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Is that what they called junk? Why does a simple cell have the DNA code for everything else when it just needs a few codes to function? Wouldn't that be a wasteful?
Why does a cell contain all DNA when it only needs a few genes ?
I interpret this question to mean "why does every cell contain the whole human genome even though it doesn't use it all, i.e. why does a liver cell contain the genes for eye color?"
If that is what you meant, then we can easily answer the first question in your actual text:
Is that what they called junk?
No, that is not what is called "junk DNA". "Junk DNA" can refer to many concepts, but generally it refers to parts of DNA that serve no function in the body: they are not transcribed into proteins, they don't serve to regulate other genes, and if you remove them or change their sequence this will have no effect on the overall organism. This means it refers to parts of DNA that are used nowhere in the body, not parts that are used in one place but not in others.
How much DNA is "junk", how useless it actually is, and why we have it are complex questions that don't all have known answers, but it is completely different from your headline question.
I don't have the time to look up a detailed answer to your first question so I will leave that to others, but here are some elements that might help:
1) I think cells use more genes than you realize. I don't know the proportion of genes that are used for the cell to live as a cell vs those that are used for the specific tasks this cell needs to do beyond maintaining itself and reproducing, but I'm pretty certain there is no cell in the body that "only needs a few genes". I would even guess all cells in the body use most of the genes they contain.
2) not all cells contain an unmodified copy of the whole genome. Some cells lose their nucleus, i.e. their DNA entirely (red blood cells); others multiply some genes that they use a lot.
3) having said all that, I would guess that liver cells indeed don't need the genes for eye color, yet they might have them. Consider that cells reproduce by copying themselves, and copying their whole genome. Is it more of a waste to keep the copy as it is, or to go around before or after the copying cutting out all the bits this specific cell won't use? Do I go around editing the code of my text editor and recompiling it to get rid of all the functionalities I don't use? I might save some space on my hard drive but it is very obviously not worth my time to do that either. If the extra DNA doesn't do enough harm, there is no reason it would be taken out; indeed the wasteful thing would be to do so.
- Whether there is junk DNA
The common view of a gene is a sequence of DNA which, upon transcription, which I assume in your understanding is a process by which DNA is read by a RNA polymerase to produce mRNA, and upon translation, produces a functional protein to regulate cellular metabolism (sum of all chemical reactions in a cell). It is not until the discipline of epigenetics emerged that we discover that most of other non-protein-coding sequences have important regulatory functions on the protein-coding sequences. Without them, the cell simply has no clue as to when it should produce more of a protein and when it should produce less, or whether the protein should be produced at all. And of course, DNA also encodes information about rRNA, which is an integral component of ribosome, which you know, is imperative for protein synthesis. Thus, the 'functions' of the DNA cannot be limited to protein synthesis, and after extension of the concept of functions, the parts of DNA we can dispense with are incredibly small.
Then let it be argued that those small parts of DNA which really serve no functions are the junk DNA. In fact, even this view is untenable because the 'functionless' DNA may be situated between the important sequences that can subtly affect the chemical properties of the protein interactions during an important biochemical process. Specifically, consider NtrC, a bacterial transcription regulator that activates transcription by directly contacting the RNA polymerase. Note that the regulatory sequence (the part of DNA the protein binds to) is very distant from the promoter of the gene(the part of the gene that RNA polymerase binds to). To directly contact it, DNA looping must occur. It is a phenomenon in which an otherwise linear DNA macromolecule is looped out(imagine bending a wire so that two extreme end of the wire touches each other) to allow for the contacts between molecules. Since the protein has such biochemical properties that allow it to contact another protein at a distance, we do not know what will happen if the 'junk DNA' the DNA spacing the promoter and the regulatory sequence is deleted. It is well possible that the two proteins will not make contacts anymore. And DNA looping is also ubiquitously found in transcription regulation of eukaryotes.
- Why a cell needs to contain all the DNA when it only needs a few genes to function
Once the notion of junk DNA is found to be elusive. This question's premises no longer hold. But let's assume there are really genes that when deleted have no observable effects on the phenotypes of the cells or their health, why does not nature delete them during differentiation of stem cells? To explain it in evolutionary terms, there are two main mechanisms nature can design to keep the 'functionless' genes at bay during differentiation of stem cells. One is to silence them by wrapping them in a compacted nucleosomal structure, or to delete them once and for all. We do not know if nature has once experimented with deletion, if it has then this design must have endowed less fitness then the wrapping model. What reasons then can we speculate about the failure of the deletion model? To delete the useless sequences, there is a widespread effects on the length of the DNA, the resultant secondary structure (topology of the chromatin). And a protein must be designed to specifically recognise what genes to delete, together with the cooperation of nucleases. This is analogous to writing a computer code that contains information that specifies some of the codes to be deleted while not influencing the instructions of the code that follow, all while being consistent in the process. This is logically possible, and we can never say this design is entirely prohibited. But computationally this is not as elegant a solution than just genes in the DNA that code for a repressor protein for the 'useless' code when the right time has come, or by just using proteins to wrap around the sequences to render them unreadable.
- Whether 'non-functional ' DNA constitutes a waste
Not at all.
It’s not ALL in the genes—the role of epigenetics
We’re pretty used to thinking ‘it’s all in the genes ’ … that we are who we are because of the genes we received from our parents. But what if we are who we are not only because of the genes our parents gave us, but also because of the environment in which our grandparents lived? Turns out, it’s not ALL in the genes—external and environmental factors can influence the way an organism’s genes are regulated. This is just part of a field of genetics known as epigenetics—‘epi’ coming from the Greek for ‘over, on top of’. Epigenetics is an additional layer of instructions that lies ‘on top of’ DNA, controlling how the genes are read and expressed.
Pretty much every cell of an organism, be it a parrot, a panther, a plum tree or a person, contains the complete set of instructions to build that organism—its DNA. DNA is a very long molecule, made up of smaller pieces known as nucleotide bases. Humans have 3 billion nucleotide bases in their DNA. The sequence of these bases is ever so slightly different between individuals, which is the key to our being unique.
DNA is a long molecule with a 'double helix' structure. Image source: Etusko Uno and Drew Berry / WEHI, used with permission.
Put certain combinations of these bases together, and you get genes, which provide the information that determines particular characteristics. So, the DNA that is contained in the nucleus of nearly every cell of our body contains all of our genes, plus much more extra DNA that is required to ensure the genes are properly controlled. Collectively, this is known as our genome.
But hang on, if every cell contains ALL the DNA and the DNA contains ALL the genes and ALL the instructions, how do we end up with all the different cells that make up all the different body parts? We obviously are not made purely of brain cells—we also need heart cells, skin cells, liver cells and lots more.
So there’s got to be some sort of control mechanism that ‘regulates’ all these genes in the DNA in our various cells—a mechanism that can turn some genes on, but keep others quiet in order to build functional cells, that can go on to build organs and tissues. This process is called ‘cell differentiation’ and is just one example, indeed, a classic example, of epigenetics—there’s an extra layer of information lying above the actual genes and surrounding DNA, telling them which ones to switch on or off to build each of the different functional cells our bodies need.
The process of cell differentiation is a prime example of epigenetics — an extra layer of information regultates the DNA in our body's cells to create all the different cell types of our body.
Epigenetics can be thought of as the interpretation of the genetic code. Just as the same piece of music will change slightly when interpreted by different orchestras, so does our genetic ‘score’ when interpreted by the epigenetic orchestra.
Key Concepts and Summary
- The entire genetic content of a cell is its genome.
- Genes code for proteins, or stable RNA molecules, each of which carries out a specific function in the cell.
- Although the genotype that a cell possesses remains constant, expression of genes is dependent on environmental conditions.
- A phenotype is the observable characteristics of a cell (or organism) at a given point in time and results from the complement of genes currently being used.
- The majority of genetic material is organized into chromosomes that contain the DNA that controls cellular activities.
- Prokaryotes are typically haploid, usually having a single circular chromosome found in the nucleoid. Eukaryotes are diploid DNA is organized into multiple linear chromosomes found in the nucleus.
- Supercoiling and DNA packaging using DNA binding proteins allows lengthy molecules to fit inside a cell. Eukaryotes and archaea use histone proteins, and bacteria use different proteins with similar function.
- Prokaryotic and eukaryotic genomes both contain noncoding DNA, the function of which is not well understood. Some noncoding DNA appears to participate in the formation of small noncoding RNA molecules that influence gene expression some appears to play a role in maintaining chromosomal structure and in DNA packaging.
- Extrachromosomal DNA in eukaryotes includes the chromosomes found within organelles of prokaryotic origin (mitochondria and chloroplasts) that evolved by endosymbiosis. Some viruses may also maintain themselves extrachromosomally.
- Extrachromosomal DNA in prokaryotes is commonly maintained as plasmids that encode a few nonessential genes that may be helpful under specific conditions. Plasmids can be spread through a bacterial community by horizontal gene transfer.
- Viral genomes show extensive variation and may be composed of either RNA or DNA, and may be either double or single stranded.
16.0: Prelude to Gene Expression
- Contributed by OpenStax
- General Biology at OpenStax CNX
Each somatic cell in the body generally contains the same DNA. A few exceptions include red blood cells, which contain no DNA in their mature state, and some immune system cells that rearrange their DNA while producing antibodies. In general, however, the genes that determine whether you have green eyes, brown hair, and how fast you metabolize food are the same in the cells in your eyes and your liver, even though these organs function quite differently. If each cell has the same DNA, how is it that cells or organs are different? Why do cells in the eye differ so dramatically from cells in the liver?
Figure (PageIndex<1>): The genetic content of each somatic cell in an organism is the same, but not all genes are expressed in every cell. The control of which genes are expressed dictates whether a cell is (a) an eye cell or (b) a liver cell. It is the differential gene expression patterns that arise in different cells that give rise to (c) a complete organism.
Whereas each cell shares the same genome and DNA sequence, each cell does not turn on, or express, the same set of genes. Each cell type needs a different set of proteins to perform its function. Therefore, only a small subset of proteins is expressed in a cell. For the proteins to be expressed, the DNA must be transcribed into RNA and the RNA must be translated into protein. In a given cell type, not all genes encoded in the DNA are transcribed into RNA or translated into protein because specific cells in our body have specific functions. Specialized proteins that make up the eye (iris, lens, and cornea) are only expressed in the eye, whereas the specialized proteins in the heart (pacemaker cells, heart muscle, and valves) are only expressed in the heart. At any given time, only a subset of all of the genes encoded by our DNA are expressed and translated into proteins. The expression of specific genes is a highly regulated process with many levels and stages of control. This complexity ensures the proper expression in the proper cell at the proper time.
Why does DNA replication need to occur?
DNA is like the instruction manual for building and operating a cell.
DNA replication needs to occur because existing cells divide to produce new cells.
Each cell needs a full instruction manual to operate properly. So the DNA needs to be copied before cell division so that each new cell receives a full set of instructions!
Here is a video which uses an animated tutorial to explain the process of DNA replication.
Primarily for cell division
Basically, every time a cell undergoes mitosis (one kind of cell division), various enzymes work to split each DNA strand in half, and then replace the missing half on the separated strands with corresponding nucleotides, leaving you with two identical strands. When the entirety of a cell's genome is copied (along with all the organelles), the cell can split into two daughter cells.
Imagine slicing yourself down the middle and splitting yourself in half, and then using each half of you as a template to recreate the other half.
That's the biology behind it, but the bottom line is that DNA is replicated in order to reproduce itself.
Design in DNA: Dual Coding Found in Nearly All Genes by Rich Deem
The information content in human DNA is enormous, but we are just beginning to understand how efficiently the DNA is encoded. Scientists had originally speculated that the human genome contained up to 100,000 genes. However, the human genome project showed that it contained only one quarter that number, mostly because each gene can code for multiple transcripts. Scientists also thought that only the protein coding DNA, comprising only 3% of the DNA, was useful. The other 97% of the DNA was thought to be junk. However, the last few decades of research have shown that the vast majority (>80%) of non-coding DNA is functional. Much of the non-coding DNA is involved in regulation of transcription (the intermediate step in which mRNA is generated, from which the protein is translated). However, scientists have now discovered that some of the protein coding DNA not only codes for the protein sequence, but simultaneously codes for sequences that bind transcription factors (proteins that regulate the transcription and expression of genes). These dual coding sequences have been termed "duons."
How the study was done
The scientists who authored the study used a naturally occurring enzyme called DNAse I, which digests DNA. It turns out that the enzyme will only degrade DNA that is not bound to proteins. Since transcription factors are proteins that bind DNA, any transcription factors that are bound to DNA when it is isolated are protected from digestion by DNAse I. Scientists isolated the DNA from 81 different cell types and sequenced the fragments of DNA that were preserved by binding to transcription factors. They had to use different cell types because those different cells differentially express genes and transcription factors on the basis of their own particular function. An example dual coding region is shown in the figure to the right, which shows the gene CELSR2, found on chromosome 1. The gene consists of 34 exons (coding regions), with the ninth exon coding for the transcription factor CTFC, which is known to regulate the transcription of numerous genes. It is interesting to note that this short transcription binding site of the exon contains two arginine residues, which are coded using two very different codons (AGG and CGC) in order to match the sequence to which CTFC binds. Although most genes consist of multiple exons (coding regions), the vast majority of duon sequences occur in the first exon, which is what would be expected if the sequences were involved in the regulation of gene expression.
Astounding levels of duons
The scientists had originally expected to find a few genes that simultaneously coded for both proteins and transcription factor binding. However, what they found was that 14% of coding sequence space were duons (which represents over 400 million base pairs). An astounding 86% of all genes expressed at least one duon sequence. Scientist already knew that intronic sequences within the DNA coded for transcription factor binding in order to regulate gene expression. However, since exon coding regions are constrained by their need to code for specific amino acids, it was never imagined that such regions of DNA could simultaneously code for the binding of transcription factors, as well. The finding shows the amazing efficiency of DNA sequences in complex organisms. Although the authors of the study recognized the obvious optimization of the code, they attributed such optimization to natural selection, rather than design:
"Our results indicate that simultaneous encoding of amino acid and regulatory information within exons is a major functional feature of complex genomes. The information architecture of the received genetic code is optimized for superimposition of additional information (34, 35), and this intrinsic flexibility has been extensively exploited by natural selection."
However, they failed to account for how selection could simultaneously select for two diverse functions in the same, overlapping sequence of DNA code.
Scientists have discovered that regulation of gene expression, originally thought to occur only in non-coding DNA sequences, is, in fact, additionally dual coded into the actual sequence of DNA that defines protein composition. Transcription factors, which bind to specific short sequences of DNA, regulate how the genes are expressed. The fact that these transcription factor binding sequences overlap protein coding sequences, suggest that both sequences were designed together, in order to optimize the efficiency of the DNA code. As we learn more and more about DNA structure and function, it is apparent that the code was not just hobbled together by the trial and error method of natural selection, but that it was specifically designed to provide optimal efficiency and function.
Reasons To Believe's Fazale Rana has written The Cell's Design, a comprehensive examination of the biochemistry of the cell from a layman's perspective. Even so, the text does not gloss over the significant details of how the cell works. As a scientist myself, I see the design within the cell as much more beautiful than even the most wonderful sunset. The cell's design certainly does reveal the artistry of the Creator.
Darwin's Black Box author Michael Behe takes on the limits of evolution through an examination of specific genetic examples. Behe finds that mutation and natural selection is capable of generating trivial examples of evolutionary change. Although he concludes that descent with modification has occurred throughout biological history, the molecular devices found throughout nature cannot be accounted for through natural selection and mutation. Behe's book claims to develop a framework for testing intelligent design by defining the principles by which Darwinian evolution can be distinguished from design.
Q: How many patients are in this study? What are the statistics on people in remission? Are there people who are not responding at all?
Issa: Our most recent results, which are based on treatment of over 100 patients, are very encouraging. Spectacular results, complete remissions, complete disappearance of the disease can be seen in almost half of the patients that receive this drug, decitabine, with MDS or the closely related disease, Acute Myelogenous Leukemia. And another 25 percent of the patients have shown some improvements. It still does not work in a small proportion of patients. Some patients do not respond to the drug early on. And some patients respond to the drug for a finite period of time and then stop responding. But we can help the majority of patients who first see this drug—quite a remarkable finding for a single drug that is now given to older people as outpatient therapy.
Q: How do you know that epigenetic drugs won't start stripping methyl tags from all sorts of other genes and wreaking havoc on the body? Why do they just remove the tags that are keeping the cells from behaving normally?
Issa: Well, this has been a concern, but the reality is we have not observed any unusual side effects for these drugs. There are two explanations for this phenomenon. One explanation is quite simple. When you give a drug to an individual, the cells that are dividing the most are going to have the most of these drugs around. And, therefore, cancer cells have essentially a higher concentration of these drugs around than normal tissues, which explains part of the differential effects of these on cancers than on normal tissues.
The other important observation is that while epigenetics may play a role in development in embryogenesis, and plays a role in maintaining our tissues, it is difficult to modify once we are adults. For a cancer cell, these epigenetic changes are absolutely essential for the cancer cell to continue behaving as a cancer. Therefore, any modification of these epigenetic changes might mean a large effect on the behavior of a cancer cell, but only a small effect on the behavior of a normal cell. Reassuringly, when we stop these drugs the epigenetic patterns of normal cells go back to essentially normal.
We are still concerned. We don't know the effects of these drugs if they are given to a very young child, and we don't know the effects of these drugs should they be given to a pregnant woman. We would expect potentially serious side effects to the fetus. There is this potential for harm.
Q: Is there hope for extending epigenetic therapy to other types of cancer besides MDS?
Issa: There is no reason why this type of therapy would work only in MDS. Now, it's not going to be easy. There are reasons why MDS cells may be easier to manipulate than breast cancer cells. They are in the blood. They have a better access to drugs. We need to figure out how to get this drug to the cancers themselves in breast cancer patients. But we are optimistic.
We are currently doing a clinical trial of this drug in patients with solid tumors. We've seen at least one quite remarkable response so far. We've demonstrated in the laboratory that, in fact, we can manipulate the epigenome of solid-tumor patients with lung cancers or breast cancers or melanomas with these drugs. And I'm absolutely convinced that in 10 or 20 years these drugs will be used to increase the cure rate of solid tumors. We just need to learn how.
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Why do our cell's power plants have their own DNA?
It’s one of the big mysteries of cell biology. Why do mitochondria—the oval-shaped structures that power our cells—have their own DNA, and why have they kept it when the cell itself has plenty of its own genetic material? A new study may have found an answer.
Scientists think that mitochondria were once independent single-celled organisms until, more than a billion years ago, they were swallowed by larger cells. Instead of being digested, they settled down and developed a mutually beneficial relationship developed with their hosts that eventually enabled the rise of more complex life, like today’s plants and animals.
Over the years, the mitochondrial genome has shrunk. The nucleus now harbors the vast majority of the cell’s genetic material—even genes that help the mitochondria function. In humans, for instance, the mitochondrial genome contains just 37 genes, versus the nucleus’s 20,000-plus. Over time, most mitochondrial genes have jumped into the nucleus. But if those genes are mobile, why have mitochondria retained any genes at all, especially considering that mutations in some of those genes can cause rare but crippling diseases that gradually destroy patients’ brains, livers, hearts, and other key organs.
Scientists have tossed around some ideas, but there haven't been hard data to pick one over another.
So Iain Johnston, a biologist at the University of Birmingham in the United Kingdom, and biologist Ben Williams of the Whitehead Institute for Biomedical Research in Cambridge, Massachusetts, modeled the problem, mathematically comparing different hypotheses for the first time. They analyzed more than 2000 different mitochondrial genomes from animals, plants, fungi, and protists (like amoebas). They traced their evolutionary path, creating an algorithm that calculated the probabilities that different genes and combinations of genes would be lost at particular points in time.
“That’s one of the innovative aspects of this work, that it uses modeling which isn’t normally included in these sorts of studies,” says Keith Adams, a biologist at the University of British Columbia, Vancouver, in Canada who was not involved in the research.
Mitochondria make energy through a series of chemical reactions that pass electrons along a membrane. Key to this process is a series of protein complexes, large protein globs that embed in the internal membrane of the mitochondria. All of the mitochondria’s remaining genes help produce energy in some way. But the team found that a gene was more likely to stick around if it created a protein that was central to one of these complexes. Genes responsible for more peripheral energy-producing functions, meanwhile, were more likely to be outsourced to the nucleus, the group reports today in Cell Systems.
“Keeping those genes locally in the mitochondria gives the cell a way to individually control mitochondria,” Johnston says, because pivotal proteins are created in the mitochondria themselves. That local control means the cell can more quickly and efficiently regulate energy production moment-to-moment in individual mitochondria, instead of having to make sweeping changes to the hundreds or thousands of mitochondria it contains. For instance, out-of-whack mitochondrion can be fixed individually rather than triggering a blanket, cell-wide response that might then throw something else off balance.
It’s like responding to a fire, says John Allen, a biologist at University College London who was not involved in the study. If a single room in a large building goes up in flames, you don’t phone the building manager to ask permission to put it out. You grab a fire extinguisher and aim.
“I think that’s a very fundamental feedback mechanism,” Allen says. In his own research, he’s found evidence suggesting that producing certain mitochondrial proteins right where they’re needed helps the cell better regulate energy production. Other structures in our cells could also benefit from this type of local control. But mitochondria, with their history as stand-alone cells, are the only ones with their own command center.
Johnston and Williams’s model points out other factors that might be important as well. For instance, genes that encode mitochondrial proteins that are hydrophobic, or water-repelling, are more likely to be made in the mitochondria. If these proteins are manufactured elsewhere in the cell, they can sometimes get stuck in transit, so it can be more efficient to produce them in the mitochondria.
The chemical makeup of the genes themselves can also influence how likely they are to stick around. Genes that are chemically able to withstand the harsh conditions inside the mitochondria instead of being broken down might be more likely to persist.
Johnston thinks that the computer program he and Williams developed is good for more than just sifting through mitochondrial genomes. The algorithm can analyze any problem where individual traits are lost or gained over time, whether those are genes or symptoms of a disease. He hopes the model will be useful for future predictions along these lines, such as looking at pathways of disease progression.
So: Genes are made of DNA, genes make proteins, proteins make cells and cells make you.
Watch the YourGenome from DNA to protein video to see how it all works
Where do your genes come from? Have you ever wondered why you have the same eye color as your dad or the same hair color as your mum? It’s because you inherit your genes from your parents. You get half from your mum and half from your dad. When you inherit genes from your parents you get two versions of each gene, one from your mum and one from your dad. For example you’ll get two versions of the genes that contain instructions for eye colour. Some versions of genes are more dominant than others if you get blue-eye genes from mum and brown-eye genes from dad you will have brown eyes because brown-eye genes are dominant. So if you inherit all your genes from your parents, why aren’t you exactly like your siblings?
Why are you different from your brothers and sister? The reason you and your siblings aren’t identical is because your mum and dad have two versions of each gene, one from each of their parents. When they pass their genes on to you they only pass on one of these versions, and it is completely random which one it will be. For example if your mum has brown-eye and blue-eye genes she could pass the blue ones on to you and the brown ones on to your sibling.
How do genes affect your health? Your genes are the instruction manual that makes your body work. Sometimes, one or a few bases of the DNA in a gene can vary between people. This is called a variant. A variant means the gene has slightly different instructions to the usual version. Occasionally, this may causes the gene to give cells different instructions for making a protein, so the protein works differently. Luckily most gene variants have no effect on health. But a few variants do affects proteins that do really important things in your body, and then you can become ill.
Play our Gene Finder game to see if you can spot the variant genes.
FUN FACT : blood group O, which is useful because it can be transfused into anyone in an emergency, is caused by a variant in the gene ABO that stops it working (a knockout ).
Geneti c conditions: Genetic conditions are diseases you develop when you inherit a variant in a gene from your parents. As a result genetic conditions usually run in families. Scientists have identified over 10,000 genetic conditions. One genetic condition is called sickle cell anemia. People with this illness have a variant in the genes that contain instructions to make haemolglobin proteins. Hemoglobin helps your red blood cells carry oxygen around your body. These sickle cell haemoglobin genes cause red blood cells to be the wrong shape, making it hard for them to carry oxygen around the body. Not all gene variants cause a genetic condition. Many variants seem to have no effects at all, others may increase your risk of developing a disease.
Genes and common conditions Scientists are looking for gene variants that can increase your risk of developing illnesses like diabetes, Alzheimer’s and cancer. It’s a tough job as a lot of illnesses can develop in a very complicated way with lots of different genes involved, and they are also affected by environmental factors like how much you exercise, your weight or if you smoke. Rarely, there are women who are particularly at risk of developing breast cancer, because they carry some gene variants. Some of these genes have been identified, and it is now possible to look at people’s genes to see if they are at risk of developing breast cancer. This can save lives.
How does your environment affect you? Your characteristics are affected by your environment as well as your genes. For example you may inherit genes from your parents that should make you tall, but if you have a poor diet growing up your growth could be stunted. To try and understand how much effect your environment can have on you, scientists study identical twins. Identical twins have the same genes, so any differences in personality, health and ability are caused by differences in their environment.
Play Troublesome Twin to discover just how much how much your environment can affect you.
Why do scientists study genes? Scientists have made huge breakthroughs in genetic research over the last few years, learning more and more about our genes and how they make our bodies work. Scientists examine our genes to work out family relationships, trace our ancestors, and find genes involved in illnesses. This gives them the tools to come up with better ways to keep us healthy. A big breakthrough in genetic research came in 2003, with the results of the Human Genome Project.
Watch the Zoom in on Your Genome video
What was the Human Genome Project? The Human Genome Project was an international research study to try and understand our entire genetic code – the complete instruction manual for how our bodies work. Thousands of scientists all over the world worked for over ten years to read every instruction inside every gene of a group of volunteers and put together a picture of the average human genome. They discovered we have around 20,000 genes in almost every cell in our bodies. Most genes are the same in all people, but a small number of genes, less than 1%, are slightly different between people. These small differences contribute to our unique features. Our new understanding of the human genome is leading to many advances in how we treat illness and disease.
How about Personalised Medicine? Soon everyone could have their genes read. In 2015, this costs about £5,000 so is not available to everyone. A doctor might use the information to give you specific medicines, tailored for your genes. At the moment many medicines are ‘one size fits all’, but they don’t work the same way for everyone. Some people respond really well to a medicine, some may not respond at all, and others experience bad side effects. Scientists are learning how differences in your genes affect your reaction to medicines. These genetic differences will help doctors predict which medicines will work for you, so they can prescribe personalised treatments.
Genes can tell us a lot about how to treat and prevent illness, but that's not all. Studying the genes of people around the world can also tell us about our ancestors.
What about the genetics of big populations? Studying your genes can reveal where your ancestors came from. Evidence suggests that humans originally came from Africa and spread out across the rest of the world. As humans migrated around the world, tiny variations in their genes developed. Over time, this happens naturally to help humans survive change. These variants were then passed down through generations. Scientists look at the genes of different populations of people around the world to spot these variations, trace them back though time, and map how our ancestors moved around.
Genetics is exciting, here's where to find out more
- The Wellcome Trust Sanger Institute, our partners and where much of the human genome project was performed, have made great yourgenomevideos and facts.
- Our Centre of The Cell has some easy and fun science and genes games.
- Inside DNA have some debates and current topics.
Written by Elise Mullis, David van Heel, Fran Balkwill and Kam Islam.