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DNA of identical twins

DNA of identical twins



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I read an article which says that identical twins have 100% similarity between their DNA, but they have different fingerprints. Does that mean the DNA is different in the fingers? What body features can be used to exactly identify the identical twins?


DNA is not the only thing in biology that determines a phenotype (observable trait, e.g. fingerprint). Far from it.

Traits can be affected by the environment (a very good example, temperature-dependent sex determination), stochastic (random) phenomena - these are know to occur in transcription ("reading DNA") or the decay of mRNA (messenger molecules which instruct protein building) - and by epigenetic phenomena. The degree to which DNA is actively read, or silenced, does not wholly depend on the DNA. In fact, this depends on the exact state of the cell or nucleus. Roughly speaking, cells in your brain (e.g. neurons) and the cells that line your lungs have identical DNA, but they are shaped, look, behave and react differently to the outside world. This is due to epigenetics, think of it as the life history of the cell.

Here's an analogy: reading the exactly same book can have different effects on people. The book is the DNA, its information unchanging, but the person and their exact status are the complicated world of the environment and the cell that is using its DNA for some purposes. PS. Terrible analogy but it may help.

By no means is my list exhaustive. Hope you can see how that identical twins with identical DNA can have a different shade of skin color (tanning!), different fingerprints (subtle and complex differences during digit development), or a different sense of fashion (psychology, cognition, what have you).


How Do Identical Twins Show up On DNA Results

Are you wondering how identical twins would match each other on an autosomal DNA test? Maybe you wonder whether their offspring will match each other at typical first cousin levels?

If you have identical twins in your family, or wonder if you do, this post will help you know what to look for as far as shared DNA between identical twins and their descendants is concerned.

This question comes up so often on social media, in my inbox, and elsewhere on the internets &ndash so I figured that a end-all-be-all post on the topic is in order.


Identical Twins' Genes Are Not Identical

Identical twins are identical, right? After all, they derive from just one fertilized egg, which contains one set of genetic instructions, or genome, formed from combining the chromosomes of mother and father.

But experience shows that identical twins are rarely completely the same. Until recently, any differences between twins had largely been attributed to environmental influences (otherwise known as "nurture"), but a recent study contradicts that belief.

Geneticist Carl Bruder of the University of Alabama at Birmingham, and his colleagues closely compared the genomes of 19 sets of adult identical twins. In some cases, one twin's DNA differed from the other's at various points on their genomes. At these sites of genetic divergence, one bore a different number of copies of the same gene, a genetic state called copy number variants.

Normally people carry two copies of every gene, one inherited from each parent. "There are, however, regions in the genome that deviate from that two-copy rule, and that's where you have copy number variants," Bruder explains. These regions can carry anywhere from zero to over 14 copies of a gene.

Scientists have long used twins to study the roles of nature and nurture in human genetics and how each affects disease, behavior, and conditions, such as obesity. But Bruder's findings suggest a new way to study the genetic and environmental roots of disease.

For example, one twin in Bruder's study was missing some genes on particular chromosomes that indicated a risk of leukemia, which he indeed suffered. The other twin did not.

Bruder therefore believes that the differences in identical twins can be used to identify specific genetic regions that coincide with specific diseases. Next, he plans to examine blood samples from twin pairs in which only one suffers from asthma or psoriasis to see whether he can find gene copy number changes that relate to either of these illnesses.

The result might also call into question the many findings of previous twin studies that assumed identical twins were indeed identical, Bruder notes. "It's pretty unlikely they're going to significantly change any of the results found so far," counters Kerry Jang, a psychologist at the University of British Columbia in Vancouver, who runs Canada's largest twin study. "We can adjust our models to take [genetic differences] into account in the same way we've adjusted for different environments."

The discovery of this genetic variation gives hope for an obscure but pressing issue in the case of a criminal suspect who is an identical twin. "If one twin is a suspect and the whereabouts of the other twin cannot be determined, then the jury is often left without the ability to find guilt beyond a reasonable doubt" in cases that rely on DNA evidence, says Frederick Bieber, a pathologist at Harvard Medical School.

"If the twin issue comes up in a criminal investigation it's possible that if there are [copy number variants] that differ between the two twins that might help sort that out," Bieber says.

Given that there are 80 pairs of identical twins in Virginia's convicted offender database alone, this might not be as small an issue as it may sound. And such genetic variation also matters to the population at large.

Bruder speculates that such variation is a natural occurrence that accumulates with age in everyone. "I believe that the genome that you're born with is not the genome that you die with&mdashat least not for all the cells in your body," he says.

Charles Lee, a geneticist at Brigham and Women&rsquos Hospital in Boston, agrees. Genetic variations can arise after a double strand of DNA breaks when exposed to ionizing radiation or carcinogens. "It reminds us to be careful about our environment because our environment can help to change our genome," he says.

Plus, these variations may predict age-related diseases. Lee adds: "As you age &hellip your chances for having a genomic rearrangement that causes a certain disease increases all the time."

The differences between identical twins increase as they age, because environmentally triggered changes accumulate. But twins can also begin their lives with differences, according to Bruder's study, and that calls into question their very name.

"Maybe we shouldn't call them identical twins," Harvard's Bieber says. "We should call them 'one-egg twins.'"


The Claim: Identical Twins Have Identical DNA

It is a basic tenet of human biology, taught in grade schools everywhere: Identical twins come from the same fertilized egg and, thus, share identical genetic profiles.

But according to new research, though identical twins share very similar genes, identical they are not. The discovery opens a new understanding of why two people who hail from the same embryo can differ in phenotype, as biologists refer to a person’s physical manifestation.

The new findings appear in the March issue of The American Journal of Human Genetics, in a study conducted by scientists at the University of Alabama at Birmingham and universities in Sweden and the Netherlands. The scientists examined the genes of 10 pairs of monozygotic, or identical, twins, including 9 pairs in which one twin showed signs of dementia or Parkinson’s disease and the other did not.

It has long been known that identical twins develop differences that result from environment. And in recent years, it has also been shown that some of their differences can spring from unique changes in what are known as epigenetic factors, the chemical markers that attach to genes and affect how they are expressed — in some cases by slowing or shutting the genes off, and in others by increasing their output.

These epigenetic changes — which accumulate over a lifetime and can arise from things like diet and tobacco smoke — have been implicated in the development of cancer and behavioral traits like fearfulness and confidence, among other things. Epigenetic markers vary widely from one person to another, but identical twins were still considered genetically identical because epigenetics influence only the expression of a gene and not the underlying sequence of the gene itself.

“When we started this study, people were expecting that only epigenetics would differ greatly between twins,” said Jan Dumanski, a professor of genetics at the University of Alabama at Birmingham and an author of the study. “But what we found are changes on the genetic level, the DNA sequence itself.”

The specific changes that Dr. Dumanski and his colleagues identified are known as copy number variations, in which a gene exists in multiple copies, or a set of coding letters in DNA is missing. Not known, however, is whether these changes in identical twins occur at the embryonic level, as the twins age or both.

“Copy number variations were discovered only a few years ago, but they are immensely important,” said Dr. Carl Bruder, another author of the study at the university. Certain copy variations have been shown in humans to confer protection against diseases like AIDS, while others are believed to contribute to autism, lupus and other conditions. By studying pairs of identical twins in which one sibling has a disease and the other does not, scientists should be able to identify more easily the genes involved in disease.

John Witte, a professor of genetic epidemiology at the University of California, San Francisco, said the findings were part of a growing focus on genetic changes after the parents’ template had been laid. This and other research, Dr. Witte said, shows “you’ve got a little bit more genetic variation than previously thought.”

In the meantime, a lot of biology textbooks may need updating.

Dr. Dumanski pointed out, for example, that as his study was going to press, the following statement could be found on the Web site of the National Human Genome Research Institute, the group that financed the government project to decode the human genome: “Most of any one person’s DNA, some 99.9 percent, is exactly the same as any other person’s DNA. (Identical twins are the exception, with 100 percent similarity).”


Some identical twins don’t have identical DNA

Identical twins were thought to be genetically the same, but a new study finds that’s not always the case.

Kumacore/Getty Images Plus

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January 7, 2021 at 12:22 pm

Identical twins may not be carbon copies at the DNA level after all.

On average, identical twins differ by 5.2 genetic changes, researchers report January 7 in Nature Genetics. The finding is important because identical twins — also called monozygotic twins because they come from a single fertilized egg — are often studied to determine whether particular traits, diseases or conditions result from genetics or from environmental influences. Identical twins were thought to be genetically the same, so differences in their health were considered to be the product of their environment. The new finding suggests that some genetic changes could also account for differences between twins.

Researchers in Iceland deciphered the complete genetic makeup, or genome, of 381 pairs of identical twins. Of those, 38 pairs were genetic duplicates of each other, but most had some differences in DNA that probably arose very early in development, either just before one embryo split to form two or shortly after the split. Some of the twins had many genetic differences, including 39 pairs who had more than 100 changes between the twins.

Patterns of mutations among twins suggest that embryos don’t split neatly when twins form, the findings suggest. Some twins may arise when a single cell or a small group of cells splits off from the embryo. The number of cells that a twin originates from may determine how genetically different they are from their twin, with more uneven splits of the embryo leading to a greater number of differences between the twins.

Questions or comments on this article? E-mail us at [email protected]

A version of this article appears in the January 30, 2021 issue of Science News.

Citations

H. Jonsson et al. Differences between germline genomes of monozygotic twins. Nature Genetics. Published online January 7, 2021. doi: 10.1038/s41588-020-00755-1.


How identical twins are helping us understand epigenetic factors in rheumatoid arthritis

Because they have identical genomes, identical twins are ideal subjects for studying the effects of epigenetic modifications - changes to the DNA which control the expression of genes but not the DNA sequence itself. A recently published study in Genome Medicine looked at 79 pairs of identical twins, where one had rheumatoid arthritis but other did not, to explore possible epigenetic factors associated with the condition.

Rheumatoid arthritis is a common and complex autoimmune disease which can have a huge impact on the quality of life of people who suffer from it. There are many factors which are known to influence the development and progression of the disease, including genetic and environmental factors such as smoking.

In recent years, over 100 genetic variants (referred to as single nucleotide polymorphisms) have been identified which play a role in the development of rheumatoid arthritis however, this still only explains a small amount of what causes the disease.

The relatively high rates of discordance of developing rheumatoid arthritis in monozygotic (genetically identical) twins indicate that environmental factors play a substantial role in the etiology of the disease. One way in which environmental exposures can influence disease is through epigenetic modifications of DNA.

Epigenetic modifications control which genes are switched ‘on’ and ‘off’ in a particular cell or tissue. This is important in the regulation of tissue development and is critical in determining cellular identity. Epigenetic marks in the DNA can be altered by many different things, including environmental factors such as diet, exercise and smoking. While many epigenetic changes are normal and happen during healthy development and ageing, epigenetics can also be disrupted in diseases.

Studying twins allowed us to see DNA methylation changes clearly, as we can be sure they are not confounded by differences in the DNA sequence.

In order to investigate if epigenetics was disrupted in rheumatoid arthritis, we compared the pattern of one type of epigenetic modification, DNA methylation, in people with the disease to that of healthy people. We did this by looking at the epigenome of 79 pairs of monozygotic (identical) twins, in which one individual had rheumatoid arthritis, and the other was healthy.

This is the ideal setup in epigenetic research, as epigenetic patterns can be influenced by the underlying DNA sequence. Studying twins allowed us to see DNA methylation changes clearly, as we can be sure they are not confounded by differences in the DNA sequence. Essentially, monozygotic twins have identical genomes, but different epigenomes.

In this study, we found that the DNA methylation patterns in the twins with rheumatoid arthritis were more variable at 1,171 sites, meaning they were less predictable and stable than the methylation profiles in the healthy twins. This could represent a disruption of epigenetics that is either causing rheumatoid arthritis, or could be a consequence of people having had the disease for a long time.

In particular, we found that the DNA methylation changes were seen in genes involved in pathways within a cell that control the reaction of cells to stress. Cellular stress can be caused by many factors, including exposures such as smoking. We believe that these changes in DNA methylation may be altering how the immune cells react to stress, which sensitizes the cells, causing an increased immune activity, consequently leading to progression of the disease.

We compared these marks with epigenetic disruption which was identified in Type 1 Diabetes, and found that the two diseases shared certain epigenetic changes. This indicates that there could be common factors which influence the epigenome, contributing to both of these autoimmune diseases.

In the future, these findings could provide insight into how rheumatoid arthritis could be treated or even better, prevented from developing in the first place.


Twins and Cancer: Nature, Nurture, or Something Else?

Is our cancer the result of nature or nurture? Are we the victims of faulty DNA over which we have no control? Or of lifestyle and environmental factors that we can change? Or is there a third option?

Epigenetics is the study of that third option. This fairly new science covers the process by which nurture might affect nature. That is, diet and exercise might actually change the way our DNA influences our body. It’s a complex new field and scientists are even having trouble defining it.

One way of illustrating it is through the lives of twins.

According to the theory of nature’s influence, we are formed by the genes we are born with—twins separated at birth grow up to live eerily similar lives, sharing marital history, criminal pasts, even athletic ability and sicknesses. The theory of the influence of nurture, however, maintains that our environment shapes us—our economic status, parental involvement, exposure to specific risks, diet, exercise, and so on.

Epigenetics, however, demonstrates that environmental factors can actually influence our genes, changing our genetic processes to make us more or less susceptible to disease. Research published in PLOS Genetics on the influence of diet and exercise on the development of breast cancer demonstrates this epigenetic component.

Twins share the same DNA, which can make one more likely to have breast cancer if the other one is diagnosed with the disease.

Identical twins are formed from the same egg and begin in the womb with identical DNA as the egg splits to become twins, the DNA likewise splits and does not necessarily divide equally, meaning that even identical twins do not have identical DNA. Fraternal twins develop from two different eggs and so they share DNA in the way all siblings do.

That’s the nature argument.

But not all twins share cancer—or any disease. It is common for one twin to get a serious illness that completely misses the other twin. This is the nurture argument—if twins share DNA but don’t share cancer, the environment has to have had some influence.

National Geographic’s January 2012 issue has a cover story on epigenetics and twins, with some compelling stories that show how unpredictable disease can be even for people with shared DNA. And that unpredictability is one of the motivators for the study of epigenetics.

As National Geographic writer Peter Miller describes it:

If you think of our DNA as an immense piano keyboard and our genes as keys—each key symbolizing a segment of DNA responsible for a particular note, or trait, and all the keys combining to make us who we are—then epigenetic processes determine when and how each key can be struck, changing the tune being played.

One way the study of epigenetics is revolutionizing our understanding of biology is by revealing a mechanism by which the environment directly impacts genes. Studies of animals, for example, have shown that when a rat experiences stress during pregnancy, it can cause epigenetic changes in a fetus that lead to behavioral problems as the rodent grows up. Other epigenetic changes appear to occur randomly—throwing a monkey wrench into the engine of nature versus nurture. Still other epigenetic processes are normal, such as those that guide embryonic cells as they become heart, brain, or liver cells, for example.

Epigenetic researcher Alejandro Burga and colleagues, writing in the journal Nature, looked at why the same genetic mutation might affect people differently, using information from the Center for Genomic Regulation in Barcelona Spain. Burga explains that identical cells do not exist:

In the last decade we have learned by studying very simple organisms such as bacteria that gene expression—the extent to which a gene is turned on or off —varies greatly among individuals, even in the absence of genetic and environmental variation. Two cells are not completely identical and sometimes these differences have their origin in random or stochastic processes.

So, while identical twins may appear identical, and while they as genetically close as two humans can be, they remain individuals on the cellular level. One may be more cancer-prone than the other even without differences in the environment.

So, what is it: Nature? Nurture? Both? Neither?

It seems to be a complex mix of all of the above, with our cancers as unique as we are.

Improving our diet and exercise certainly have been shown in multiple studies to reduce our risk of breast cancer. But sometimes the environmental risks that make one twin more prone to illness are no more under their control than their DNA. The way the fetuses develop in the womb, for example, might improve one twin's health while imperiling the other's. And sometimes, that tiny variation in DNA between twins makes all the difference in susceptibility to cancer.

Epigenetics, while not answering the question of what causes cancer, is absolutely getting us closer.

• For another perspective on Epigenetics: Can Human DNA Help Guide Reforestation?


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TWINS: EXPLAINED

Twins are two individuals who form in the same uterus. There are a few different kinds:

1. FRATERNAL TWINS (non-identical)

These account for two-thirds of twins.

Two eggs are fertilized by two sperm and both implanted into the walls of the uterus at the same time.

These eggs form separately, in separate sacs adjacent to each other.

They share 50 percent of their DNA, as they would with their other non-twin siblings.

They can be different genders, though most (around 60 percent) are same-sex twins.

Research suggests fraternal twins run in families, typically down the maternal line.

A single egg is fertilized by one sperm and embeds in the uterus wall.

But at some point, it splits from one zygote into two.

They do not always share the same amniotic sac, but they always share the same placenta.

Those that share the same amniotic sac are known as monoamniotic, while those that have their own are diamniotic.

Most identical twins split within eight days of conception.

Those that split between eight and 12 days are known as mono-mono twins - incredibly rare.

Those that split after 12 days tend to be conjoined.

Identical twins – or monozygotic (MZ) twins – may start out from the same egg, but each take on their own mutations as they develop.

It’s these mutations that could help to reveal who in a pair is tied to a given DNA sample.

Doing this accurately would require ‘a genome-wide search for those few mutations that occur during early embryonic development and hence allow distinguishing between MZ twins in later life,’ the researchers say.

Lead author Michael Krawczak has been investigating the possibility of comparing twins’ unique mutations for years, and published a set of initial calculations in 2012 to settle a hypothetical paternity dispute.

A team at Eurofins Scientific in Brussels then picked up on the research and tested it out themselves using DNA from a pair of identical twin volunteers, and the wife and child of one of the men, according to the New York Times.

And in a proof of concept for the technique, the researchers were able to distinguish between the child’s father and uncle by comparing their whole genomes.

Krawczak’s team has now published a general mathematical framework to back up the method, in a step toward its use in forensic investigations.

But, it’s still in the early stages and will require much more testing before it can be adopted by the courts, experts note.

Steven A. McCarroll, a Harvard Medical School geneticist who was not involved in the study, told NYT, ‘It would be really nice to know that we could do this kind of analysis over and over and over again and never get it wrong.’


Identical twins can share more than identical genes: Molecular similarity

An international group of researchers has discovered a new phenomenon that occurs in identical twins: independent of their identical genes, they share an additional level of molecular similarity that influences their biological characteristics. The researchers propose a mechanism to explain the extra level of similarity and show that it is associated with risk of cancer in adulthood. The results appear in the journal Genome Biology.

"The characteristics of an individual depend not only on genes inherited from the parents but also on epigenetics, which refers to molecular mechanisms that determine which genes will be turned on or off in different cell types. If we view one's DNA as the computer hardware, epigenetics is the software that determines what the computer can do," said senior author Dr. Robert A. Waterland, associate professor of pediatrics -- nutrition at the USDA/ARS Children's Nutrition Research Center and Texas Children's Hospital and of molecular and human genetics at Baylor College of Medicine.

Epigenetics works by adding or removing chemical tags to genes to mark which ones should be used in different cell types. One of the better studied tags, known to play an important role in development and cancer, is the methyl chemical group. Here, in a large group of identical and fraternal twin pairs, Waterland and his colleagues studied a group of genes called metastable epialleles. Previous work indicated that methyl tags are randomly added to metastable epialleles during early embryonic development and maintained throughout life.

"We expected that the patterns of methyl tags added to metastable epialleles would be equally random in identical twins and fraternal twins," Waterland said. "Instead, we found that the methylation patterns matched almost perfectly in identical twins, a degree of similarity that could not be explained by the twins sharing the same DNA. We call this phenomenon 'epigenetic supersimilarity.'"

Identical twins are formed when the very early embryo -- essentially a ball of cells -- splits into two parts, and each continues to develop into a separate human being. The authors proposed and tested a simple model to explain epigenetic supersimilarity.

"If, in this group of genes, the epigenetic markers are established before the embryo splits into two, then the markers will be the same in both twins," Waterland said. "In essence, both twins inherit an intimate molecular memory of their shared developmental legacy as a single individual. On the other hand, genes at which epigenetic markers are set after the embryo splits can have greater epigenetic differences between the two twins."

Cancer connection

Epigenetic supersimilarity seems to occur in a relatively small group of genes, but, as the researchers discovered, many of these are associated with cancer. To test whether these epigenetic markers might affect risk of cancer, the scientists in Houston teamed up with cancer epidemiologists running the Cancer Council Victoria's Melbourne Collaborative Cohort Study in Melbourne, Australia. Back in the 1990s, this large study was set up to assess different risk factors for cancer.

"By analyzing peripheral blood DNA samples from healthy adults in our study, we have been able to show that methylation at epigenetically supersimilar genes is associated with risk of subsequently developing several types of cancer, including lung, prostate and colorectal cancer," said Dr. Roger Milne, associate professor and head of Cancer Epidemiology at Cancer Council Victoria, and an author on the study.

This study shows that, at the epigenetic level, identical twins are more similar to each other than previously recognized.

"Our findings should prompt a re-evaluation of previous genetic studies on twins," Waterland said. "For decades, researchers have studied genetically identical twins to estimate what proportion of disease risk is determined by one's genes. To the extent that epigenetic supersimilarity affects risk of disease, as our results indicate, genetic risk estimates based on twin studies have been inflated."


The role of epigenetics

In addition to this, genes can be switched on and off in different cells. In fact, they have to be. If all of our genes were switched on all of the time in all of our cells then we would not be able to grow different tissue types and organs from a single set of biological instructions.

One of the main processes switching genes on and off is an epigenetic process known as DNA methylation. By controlling which genes are on or off in any given cell, we are able to grow kidneys, heart, skin, etc and control how these cells behave and what they look like.

DNA methylation marks can be inherited across generations, but, equally, they can be altered by relatively short-term stimuli such as exercise or nutrition. More importantly, there is evidence that the genes involved in controlling eye, skin and hair colour are subject to this epigenetic control.

So whether they had a different experience in the womb – such as one twin receiving more nutrients due to a better connection to the placenta – or whether there was some chance epigenetic reprogramming, it seems likely that epigenetics will have a role in explaining the difference in the appearances of Amelia and Jasmine.

Although a few eyebrows may be raised when Amelia and Jasmine are described as identical twins, biologically they are as identical as any other pair of identical twins. The differences between them are just more visually striking.


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