We all know the old saying that men already have their hands full just trying to make bottles for their infants. If they also had to nurse, they wouldn’t have a chance. Thankfully, nature has saved them the trouble by just giving them two little pink bumps on their chest to serve as nipples. When considering the function of every part of the human body, the nipples on men may stand out as the most pointless. But why did nature retain them if they didn’t provide any milk? Just a matter of style, then?
Why do males need nipples? Except for maybe looking good on their chests, they have no practical use. And even then, this is only for the most muscular of them. Male nipples could have been lost to evolution since they are incapable of producing even a trace of milk. However, mother nature disagreed and insisted on keeping them where they belong. But to what end did this occur?
Nipples have to be traced all the way back to their beginnings so they can be properly understood. The point of this starts even before a baby is born.
During the earliest stages of development, embryos of both sexes contain basic structures that may eventually become either male or female reproductive organs (or rarely both). Whether a newborn is born male or female is determined by a combination of genes. An important master gene is located on the Y chromosome’s short arm and is known as SRY (sex-determining region Y).
About seven weeks during embryonic development, SRY is switched on. When turned on, it causes the female reproductive system to disappear while also causing the male reproductive system to develop.
However, breast and nipple development start between weeks four and six, far before the SRY gene is turned on. When this happens, there are two bumps (mammary ridges) between primitive axilla and groin. Thus, even when the mammary ridge fades later in male development, the cells that produce the primitive nipples and the nipple smooth muscle still persist in that area. The remaining cells develop into the complete breasts and nipples.
According to other scientists, nipples exist on men because the area is very sensitive for certain people. And our bodies’ erogenous zones seem crucial for reproduction.
An Early Stage of Development
In the initial few hours following fertilization, the embryo undergoes rapid and dramatic changes. Nipples are a part of normal male and female development up to a particular age. Paleoanthropologist Ian Tattersall from the American Museum of Natural History in New York, USA, says, “To put it simply, men and women are all built from the same genetic blueprint.”
However, distinctions start to become visible during the sixth and seventh weeks of pregnancy. This is because of Y chromosomal genes, which are only found in males. These predisposed male genes eventually promote testicular growth, leading to the production of the hormone testosterone. Multiple effects on the developing embryo are brought about by the chemical.
Its masculine traits mature and its genitalia fully form, but any potential for a future feminine identity is hindered. And the nipples still persist after this abrupt halt. There is no way to remove them after they have been set. The emerging male will wear them like badges of honor for the rest of his life.
Infant males and females have identical nipples and breasts. Only in puberty, when hormones are at work, do they start to alter. Both sexes experience a growth in the size of their nipples, albeit the female nipple expands more. As the female breasts enlarge and change form, the male ducts contract. The mature male nipple is smaller and more uniform in shape than the female counterpart.
What Accounts for the Evolutionary Survival of Human Nipples?
In humans, a child receives one copy of each gene from each parent at birth. Thus, a boy’s inherited characteristics should be a blend of his parents’ characteristics. From a genetic perspective, we must then ask backwards: how can men and women differ if genes are acquired from both parents?
Common examples of sexual dimorphism are the different plumage colors seen in birds and the varying sizes of male and female insects. Unless the same feature (color, for example) in men and females has been genetically dissociated, it is impossible for such disparities to arise.
This occurs when a characteristic is controlled by a distinct set of genes in males and females, when the relevant genes are situated on separate chromosomes, or when the genes’ expression has become conditional on environmental factors (if the genes are in a male or female genome). Evolutionary geneticists often assess a statistic known as genetic correlation, which represents the assumption that two qualities (here, in men and females) have a common genetic base. As a matter of course, evolution works on the assumption that sexes are genetically similar.
If the attribute is vital to the reproductive success of both men and women, yet the better or ideal trait is different for a male and a female, then we have a case of decoupling between male and female features. If the trait is essential in both sexes and has a comparable “optimal” value in both, then decoupling is unlikely to develop; conversely, decoupling is likely to occur if the attribute is important in one sex but not the other.
This is especially true for nipples. If you look at their reproductive success rates, it’s obvious that they have a distinct edge when it comes to females. The occurrence of nipples in men is likely best described as a genetic connection that survives owing to a lack of selection against them, rather than selection for them, given that the genetic “default” is that males and females share features. What this means is that evolution has not eliminated the male nipple for any reasonable cause.
Don’t Fix Something That Isn’t Broken
For what reason did mother nature make this choice? Men’s nipples aren’t very attractive, but they’re not exactly a waste of time either. Because having nipples doesn’t have much of an effect on your metabolism. Then, why get rid of something that has no purpose, does no harm, and provides no benefit? Perhaps they provide a touch of sexiness to otherwise macho physiques.
Sadly, this seems like a bit of a delusion that may end up costing a lot for some men. Because males may also have breast tumors, the disease is not limited to females. But male breast cancer accounts for fewer than 1% of all instances, and the chances are much lower for men who live healthy lifestyles.
Two of the most significant contributors to breast cancer are excess weight and alcohol intake. The key to maintaining toned nipples is a healthy diet and limited alcohol use. Those are literal “nipple-breakers.”
Cancer is a terrifying pandemic that hangs over our heads like the sword of Damocles. Innumerable individuals are afflicted by this multifaceted illness, and tens of thousands more must live with the diagnosis every day. Even with the best diagnostic tools and treatment options available, many people still die from it. Doctors are working tirelessly to determine what has triggered this cancerous multiplication of cells.
Some of the possible causes of cancer have been identified as exposure to toxins or radiation or a family history of the illness, although unlike with many infectious diseases, a direct correlation between cause and effect is usually not sufficient for cancer. The catastrophic transition from a healthy body cell to a tumorous cancer cell is often set in motion by the confluence of a number of elements. However, scientists have barely scratched the surface of this interaction’s intricate complexity.
Tumor viruses are one aspect that has gained the attention of scientists. The earliest signs that viruses may cause cancer were identified by scientists around the turn of the past century, but this information was largely disregarded for decades. In the past, there was no link between infectious agents and tumor diseases.
Despite the fact that the link between cancer and viruses was finally proven, scientists in this area faced an unprecedented wall of opposition. Ignorance, but also tenacity, has a long and illustrious history that continues up to the present day. As such, it served as a near-perfect illustration of the typical sequence of scientific progress described by Austrian engineer and author Robert Musil: “Every few years that something till then held to be in error suddenly revolutionizes the field, or that some dim and disdained idea becomes the ruler of a new realm of thought.”
More and more viruses are being added to the list of “suspects” by cancer researchers, and roughly a dozen have been recognized beyond question, demonstrating the “new realm’s” visible growth. The human papillomavirus and various herpes viruses are two examples of these ubiquitous yet purportedly innocuous infections. Viruses’ causal pathways in cancer are very vaguely understood, but researchers are working to fill up the gaps.
The discovery of the cancer virus
Chickens to revolutionize science
In the year 1909, a farmer pays a visit to a young physician and biologist Peyton Rous at his new job at New York’s Rockefeller Institute for Medical Research. He is concealing a jar with a cancerous chicken under his arm. A sarcoma, a huge cancerous tumor of connective tissue, had developed on the right side of the breast of this striped Plymouth Rock chicken.
At the time, research on cancer was still in its infancy, but Rous, who worked on the subject, jumped at the chance to do a battery of experiments using the chick and its tumor. So, he decided to produce an extract from the diseased tissue, filter it to remove any remaining cells, and then inject it into young chickens of the same breed. Unusually for the period, the healthy animals also got cancerous tumors of the same sort as a consequence of this experiment.
With this in mind, Rous deduced that the tumor was caused by a microscopic pathogen present in the extract. He suspected a parasitic creature, probably one of the recently identified viruses. Rous attempted to prove his hypothesis by successfully transmitting additional chicken cancers via this route. His findings and theorization of a cancer-causing virus were published in 1910, setting off a real “tumor wave.”
Standing on the sidelines
However, no success was found in using this method to induce growth in any other animal species. Soon after, Rous was marginalized in the scientific community, and his viral tumors were deemed to be a chicken-specific anomaly. In his acceptance address for the Nobel Prize in 1966, Rous recalled, “The results of the sarcoma virus were met with absolute disbelief.” However, “spontaneous” chicken tumors with different morphologies were successfully transplanted and a virus was found in each of them not long after.
In the 1930s, Richard Shope, a colleague of Rous’s, obtained comparable results using an extract of a benign skin tumor, a papilloma, from the skin of a wild rabbit species. However, these findings were disregarded since they were not thought to be relevant to cancer.
“Milk factor” instead of viruses
The standard medical view, that cancer was at most related to a person’s genes or their environment and could not be caused by viruses or other pathogens, appeared to be impervious to new evidence. Under the banner of “What must not be, cannot be,” any and all theories involving viruses that cause cancer were dismissed as ridiculous. In the 1930s, the United States’ highest health authority convened a council of specialists who issued a formal guiding principle that viruses and other organisms could be ruled out as causes of cancer.
Due to the atmosphere, few scientists were willing to publicly provide proof of the presence of cancer viruses. Breast cancer-causing viruses were first identified in mice by John Bittner, a researcher at the leading cancer research facility in the United States, in the late 1930s. Instead of calling the cancerous agent a virus in his paper, he called it a “milk factor,” neutrally avoiding the risk of losing his job and future research funding.
The breakthrough
The significant change, and the subsequent rise of cancer virus researchers, did not come until the late 1950s. There were two primary causes that resulted in this change: Scientists found that some viruses could introduce their genetic material into the host cell’s DNA. This modified the cells irreversibly without killing them. However, numerous scientists started to find tumor viruses in their lab tests, making it impossible to deny the undesirable reality.
According to a long-held theory, cancer and infections produced by viruses or other organisms could not be linked to one another. But a decade later, in 1966, Peyton Rous was honored for his foresight and tenacity with the Nobel Prize in Medicine, and the virus he discovered was given the honorific name “Rous sarcoma virus.“
Looking for the virus-cancer mechanism
Genome thieves
Cancer cells are the progenitors of more cancer cells and pass on their destructive capacity to their children, making them the ultimate misfits. Yet they originate in healthy tissue. But, how? What part do viruses and other pathogens play in this process? Caltech cancer researcher Renato Dulbecco was pondering this very subject. As a result of Peyton Rous’s rehabilitation, study into tumor viruses is no longer taboo, although still very little is known about how they work.
In 1960, he and his colleague Marguerite Vogt undertook laboratory experiments in which they infected hamster cells with a polyoma virus, a DNA virus with little complexity. The cells started to transform as expected, and tumors started to form. However, they immediately noticed something peculiar: the viral reproduction ceased along with the transition to cancer cells. Their numbers did not increase or decrease as they would during an actual infection since they were not able to exhaust the cell’s resources on viral production. Sure, but why?
The virus always leaves behind traces
Dulbecco could only think of two possibilities: either the virus got killed out in the process of the cell’s metamorphosis, or it survived the transformation but was unable to multiply. After much effort and testing, the scientist finally got an answer. He discovered the virus’s “footprints” in the changed cells, disproving the original hypothesis and confirming the infection was still there.
Using molecular biology techniques, he was also able to show that the virus was inactive since a key piece of its DNA had been incorporated into the host cell’s genome, rendering it inaccessible for viral replication. Only around seven proteins were encoded by the viral DNA that was added, but that seemed to be enough for cell processes to go haywire.
Contrary to dogma
A young scientist at the University of Wisconsin named Howard Temin had less luck than Dulbecco did when he published his findings and received both praise and criticism for them. Unlike Dulbecco, Temin studied an RNA virus (the Rous sarcoma virus) in his tests; yet, he reached the same conclusion as Dulbecco in a 1964 paper: the virus must add something to the cell’s genome that initiates the cell alterations. According to him, before inserting its genetic material into cellular DNA, the virus was “translating” its RNA genome into DNA, called the “provirus.”
However, he made a huge “error” by proposing this theory, since it challenged the prevailing paradigm in molecular biology at the time. This dogma states that information in live cells always flows from DNA to RNA and then to protein, but never the other way around. For this reason, most of Temin’s scientific peers would have considered his concept of a provirus that employed this “wrong” path to be heretical. The response was just as furious and condescending.
Again, it took almost a decade and the “administrative aid” of a coworker before the previously disgraced scientist was vindicated. Temin and the biologist David Baltimore delivered the killing blow to the doctrine at the decade’s close in the 1970s. Both separately found an enzyme in tumor virus-infected cells that can convert RNA to DNA. There was experimental proof that this “provirus DNA” was integrated into the cellular genome.
The seminal work on the biology of tumor viruses by Dulbecco, Temin, and Baltimore was recognized with the Nobel Prize in 1975. However, the three of them were unable to resolve the lingering mysteries of how viruses cause cancer and whether or not they also cause cancer in humans. “I do not believe that infectious viruses are the causes of most human tumors, but I think that viruses can provide us with models for the development of cancer,” Temin said cautiously in his Nobel Prize acceptance address.
Looking for a cancer gene
Can cancer viruses replicate without causing disease?
Two researchers at the U.S. National Cancer Institute, Robert Huebner and George Todaro, experimented with the Rous virus on various mammals in the 1970s, shocking the scientific community just as they were coming to terms with the discovery that cancer viruses, including and especially RNA viruses, incorporated part of their genetic information into the DNA of the cell. They found, to their shock, that viral DNA could be detected in tumor cells even when the tumors had not been caused by the virus but rather by physical or chemical effects. How could this be explained?
The “virogen-oncogene hypothesis”
Huebner and Todaro proposed that viral DNA doesn’t come “out of nowhere” since cells must already have viral genes embedded in their genetic material, which were incorporated into the genome at some point during evolution. These conserved DNA regions are inactive under normal conditions but become functional when exposed to certain stimuli, allowing them to produce viral proteins and, in turn, new viruses. However, they postulated that some of these “virogens” also operated as “oncogenes,” causing the development of tumors as well.
Hunting down the tumor gene
If this hypothesis were to hold, then the Rous oncogene must also be present in the cellular DNA of normally developing animals. Michael Bishop and Harold Varmus of the University of California, San Francisco, began a mission to match the genome of the Rous sarcoma virus with chicken DNA for this very aim. But this would be very difficult to do without high-tech equipment like PCR or sequencing devices.
Fortunately, in 1971, a serendipitous discovery by Peter Vogt of the University of Southern California revealed a viral mutant that was capable of replication but seemed to lack the potential to produce malignant tumors. The virus’s genome was 15 percent shorter than average, suggesting that this missing part could include the critical tumor gene(s).
This was the key piece of information that helped Bishop and Varmus solve the case. This allowed them to determine whether or not the “src” gene fragment was present in the cellular DNA of their guinea pigs and, if so, whether or not it functioned as a possible cancer gene. However, scientists were surprised to discover that the virus was present not just in chickens, the primary hosts of the Rous virus, but in birds of every genus and subgenus.
But that wasn’t the end of it; other researchers soon identified src variations in guinea pigs, rabbits, rats, snakes, and even humans. The oncogene postulated by Huebner and Todaro seemed to be found. Bishop and Varmus, though, were not confident in the claims. They were wary about its extraordinarily widespread distribution. The origin of the gene still remained unknown; did this gene really come from the Rous virus?
Oncogenes: a biological enigma
The enemy within
An essential step forward accomplished with the discovery of a cellular proto-oncogene. Not much time had passed, yet scientists had already uncovered over 40 distinct retroviral oncogenes. They speculated that the majority of cells had gene sequences that were homologous to a viral gene known to cause tumors. Tumor viruses and other external factors could contribute to tumor development, but there was also an “internal adversary” that might be just as crucial.
However, more questions were created by the new data than they answered. Among the most crucial, in Varmus’s words, “Did the evolutionary conservation of the src gene indicate its cellular origin? Or could it still be a virus-derived gene that was just better conserved than comparable viral elements?”
Own cell instead of being smuggled in
Rapid responses to this question emerged from many different fields. Sequence analysis, however, provided the clinching evidence. It demonstrated that the src gene was broken up into many segments by introns (“junk DNA”), which were typical of biological DNA but were rarely seen in viral genes.
Harold Varmus reflected on this, saying, “All our arguments and experiments led to only one conclusion: the precursor to src was a conserved – and therefore vital – cellular gene that found its way into the Rous sarcoma virus by recombination.” So, it seemed that the proposed evolutionary route of the “virogen oncogene” concept must have followed an exactly opposite direction.
Since the oncogene’s precursors have been conserved throughout evolution, this explained why they are found in so many different types of cells. “Far from being a harmful element just waiting to be activated by a carcinogenic signal, the precursors of viral oncogenes seem to have an impact on the organism to have an important function, otherwise they would not have been preserved in the course of evolution,” said Varmus. These genes are, in fact, involved in essential cellular processes, including multiplication and differentiation.
Hostile takeover
How, therefore, could this normally helpful gene cause an infected cell to go berserk? Bishop and Varmus hypothesized that the retrovirus identifies the benign proto-oncogene during infection and alters it into the malignant oncogene. During this process, known as transduction, the virus inhibits the gene’s regular function and removes it from the organism’s regulatory system. Therefore, the misplaced and overactive genes have undesirable effects, such as excessive cell multiplication.
The two scientists speculated that Huebner and Todaro’s peculiar results might be explained if the transition was triggered by chemical or physical forces. In 1983, researchers found a group of cellular genes that were structurally similar to viral cancer genes and oncogenes from non-viral cancers, lending credence to this theory.
Viruses as a possible cause of human cancer
Initial evidence for human T-virus type 1
By pinpointing the “inner enemy” and showing that viruses might play a role as triggers in carcinogenesis, Bishop and Varmus have thrown open the floodgates for contemporary cancer research. They shared the Nobel Prize in Medicine in 1989.
However, they encountered resistance and even contempt for their ideas. Their hypothesis, that a comparable process could possibly contribute to human tumor formation, was at odds with the current scientific consensus. But this perspective held that although viruses were identified as a cause of tumor disorders in animals, there was less evidence to support a similar link in humans. But they weren’t completely wrong since hereditary or environmental factors are still considered to be the main causes of cancer in humans.
The first human retrovirus
However, this started to change in the early 1980s. In 1980, a patient with cutaneous T-cell lymphoma, a benign skin ulcer, was investigated by virus researcher Robert Gallo and his colleagues at the National Cancer Institute in the United States. He analyzed the tissue samples and found a retrovirus, a kind of virus that had never been seen in humans. While these RNA viruses, to which the Rous sarcoma virus also belongs, had been studied for quite some time in animals, this was the first time that they had been found in people.
Gallo and his Japanese colleagues continued studying its biology and ecology in the years that followed. Scientists found an unexpected link between the virus and adult T-cell leukemia lymphoma; whereas most infected people had relatively mild skin changes over time, a small percentage had acquired this aggressive type of leukemia.
This kind of cancer often does not manifest until the age of 60, but once it does, it generally results in a swift death. It is estimated that just 1–4% of infected people actually acquire leukemia, but all patients carry the virus anyway.
And the Leukemia
So, was the virus the cause of cancer? There had to be more evidence than just finding a virus in a cancer cell. But in 1982, Gallo and his group found the viral “culprit” in the virus’s DNA. Since there was no homolog of the viral gene “tax” in the human cell genome, “tax” could not be considered an oncogene in the traditional sense. But when it was inserted into the cell’s DNA, it activated particular T cell growth factors, leading to the unchecked multiplication characteristic of leukemia. The specifics of this mechanism were, however, still little known.
The pathogen, now known as HTLV-1, or human T-cell leukemia virus, made medical history as the first virus known to cause cancer in humans. This discovery sparked what has become a decades-long effort to identify and characterize additional viruses that might cause human tumors. Even while the hepatitis C pathogen was now thought to have a role in certain kinds of liver cancer and maybe even in some forms of non-lymphoma, Hodgkin’s other RNA viruses had thus far been on the suspect list at best, with nothing yet confirmed.
Human papillomavirus (HPV) and cervical cancer
Forming a model
Human papillomavirus (HPV) is a tiny, contagious virus that may manifest in anyone’s cells. The current global prevalence of this DNA viral infection is estimated to be above 25 million. The sexually transmitted disease affects almost half of the male and female population.
Infected people may not even realize they have it. The virus is asymptomatic and may live in the skin and mucous membranes for a long time; in rare instances, benign warts may appear. In addition to its pervasiveness, HPV is also remarkably diverse, with over 130 distinct strains having been found to date. And 18 of them are particularly worrisome since they belong to high-risk categories and may cause cancer. Discovered in 1983, this link between a virus and cancer is now one of the best studied and proven anywhere. Some virologists think that HPV is responsible for at least 600,000 instances of cancer globally; other estimates place the number at between 12 and 15 percent of all tumor cases.
Two proteins that sneak into cells
The human papillomavirus types 16, and 18, are mostly to blame. More than 90% of head and neck cancers and 99% of cervical cancers have these abnormalities. In most cases, the human immune system can clear up an HPV infection in around ten months. Changes occur, however, when risk factors are introduced, such as smoking, an impaired immune system, or a particularly aggressive viral strain:
Two viral proteins, E6 and E7, are produced by the infected cells. When bound to a particular cell protein, E6 triggers that protein to label the tumor suppressor gene P53 for destruction. Consequently, the cell is deficient in a key component for preventing mutations and cancerous transformations. Another viral protein, E7, is responsible for cell death by “hijacking” a cellular protein engaged in crucial regulatory mechanisms. This causes the release of transcription factors that actively promote cell multiplication. Two proteins assist the virus in disrupting the cell’s basic metabolic and developmental processes, leaving the cell vulnerable to mutations.
However, this is by no means the sole mechanism by which HPV causes cervical cancer. In fact, new mechanisms are disclosed virtually every week. These two, though, are the sharpest and most consequential.
The dirty dozen
Researchers have had a hard time finding new tumor-inducing viruses due to the intricacy and variety of the processes and regulatory systems already engaged. This is one of the reasons why just a handful of anti-cancer drugs that target viruses have been shown to be effective in people.
Epstein-Barr virus (EBV) for nasopharyngeal cancer and Hodgkin’s lymphoma; hepatitis viruses B and C for liver cancer; human T-cell lymphotropic virus type 1 (HTLV-1) for cervical cancer; and human herpesvirus 8 (HHV-8) as a trigger for Kaposi’s sarcoma are all well-established viruses that cause cancer in humans. Polyomavirus and hepatitis C for non-Hodgkin’s lymphoma, and an unidentified agent for a kind of pediatric leukemia, remain on the list of possible tumor-causing viruses. The tally of cancer viruses in humans that have been “condemned” continues to increase today.
Helicobacter pylori and stomach cancer
Several kinds of cancer in humans now have a known link to infections with certain viruses, bacteria, and parasites. 15–20% of all malignancies are believed to have an infectious cause. But we weren’t always aware of the cancer-causing bacteria. In fact, this medical dogma was toppled anew by a dogged scientist, a little bit of self-experimentation, and a giant leap forward. The Australian scientist Barry Marshall, his colleague Robin Warren, and the rod-shaped bacteria Helicobacter pylori are the story’s primary characters.
In 1982, the medical community accepted the dictum that “Bacteria are everywhere—but the human stomach is bacteria-free.” Because of the very acidic conditions present in the stomach, it was often believed that no bacteria could thrive there. And that was not all. The majority of medical professionals and scientists in the field of pharmacology, as well as patients, attributed the pain of gastric mucosal inflammation and subsequent gastric ulcers to the presence of acid in the stomach. The pharmaceutical industry promoted acid blockers of different sorts with the slogan “No acid, no ulcer,” and sales were booming as a result.
Its home is the stomach
Pathologist Robin Warren found something that shouldn’t be there when he examined tissue samples from stomach ulcers and irritated stomach mucosa under a microscope: bacteria that are full of mucus. And that was the case in over half of the samples he tested. The number of these cells seemed to be correlated with the degree of inflammation. Warren consulted with doctor Barry Marshall after concluding that his finding must be significant.
As a team, they achieved the first successful cultivation of the bacteria. They could now undertake microbiological experiments to learn how the bacteria manage to thrive despite the harsh circumstances of the stomach. To begin attaching to the mucosal cells, bacteria first use their flagella to dig deeply through the protective mucus layer. Meanwhile, they used an enzyme called urease to convert the uric acid produced by the cells into carbon dioxide and ammonia. This created a neutral environment that bypassed the stomach’s defense against microbes.
A sip alters the course of history
However, these results did not establish beyond a reasonable doubt that this particular bacteria caused an inflammation or cancerous tumor. Because the conclusive evidence was still absent. In July of 1984, after months of testing, Marshall decided to take a daring step: he began testing on himself. On the informal principle of “a small sip for a person-a big sip for medicine,” he consumed a brackish solution containing billions of germs. As Marshall reflected, “Everyone said, you’re crazy. It seemed like too incredible an explanation for something as complex as stomach ulcers.”
In a matter of days, he started feeling sick, like he had the flu, and in two weeks, he had gastritis. With the use of a tissue sample, he was able to see that his mucosal cells were covered in a thick layer of germs. Thus, Marshall successfully exposed Helicobacter as the true culprit in the inflammatory process. At that time, though, the link he suggested between the bacteria and stomach cancer had not been proven.
The murderer’s in the blood
However, since then, his theory has been independently verified: antibodies may indeed identify the bacteria in the blood. Three further significant epidemiological investigations followed this. Scientists looked for Helicobacter antibodies in the blood of thousands of stomach cancer patients, whose blood was collected and preserved decades ago as part of earlier research, and compared the findings to the values of a similarly large sample of patients who did not have cancer of the stomach.
Those who were infected with Helicobacter 20 years ago had a six-fold increased risk of developing cancer compared to those who were now free of Helicobacter. These findings were so compelling that in 1994, the World Health Organization’s International Agency for Research on Cancer (IARC) officially labeled Helicobacter pylori a class 1 carcinogen, the first identified bacteria capable of causing cancer.
Terms related to viruses, cancer, and genes
Most of what we know about how genes play a role in cancer was uncovered via studies of tumor viruses. The relative simplicity of the viral genome has been the only thing that has allowed researchers to identify, or at least narrow down the DNA building blocks involved in the formation of human cancer.
The link between viruses and cancer has been recognized to exist in animals since the middle of the past century, but only in people since the 1980s. Unlike animal tumor viruses, however, the link between human cancer viruses and the disease is based on correlations or presumed processes rather than a clear cause-and-effect premise. The viruses have a role as either cofactors or cocarcinogens in this scenario. This demonstrates undeniably that the process of carcinogenesis in humans is intricate and multi-staged.
At least six families of DNA viruses and two families of RNA viruses are suspected in the development of cancerous human tumors. Among the examples are Retroviridae and Flaviviridae as RNA virus families and Hepadnaviridae, Herpesviridae, and Papillomaviridae as DNA virus families.
RNA viruses:
Those are the viruses that employ RNA rather than DNA to store their genetic information. Single and double-stranded forms of the RNA are possible. Examples of RNA viruses include influenza, polio, and Ebola; the hepatitis C virus has been linked to cancer.
Retroviruses:
The retrovirus family is also an RNA virus. To integrate their genome into the host cell’s chromosome, retroviruses employ the enzyme reverse transcriptase to create a DNA translation of their genome. Here, it is incorporated into the DNA of the cell for good. The AIDS virus and HTLV-1, a virus linked to leukemia, are examples of such pathogens.
DNA viruses:
These viruses have their genetic material in the form of DNA and may thus integrate it into the host cell’s genome without first requiring “translation.” Herpes viruses, human papillomavirus (HPV), linked to cervical cancer, and Epstein-Barr virus, linked to certain types of leukemia, are all examples.
Transduction/transformation:
This is the process through which healthy cells mutate into cancerous ones. This mechanism has been greatly elucidated by the capacity of viruses to convert cells in culture. The altered cells display hallmarks of cancerous tumors, including unchecked multiplication, reduced reliance on supporting tissue, and less need for external growth hormones. When transplanted into a new host organism, some altered cells may potentially become cancerous.
Tumor virus transformation of a cell always exhibits the following three characteristics: it is a “one-hit” process, meaning that the transformation is triggered by a single viral infection of the cell. In addition, the cell retains some viral genetic information, and the transformation is maintained by the continued production of a subset of viral genes.
Oncogene:
A gene that has a significant role in causing or facilitating the progression of cancer. Point mutations, rearrangement of its DNA building blocks, loss of individual segments, and excessive, uncontrolled gene expression triggered by viruses all contribute to its activation and transformation into a tumor gene. The Greek term for “mass” or “lump” is whence we get our modern word “onco.”
Cellular Oncogenes:
An oncogene may mean either a normal gene that has been changed to become active in tumor cells or a cellular gene that has been activated in tumor cells.
Viral Oncogenes:
DNA viruses may cause cancer because they include a gene that isn’t found in cells but has the potential to do so when infected, or because they contain a version of a normal cellular gene that has been changed or activated to operate as a tumor inducer.
Proto-oncogene:
A precursor of both viral and cellular oncogenes, a normal gene of the cell that may be turned into an active oncogene by external factors.
Tumor suppressor gene (TSG):
Genes encoded by a cell’s own DNA inhibit cancerous transformation. These genes may have a bigger effect on carcinogenesis than the active oncogenes.
Woolhouse M, Scott F, Hudson Z, Howey R, Chase-Topping M (2012). “Human viruses: discovery and emergence”. Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences.
The written version of our genetic instruction manual, which has 3 billion letters, would take up many volumes’ worth of space in real life. However, it is only contained inside the tiny cellular structure of our body. From our gender to our physical characteristics to our susceptibility to disease, practically every aspect of our lives is determined by the choices our ancestors made. However, for a very long time, no one knew what this genetic code looked like and what it contained. Scientists eventually uncovered the shape, language, and exact function of our DNA, with some unexpected findings along the way.
The genetic specifications for all known creatures and many viruses are stored in a deoxyribonucleic acid or DNA, a polymer made up of two polynucleotide chains that coil around each other to create a double helix. DNA governs development, functioning, growth and reproduction.
Two men did change the world of science
In a statement made 70 years ago, according to James Watson, only a few discoveries have been of such exquisite beauty as DNA. Watson was referring to the double helix, a structure that is 2.5 nanometers in diameter, looks like a helically twisted rope ladder, and stands 7,2 feet (2,2 meters) in length if fully unfolded.
On April 25, 1953, James Watson and Francis Crick published a single page in Nature proposing a model for the three-dimensional structure of deoxyribonucleic acid (DNA), the molecule that encodes human genes.
It seemed that the two researchers were confident in the long-term relevance of their model since they cited “novel features of considerable biological interest” at the start of their paper.
Zero interest in chemistry
Although at first glance, it did not seem likely that two “scientific clowns,” as scientist Erwin Chargaff dubbed them, would produce such a groundbreaking discovery. James Watson, who was very talented, began studying biology at the University of Chicago when he was only 15 years old. Birds were his major focus at the time, thus he was able to avoid taking any science classes.
The zoologist’s understanding of chemistry and physics was quite limited when he first arrived at the Cavendish Laboratory in Cambridge, England, in the autumn of 1951, at the tender age of 23. In England, he met British scientist Francis Crick, who was 13 years older and whose loud laughing was the bane of his colleagues’ existence. Francis Crick’s prior life as a researcher was summed up by the institute’s director, Sir Lawrence Bragg. According to him, Francis was talking ceaselessly and had come up with next to nothing of decisive importance.
A scientific footrace
In 1949, Erwin Chargaff discovered that the DNA bases adenine, thymine, cytosine, and guanine always occur in DNA at a 1:1 ratio, or most likely in pairs. The next step was to figure out the structural integrity of the bases and how they fit together. Watson, who was originally uninterested, attended a presentation by neighboring King’s College London scientist Rosalind Franklin in November 1951, during which she shared recent X-ray diffraction photographs of DNA.
Waston found intriguing her speculation that DNA could exist in a twisty helical shape with two, three, or four twists. As soon as Watson and Crick got back to Cambridge, they set out to try to replicate this structure. They hypothesized, based on chemical calculations, that the structure would consist of three chains joined in a helix by magnesium ions, with the molecular arms pointing in all directions.
Success through failure
Watson, however, was not paying close attention, and the team’s model of the chemical reaction turned out to be incorrect. They made a disappointing appearance in front of Rosalind Franklin and London-based biophysicist Maurice Wilkins.
Colleagues were quite harsh in their criticism. Previous X-ray images produced by these two scientists had demonstrated conclusively that the supporting chains could not lay within, refuting the premise of Watson and Crick, and that magnesium ions were scarcely capable of maintaining this structure.
In July of 1952, Erwin Chargaff visited Watson and Crick in the lab and delivered a similarly damning assessment of their scientific prowess: “enormous ambition and aggressiveness, coupled with an almost complete ignorance of, and a contempt for, chemistry…”
When it became public that famous scientist Linus Pauling, on the other side of the Atlantic, shared a fascination with the structure of genetic information and suggested a model for it, the scientific reaction intensified. Urgency necessitated swift action.
Then, towards the end of 1952, Maurice Wilkins offered Watson and Crick an X-ray structural study of his colleague, Rosalind Franklin, which proved to be a pivotal event that ultimately led to triumph. It was, in fact, a picture of a recently discovered DNA structure. But this was all without Franklin’s consent.
By the end of the study, the two scientists had reached a consensus: DNA is made up of two strands that intertwine with each other like rungs on a rope ladder. Hydrogen bonds hold their molecular appendages, the complementary bases, together. Finally, Watson and Crick assembled their metal double helix structure like pieces of a jigsaw. This variation won over even the most skeptical people.
Recognition and respect
Many scientists date the beginning of molecular genetics to the publication of the “Watson-Crick Model” of the structure of DNA. James Watson, Francis Crick, and Maurice Wilkins all split the 1962 Nobel Prize in Medicine and Physiology equally. In contrast, Rosalind Franklin, whose research offered the last vital piece of the puzzle, came up empty. Sadly, she passed away from uterine cancer in 1958, when she was only 37 years old, without seeing the fruits of her labor. It’s safe to say that most people nowadays have forgotten who Franklin and Wilkins were. But the names Watson and Crick will forever be linked to the double helix model of DNA.
The exchange of information
Translation of genetic code
Since 1953, scientists have understood the fundamental nature of our DNA and that it includes the blueprints for every aspect of our identities, from physical appearance to health. It was quickly understood that each base pair represented a different letter in the manual. The question is how to give form to these inscrutable directives and create a live, breathing, and authentic human being.
In every human cell, two sets of 23 chromosomes are created when an egg from the mother and a sperm from the father fuse. The maternal contribution to these roughly X-shaped structures is half, whereas the paternal contribution is half.
We store and carry our DNA, or genetic information, in a compact form called chromosomes. All of our DNA, together with its protective envelope structures, is stored in a very condensed form on the many chromosomes in our bodies.
The sequence of bases as the alphabet of life
The typical RNA codon table is structured in the form of a wheel.
Adenine (A), Guanine (G), Thymine (T), and Cytosine (C) are the four bases that make up DNA. The two strands of DNA’s framework are held together by the pairs A-T and C-G. They serve as the rungs on this hereditary ladder. When you align the ladder segments of a single DNA strand, you’ll see a lengthy string of base letters.
And it is in them where the genetic code is found. Three of these letters are put together to spell out a word that specifies where in the process the production of protein should include a certain amino acid. A string of these letters forms a phrase, which in turn becomes the blueprint for a protein. And these molecules, in turn, play the role of a biochemical housekeeper who makes sure everything from cell and tissue formation to signal transduction and metabolic processes go smoothly.
Transcription and translation of DNA
Genes and proteins
How, however, does the blueprint for a structure end up as a protein? The process of making proteins from scratch is called biosynthesis. At this phase, the genome must be unpacked so that the information for a protein can be read from DNA. Generally found as a double strand, DNA separates into two single strands. Thus, the free arms of the rope ladder become accessible.
Enzymes have now made it possible to make carbon copies of this segment of the strand by simply joining a complementary base to each of the free arms. This time around, though, the base uracil bonds to the adenine instead of the thymine. In this case, however, the ribonucleic acid (RNA) serves as the scaffolding for these newly joined bases. After the copy is complete, enzymes cut the RNA strand and its accompanying DNA bases away, creating a copy of this region of the genome that can be moved throughout the cell, the messenger RNA (mRNA). Transcription refers to this process of making a copy of the genetic material and rewriting it.
Translation into protein building blocks
A ribosome’s translation of mRNA and protein synthesis is shown in this diagram.
However, this is just the beginning. mRNA now transports the genetic information copy from the nucleus into the cell plasma, where it will be read by the ribosomes and used to make proteins.
The mRNA is sandwiched between the two subunits, one larger than the other; this creates a reading unit similar to the needle on a tape recorder. It decodes the genetic code by identifying which of the three bases (and hence which genetic code word) is present in each instance.
Simultaneously, many of the amino acids that will make up the future protein accumulate on the ribosomes, each of which has a tiny piece of RNA consisting of precisely three base letters connected to it. These letters and numbers serve as a label, identifying the specific amino acid bound to this transport RNA (tRNA). It is the job of the ribosome to dock and connect the component of the amino acid that corresponds to the coding of the next amino acid in the read-out mRNA.
Polypeptides, or chains of amino acids, are produced in this fashion and are the building blocks from which proteins are assembled. DNA can only perform its job via translation, the process by which the genetic information is converted into a chain of amino acids.
Junk DNA
Discarded material transformed into a control center
A gene is a set of instructions for making a particular protein; it consists of a specific sequence of the base pairs cytosine, adenine, guanine, and thymine. It’s the blueprint for these critical messengers of our body’s processes.
It was quickly discovered, however, that significant portions of human DNA lacked any recognizable construction instructions. Sequences in an organism’s DNA that do not code for proteins are known as noncoding DNA (ncDNA). They looked to be made up of illogical and repeated DNA sequences that had no discernible purpose. Therefore, scientists called these pieces of DNA “junk DNA.”
Only 2% of your genes are real
However, scientists were baffled when they looked more closely at the breakdown of our genetic material and saw that around 44% of it is “junk” in the form of several copies of genes and gene fragments (repeats).
In addition, 52% seems to be useless as well and does not code for proteins. However, only around 2%–4% of human DNA is made up of genuine protein-coding genes.
It has long been a puzzle as to why evolution has preserved so much irrelevant DNA in addition to these gene sequences. But this issue was first answered by research in 2004. Scientists in the United States revealed a startling discovery about this “living genome deserts” that many regions of DNA that do not code for proteins were far from inactive. They include sequences that may activate or silence other genes, even if they are located far away.
A regulator made of “junk”?
This suggests that the genome’s so-called “junk” is playing a significant role in regulating gene activity, helping to shed light on the basic differences across species even though their genes are, on average, just a few percent different.
Also, scientists from LLNL and JGI found that different parts of junk DNA have experienced different degrees of modification during evolution. There are several non-coding regulatory elements in the “desert areas” that are resistant to rearrangement and defend themselves via repeating junk DNA patterns. It appears that genomic regions known as stable genome deserts are essentially hidden gene regulatory components that preserve the intricate function of neighboring genes.
About two-thirds of the genome deserts and about 20% of the overall genome could be gene segments that are completely useless for biology, indicating that most of the genome is redundant. At least, 75 percent or more of our genetic material is really just junk and only around 8–14% of our DNA is functional in some way.
Our genome is governed by junk DNA
Junk DNA and genome desert.
The term “junk DNA” refers to the 98% of the human genome that does not code for proteins but the truth is actually more complicated.
Because this notion of mostly useless junk DNA kind of shattered in 2011. The international ENCODE project discovered something astounding: almost all of our junk DNA functions as a massive control panel for our genome, containing millions of molecular switches that can activate and deactivate our genes as needed, including in regions where only an “unstable desert” had been suspected.
The “junk” has millions of switches
Scientists created a detailed map of the locations and distributions of control elements, which revealed that the control switches are often located in inconveniently distant genomic regions from the genes they regulate. However, due to the complex three-dimensional shape of the DNA strands, they can still come close and exert their regulatory effects.
That means, our genome is only functional because of switches: millions of buttons that control which genes are active.
Genes derived from junk DNA
But junk DNA has other, non-regulatory functions too; scientists from Europe identified a gene on mouse chromosome 10 that appeared out of nowhere but originated between 2.5 and 3.5 million years ago via genome-wide comparisons. The gene was the only one positioned in the center of a lengthy non-coding chromosomal part. This area is present in all other mammalian genomes as well. However, the gene is only found in mice.
There was some speculation that a gene may emerge at a place in the genome that had never been used before, but no evidence for this had ever been found. Yet it was discovered that the mutations that only occur in mice could be responsible for the new formation of the gene.
This demonstrates that the regions of DNA that do not code for proteins are an essential component of our genome and that they have long played a significant role in a variety of modern genetic analyses.
DNA and forensic science
It was all solved via a DNA analysis
You can identify a criminal by his genetic fingerprint from as little as a drop of saliva on a Coke bottle or cigarette filter, a few skin cells beneath the victim’s fingernails, or blood on his clothes.
Most of our bodily fluids also contain cells from our body, and with them our genetic information. Skin cells are always left behind when a hand is dragged along a rough surface or is scratched, and these cells carry our DNA.
However, there is a catch: there is far too little genetic material in the crime scene that remains for analysis, and this is precisely the reason why DNA analyses from such relics were unattainable for a long time. These genetic material remains can tell investigators whether or not their suspect was the perpetrator.
The polymerase chain reaction for DNA testing
But in 1983, US scientist Kary B. Mullis came up with a plan to multiply the few amounts of DNA that obtained and, in the process, devised one of the most pivotal techniques in genetics and biotechnology: the polymerase chain reaction (PCR).
A DNA fragment of up to 3,000 base pairs in length is heated to 201 to 205 degrees Fahrenheit (94 to 96 degrees Celsius), which breaks the hydrogen bonds between the bases of the double strand, resulting in the separation of the helix into two single strands. Two primers are then added to the DNA solution.
They bind to certain places on the DNA segments (based on their structures) and signal the beginning of the copying process, which is carried out by a heat-stable enzyme called polymerase.
At a temperature of 140–160 degrees Fahrenheit (60–70 degrees Celsius), it joins DNA-building components floating in solution to produce a perfect replica of the sequence designated by the primers, leading to another double strand and doubling the original amount of sequences.
Once the PCR is finished, the few remnants from the murder scene become a solution containing millions of copies of the perpetrator’s DNA, thanks to the process of repeated cycles in which the double strands are split from one another and then supplied with new halves by the polymerase.
A unique repeat pattern
The testing phase can now begin, with researchers comparing only small fragments of the DNA rather than the full sequence (which would take too long and be too laborious).
These fragments are found in the genome’s non-coding regions and are made up of several repeating base sequences termed “short tandem repeats” (STRs), which provide a unique genetic fingerprint since their numbers vary from person to person.
In many countries, a standard DNA analysis at a criminal lab includes testing for eight STR systems over several chromosomes and one sex-differentiating characteristic, which should be more than enough to rule out the possibility of a chance match.
Estimates suggest that the number of people with whom our unique STR pattern is shared is less than one in a billion, with the exception of identical twins. If a suspect’s genetic fingerprint matches that found at the crime scene, then it’s likely that s/he committed the crime in question; her/his own DNA has in fact convicted him.
Probing the paternity of a child
The mother’s identity is generally evident since she gives birth to the kid (barring surrogate moms), but the identity of the father is not always so clear.
It’s possible that the question of paternity won’t come up until the child is an adult if the woman has cheated on her partner in secret or if she gets pregnant shortly before breaking up with her partner and keeps the baby from him.
Numerous laboratories around the world have long offered such gene-based paternity tests online, and the process for those willing to take the test is very simple: just send in a saliva sample, a few hairs with a hair root, a baby’s pacifier covered with spit, or a piece of chewing gum that has been well chewed.
First, the DNA is extracted from the samples and amplified by polymerase chain reaction (PCR) in the lab; next, the DNA is compared to samples of the same genetic material from the child’s father or, ideally, the mother.
Short tandem repeats (STRs) are also used in forensic DNA analysis, and the frequency with which a given base sequence is repeated within an STR marker varies from person to person but is passed down from parents to offspring. Each person carries two STR marker variants at each gene locus, one inherited from mother and one from father.
In contrast, if the genetic material of the parent and child differs at three or more STR markers, paternity or maternity is considered to be ruled out. The probability that two unrelated people will have the exact same pattern of repeats at these markers is just one in 100 billion, according to current estimates.
The Human Genome Project (1990-2003)
Human Genome Project. Image credit: Encyclopædia Britannica, Inc.
Learning by reading life’s book
In the year 2000 in the United States, Bill Clinton and his British counterpart, Tony Blair, arranged for an unusual news conference in Washington. Nothing less than the human DNA itself was at stake here. The decoding of our genetic composition has been publicly announced by Clinton and, following him, by representatives of two rival research organizations, one government and one private.
And in 2022, scientists finally announced that they finished decoding the entire human genome. According to that, about 30,000 human genes are housed in the nucleus of each human cell, where they are contained in 23 chromosomal groups.
Humanity’s next big thing
An early version of the “Book of Life” has been deciphered by both the worldwide Human Genome Project (HGP) scientists and genetic engineering pioneer Craig Venter and his business Celera. About 3.1 billion letters make up our genome, which is composed entirely of apparently random sequences of the four nucleotide bases (adenine, cytosine, guanine, and thymine).
From the neurons that carry impulses throughout the brain to the immune cells that help protect us from external attack, each of the trillions of cells that make up our bodies has the same 3.1 billion DNA base pairs that make up the human genome.
It’s still not fully known what words and sentences may be constructed from these letters, as well as where certain functional units of genetic material are buried.
The decipherment of the human genome paved the way for novel approaches to illness prevention, diagnosis, and treatment. But these 3.1 billion letters of sequence in one human DNA were only the beginning of the long road to deciphering the human genome.
Interesting, but impossible
Things looked very different 25 years ago. In 1985, a group of genetics experts at the University of California, Santa Cruz, were approached by biologist Robert Sinsheimer with an unusual proposal: Why not try to sequence the human genome? The response was as unanimous as it was unequivocal: bold, exciting, but simply not feasible. Decoding even small sections of DNA was still too laborious at this time.
However, one of the researchers involved, Walter Gilbert of Harvard University, did not give up on the idea. About 20 years ago, he and a colleague were the first to develop a method for reading out the genetic code or genetic sequencing.
However, potential backers were still cautious, asking, “What if it turns out that the entire thing is not worth the massive effort?” and “Shouldn’t we possibly start with the genome of a small, less sophisticated creature, such as a bacterium?”
Genome arms race
Finally, in 1988, the U.S. National Institutes of Health (NIH) was convinced to organize a project to decode the human genome, led by none other than James Watson, one of the two discoverers of the double helix structure of DNA.
Understanding of the disease genes
However, progress has been sluggish since researchers were always debating whether or not it would be more efficient to begin by searching for illness genes rather than meticulously sequencing everything.
Craig Venter, a geneticist at the National Institute of Neurological Disorders and Stroke (NINDS), stood out because he and his colleagues had created a novel approach to discover gene fragments at an unparalleled rate, but without understanding their function.
Watson opposed and publicly complained about the sellout of genetic material which was met with early enthusiasm by NIH leaders since, if patented, these genes could be converted into cash. The fallout was seen when Watson was replaced as project head by Francis Collins in April 1992.
Not fast enough
Collins made a dismal prediction in 1993 that human genome sequencing wouldn’t be finished until 2005 at the earliest if things kept moving at their current rate. Part of the reason for this was the lack of resources that have so far prevented the development and widespread use of state-of-the-art DNA sequencers, which would greatly facilitate the automation of the genome decoding process.
On the other side, achieving a success rate of 99.99 percent was a need. After all, international research institutes were joining the effort at an increasing rate.
Upon meeting Craig Venter in 1995, the HGP researchers and management were rudely roused. As part of his new job at a commercial corporation, Venter released the first genome of a fully developed organism, that of the Haemophilus influenzae bacteria. He had accomplished it in a year because of the cutting-edge computing power available at the time. While progress was being made by Collins and the HGP researchers, it was slower than some would like.
Head to head
At the 1998 annual gathering of genetic experts, Venter pulled off his next move by announcing that his new firm would be able to decode the human genome in three years for a quarter of the cost of the HGP. He would be assisted by an automated sequencing system currently under development.
At this point, Collins and his group must take action. Six months later, they announced that instead of waiting until 2005, full genome sequencing was now expected to be completed in 2003 thanks to increased efforts. They wanted to provide the first functional version of the human genome that is around 90% valid by spring 2001.
It seemed like Craig Venter and his business, Celera, were in for a close finish. In reality, though, efforts to establish a mutually agreeable human genome resolution had already begun behind the scenes.
The HGP suggested holding a combined press conference to announce the initial versions of both projects at the same time on July 26, 2000. While the HGP had been publishing their sequencing in the British journal “Nature,” Venter and his colleagues had been contributing to the rival American journal “Science.” The unveiling of the virtually entire human genome was announced two years ahead of schedule, on April 14, 2003.
Thus, in April 2003, the Human Genome Project (HGP) was announced as completed but only around 85% of the genome was actually included. 15% of the remaining human genome was sequenced only by January 2022.
Dictionary of genetics
Amino acids
20 amino acids are the fundamental building blocks of proteins, and the genes determine the order in which these amino acids are put together to create a chain.
Bases
The nucleotides adenine (A) and thymine (T) and cytosine (C) and guanine (G) are paired with one another in double-stranded DNA through the complementary base pairing concept. Thymine (T) is switched out for uracil (U) in the ssRNA (single-stranded RNA).
Chromosomes
Chromosomes, which contain an organism’s genetic information, number 46 in humans thanks to the duplication of the 23 chromosomes found in each of our cells.
Codon
An amino acid’s genetic code is encoded in a sequence of three bases.
DNA
Deoxyribonucleic acid is a double-stranded molecule composed of a sugar backbone (deoxyribose) and a phosphate group, and a linear series of base pairs. The two single strands are complementary to each other, run in an antiparallel direction, and are kept together by base pairs.
DNA sequence
An order of the DNA molecule’s construction order.
Dolly
A well-known cloned sheep that was cloned in 1996 from an adult sheep’s single cell.
Gene
Genes are sections of DNA. In eukaryotes, genes are often made up of coding sections (exons) and noncoding sections (introns). Coding portions (exons) carry the genetic information for creating proteins or functional RNA (e.g., tRNA).
Genetics
Molecular genetics investigates the fundamental laws of heredity at the molecular level, whereas classical genetics focuses on the inheritance of characteristics, especially in higher species. Applied genetics focuses on the breeding of economically highly productive crops and animals.
Genetic code
The genetic code is a kind of encryption used to store information on DNA, and it is represented by a set of three-base pairs in all known forms of life.
Genetic fingerprint
Genetic fingerprints are unique to each person and are generated by using so-called restriction enzymes and undergoing further analytical processes.
Genome
A genome refers to the whole set of genetic instructions for a certain organism.
Human Genome Project
An international effort funded by many agencies to investigate the DNA sequence, protein function, and regulatory mechanisms of the human genome.
Gamete
Gametes are sexually reproducing cells (eggs, sperm) that contain just one copy of each of the 23 genes found in the human genome, which is called haploid (in humans).
Cloning
Producing offspring with the same genetic material by cell division or nuclear transplantation.
Mutation
Mutations, which may be caused by anything from exposure to ultraviolet light or naturally occurring radioactivity to the simple passage of time, are the fundamental mechanism by which new species are created and evolve.
Nucleic acids
Both DNA and/or RNA
Nucleotides
A phosphate group, a sugar, and a base make up the three components of the DNA-building block.
Nucleus
The nucleus is the membrane-bound organelle that houses the cell’s chromosomes.
Peptides
Peptides are compounds made up of two or more amino acids, which can be the same or different. Peptides are classified according to their length, with dipeptides consisting of two amino acids, tripeptides of three, oligopeptides of two to nine or ten amino acids, polypeptides of ten to ninety-nine or one hundred amino acids, and macropeptides of one hundred amino acids or more being considered proteins.
Polypeptide
Chain of ten or more amino acids held together by peptide bonds.
Polymerase
The protein-making enzyme uses DNA as its template.
PCR (Polymerase Chain Reaction)
In 1985, Kary Mullis devised a method of enzymatically amplifying tiny amounts of DNA to provide enough material for genetic analysis of nucleic acid sequences.
Protein biosynthesis
Translation and transcription are two steps in the protein production process, which takes place on ribosomes inside a cell. Enzymes, hormones, and antibodies are all examples of proteins. Protein is a class of molecules that is predominantly made up of 20 distinct amino acids.
Proteome
Complete set of proteins in a cell, organ, or tissue fluid.
Purine bases
Adenine and guanine are two examples of purine bases.
Pyrimidine bases
DNA and RNA both use the pyrimidine nucleotide uracil, however, RNA uses cytosine and DNA uses mostly thymine.
Restriction enzymes
DNA scissor enzymes are enzymes that detect a particular sequence of letters on DNA and cut the DNA at that sequence.
Ribonucleic acid (RNA)
Ribonucleic acid (RNA) is the “little sister” of deoxyribonucleic acid (DNA), a single-stranded nucleic acid molecule involved in protein production in which the nucleotide uracil (U) replaces thymine.
Ribosome
The ribosome is the cell’s “protein factory,” where proteins are made by reading a copy of a gene.
Telomeres
Normal cells may undergo around 2,000 cell divisions before showing signs of wear and tear, during which time DNA ends (telomeres) that do not carry genetic information shrink.
Transcription
The overwriting of a gene’s DNA into messenger RNA (mRNA).
Translation
The method carried out by ribosomes whereby a protein is synthesized from its constituent amino acids.
Virus
Pathogenic biological structure made up of proteins and nucleic acids that may infect, replicate, and kill host cells.
Viruses are dangerous because they rely on a “host” organism for their metabolism.
Cell
DNA is packed into chromosomes in the cell nucleus, making the cell the smallest reproducing unit in higher animals.
Ouch! When you accidentally bump into anything or strain a muscle, you feel it right away. Instinctively, you go for the source of the pain. You try to stroke the pain away by gently rubbing your fingers over the hurt spot. But, why do we do that? The question is whether or not this touch has the potential to alleviate discomfort.
Actually, yes. Massaging the skin may really relieve severe agony. As a result of the nerve impulses stimulated by this contact, the experience of pain is lessened. This is because stroking sends information directly to the brain, bypassing the spinal cord. The slow, repeated touches are sent not as regular tactile stimuli but rather as a special form of pain input. By grasping the area in pain, this new stimulus takes the place of the actual pain stimuli in a way.
The skin where this grasping or touching happens consists of special nerve fibers called C-fibers. These thin nerve cords do not have a myelinated sheath and therefore only conduct signals slowly. The ends of these fibers are located in all the hairy skin areas of our body. Each C-fiber collects the signals from about 0.155 square inches (1 square centimeter) of skin and passes them on to the brain.
There are two possible pathways for the onset of pain
But how does rubbing the painful area on the skin function in practice? The skin’s pain receptors are among the first to go into warning mode after bumping into something. There are now two pathways for transmitting this pain signal to the brain. Extra-quick pain-sensing nerve fibers make sure we feel the damage as soon as it happens, often in the form of a sharp stab. In the case of a hot stove top, for instance, this early warning allows us to avoid injury. Or to automatically reach the location where we banged into anything.
However, at the same time, the slower C-fiber transmits the pain signal. The dull, constant discomfort is caused by the signal reaching the brain. You then send positive “stroking signals” to the place that hurts by rubbing your palm over it. Even if the brain gets pain signals from the same location at the same time, these rubbings are not actually blocked. In fact, these stroking impulses serve as a barrier against actual pain.
What makes self-touching so effective against pain?
It’s worth noting that self-touch enhances the efficacy of these strokings. So far, this is what the findings of a study led Patrick Haggard of University College London show. The scientists had participants rate the intensity of a heat ache on their finger after touching their hand or after having it touched by another person. A decrease in discomfort of 64% was seen only when the test subject touched the area with their own hand.
The intensity of our pain sensation is determined not only by the strength of the pain impulses that make it to the brain but also by how the brain combines those signals into its picture of the body. Apparently, self-touch aids the brain in assigning and integrating information from the damaged body region. Consequently, this tends to lessen the sensitivity to touch.
Even in the womb, unborn offspring respond to taste cues, learning what their mother consumes via the amniotic fluid. Recently, scientists have used ultrasonography to directly see this response for the first time. Babies seemed to smile when they tried the sweet carrots, but their mouths scrunched up when they smelled the bitter-tart kale. The smell of kale causes the fetus (in the picture above) to put up a defensive face.
The unborn child’s sense of taste develops before its other senses, including hearing and sight. In the eighth week of pregnancy, the first taste receptors appear, and by the time the baby is 15 weeks along, it is able to taste the amniotic fluid it is ingesting. By this time, the infant has picked up on the mother’s eating habits. Numerous studies with infants provide evidence that these first tastes significantly influence what kids want to eat as they grow up.
Vegetable Smackdown: Carrots vs. Kale
Now, researchers led by Beyza Ustun of Durham University are utilizing high-resolution 4D ultrasound pictures to show how a fetus reacts to different tastes in the amniotic fluid. These photographs provide the first clear glimpse into the unborn child’s reaction to various flavors. In their research, for the first time, they were able to see these responses.
One hundred pregnant women consumed a capsule of a test flavor on an empty stomach at 32 and 36 weeks of pregnancy. Each capsule included either 400 milligrams of sweet carrot powder, 400 milligrams of tart and bitter kale powder, or 400 milligrams of a neutral-tasting control material. In order to prevent her reaction from influencing her child, the mother was unable to tell which flavor she was receiving while swallowing. The researchers started documenting the baby’s responses through ultrasonography after the capsule had made its way through the stomach.
Unborn Babies Expressed Their Emotions Clearly
After consuming amniotic fluid, this unborn kid smiles because it responds favourably to the delicious carrot powder that the mother had previously consumed. (Image: “Fetal Taste Preferences Study (FETAP)/ Durham University)
Indeed, fetuses’ facial expressions were seen within 30 minutes after the mothers ingested the aroma capsules. In this little time frame, the aroma compounds had made their way from the small intestine into the circulation and then through the placenta into the amniotic fluid. The unborn babies’ mostly neutral facial expressions were altered in a distinctive manner depending on the exposed aroma.
When their mother had ingested the delicious carrot powder, the offspring would open their mouths wide, as if smiling, or pucker their lips, as if sucking. The expression was different when the pregnant women were exposed to the bitter taste of kale, as their unborn children’s responses included squeezing their lips together and/or rising their upper lips. According to the research group, their faces mirrored the defensive emotions of a newborn child.
Watching the babies’ faces light up as they smelled the sweetness of carrots or the earthiness of kale, and then sharing that moment with their moms, was a genuinely unforgettable experience, according to the team.
Perception of Taste in the Womb Has a Long-Lasting Effect
These findings provide conclusive evidence that fetuses can detect the aroma of their mothers’ foods while still in the womb. Scientists discovered advanced fetal perception and its capacity to discriminate between distinct taste cues from the mother’s diet.
Prenatal exposure to a variety of tastes helps shape a child’s food preferences. According to scientists, the potential long-term effects of these early sensory experiences are significant. This is because a mother’s diet influences her child’s food preferences from a young age via early exposure to tastes. Scientists now want to understand if the habituation effect dampens these initially adverse responses. (Psychological Science, 2022; doi: 10.1177/09567976221105460)
Some of nature’s most eye-catching displays of color may be seen on the wings of butterflies. They have spots that are green, blue, or red, and they appear to change color as they move. Morpho rhetenor is a butterfly native to tropical regions with a brilliant blue coloration that can be seen from more than half a mile away. The work of British physicist Peter Vukusic has led to this conclusion. But where does this brilliant glow exactly come from?
Pigments are what give flowers, fur, and most other common items their colors. They seem to be different colors because they reflect just part of the visible spectrum. But butterflies and the ones that glisten in the sunlight are different from other insects. Most of the time, they lack any visible pigments. But what causes them to glow in the first place?
The famous scientist Isaac Newton began to suspect something was amiss as early as 1672. As far as he could tell, insects use small physical structures to influence light. We now know that the anatomy of a butterfly’s wing holds the key to understanding the iridescent colors it displays.
Reminiscent of Roof Shingles
Butterflies have thousands upon thousands of tiny, overlapping scales covering their wings. These scales are 1–3 micrometers thick and laid out in a pattern reminiscent of roof shingles. Each scale is constructed from a number of very thin layers of keratin. The protein keratin is also found in hair and fingernails. There is a minimal amount of space between each keratin layer.
The topmost of these transparent layers reflect some of the light that penetrates them. Keratin is penetrated by the rest. Another portion of the light is reflected from its underside as it travels through the air. Light waves that are reflected from the wing undergo a little redistribution as a result of this offset reflection. The two reflected waves no longer have parallel troughs (dips) and crests (peaks).
Scientists liken it to the action of waves on a small channel between two harbors: Sometimes a bigger wave is formed when the crests of two waves collide. And sometimes a crest and trough cancel each other out.
The nanostructure of the scales on a butterfly wing makes some colors and wavelengths of light more intense than others.
Butterfly Colors Change Due to Directional Reflection
However, the wing scales are capable of doing more, since each individual layer selectively emits the reflected light. That’s why the butterfly wing might seem brilliant blue one moment and subtly green the next time you look at it.
Generally speaking, pigment colors don’t shine very brilliantly due to their inefficient light reflection. By reflecting light in a specific fashion, structural colors like the ones seen on butterflies may achieve extremely high and varying intensities. Thanks to these, the male butterfly in the morphed form can still attract females from hundreds of feet away with its dazzling blue display.
Every time you sneeze, it’s like an explosion with high-pressure air shooting out of your mouth and nose with droplets and other mucus fluids. Muscles in your face stiffen up without your knowledge, and you find yourself temporarily closing your eyelids. But for what purpose do you close your eyes when you sneeze?
Maybe it’s to keep you safe from the bacteria and mucous that are released during the sneeze. Or, can hiding your face protect your eyes from the internal pressure that may cause them to bulge and be permanently damaged? Both of those renditions are widely shared on the Web. It’s widely known that you can’t keep your eyes open when sneezing since it’s a reflex. Does this hold water, though?
Not a true reflex
The act of sneezing does not constitute a true reflex. The sneeze stimulus is more nuanced and is not under pure spinal-cord control. Foreign objects in the nose, infections, and allergies are only a few of the many causes of sneezing.
Those pesky irritants on the nasal mucosa are shot out the window as the air is released at a speed of around 90 mph (150 kph), the head is jerked forward, and we hear “explosion” sounds. However, closing your eyes as a result of a sneeze is not always a reflex. There are actually recordings of individuals sneezing with their eyes open.
How does it work?
There are two widely shared theories for why people have to automatically shut their eyes when they sneeze. To start, the whole body, not just the chest and breathing muscles, tenses up when you sneeze. That is why a drop of pee or gas may be released during a sneeze.
The face and the eyes in particular are tense during a sneeze. When you tense up, the muscles around your eyes shut your lids.
But the idea that this response is meant to shield the eyes from the resulting higher pressure is nonsense.
Nerve network joins nose and eyes
However, there is a nerve that runs between the eyes and the nose. The nasociliary nerve divides into two branches, one of which travels to the top of the nose and the other to the eyelids and the sclera (whites of the eyes). This is because there is a tight relationship between the nose and the eye. Sneezing is an example of an inflammatory response in the eye region, which may also be caused by irritation to the nerve branch that leads to the nose.
Some individuals, for instance, may sneeze in response to really bright light, demonstrating the intimate relationship between the eye and the nose. This is due to the proximity of the optic nerve to a branch of the nasociliary nerve. The sun’s rays stimulate the optic nerve, producing an electric current. When this current goes down the nerve fiber and across to the next nerve, it makes you sneeze.
In any event, shutting your eyes when you sneeze makes biological sense. One of the first forms of self-defense is the simple act of closing your eyes. All painful stimuli cause you to shut your eyes automatically. Our ancestors knew this organ was critical to their existence; therefore, they guarded it instinctually.
Even when we believe we are focusing on a single target, our eyes are actually moving rapidly from one location to the next. This occurs even when our attention is focused on a single place. When we move our heads from side to side, our eyes jerk very quickly and shake violently. This also occurs when we alter the direction in which we are looking. We, on the other hand, are so used to these unpredictable eye movements that we rarely perceive them at all. Then, what might be the cause of this?
Jerky eye movements
It is a straightforward experiment in which you start by focusing on your right eye while standing in front of a mirror. After then, you allow your sight to slowly shift to your left eye. Whatever you do, you do not see your own eyes moving. Observers have been able to show that our eyes don’t stay still when we move our focus from one place to another.
This is because of a combination of two factors: first, the motions of our eyes, and second, the method by which our brain interprets those movements. Saccades are short, jerky, and, most crucially, very rapid motions that occur when the eyes move. Saccades are the technical term for these types of eye movements. When we allow our focus to wander, the movement of our eyes is not equal. Instead, our attention skips about from one thing to another, and it almost always goes to the places and things that capture our eye.
The brain fills in the blanks
But why is it that we don’t even seem to notice these jumps? Because saccades are performed at such a high rate of speed, the images that are shown on the retina of the eye become distorted at the time that they are being performed. Because the brain is unable to make use of this picture in any way, it is simply thrown away. The brain automatically fills in the gap of a few microseconds so that we do not experience temporary blindness. The gap is filled with a picture of the target point rather than the starting point. What we think we are seeing is actually always delayed by a few microseconds.
This can be proven with another simple experiment: while watching a ticking clock, it is common to see that the initial second appears to last for an exceptionally long amount of time. After that, the hand moves ahead at its usual slow and steady speed. This particular optical illusion is sometimes referred to as “chronostasis,” which literally means “time standing.”
This happens because the brain is able to make a connection between the moving eyes and the still picture of the clock. This may account for as much as one-tenth of a second of the total time. Now, if you look at the clock precisely when the hand has just moved, you will see the whole second, as well as a tenth, added onto it.
