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No; only a small percentage of mutations cause genetic disordersamost have no impact on health or development. For example, some mutations alter a gene's DNA sequence but do not change the function of protein made by the gene. Often, gene mutations that could cause genetic disorder are repaired by certain enzymes before a gene is expressed and an altered protein is produce. Each cell has a number of pathways through which enzymes recognize and repair errors in DNA. Because DNA can be damaged or mutate in many ways, DNA repair is an important process by which the body protects itself from disease. A very small percentage of all mutations actually have a positive effect. These mutations lead to new versions of proteins that help an individual better adapt to changes in his or her environment. For example, beneficial mutation could result in protein that protects individuals and future generations from new strains of bacteria. Because a person's genetic code can have large number of mutations with no effect on health, diagnosing genetic conditions can be difficult. Sometimes, genes thought to be related to particular genetic condition have mutations, but whether these changes are involved in development of condition has not been determine; these genetic changes are known as variants of unknown significance or. Sometimes, no mutations are found in suspected disease - related genes, but mutations are found in other genes whose relationship to particular genetic condition is unknown. It is difficult to know whether these variants are involved in disease. The University of Utah Genetic Science Learning Center provides information about genetic disorders that explains why some mutations cause disorders but others do not. The National Human Genome Research Institute provides information about human genomic variation. Cold Spring Harbor National Laboratoryas DNA From Beginning explains the discovery of DNA repair mechanisms in cells and introduces researchers who work to understand these mechanisms. Force explains the significance of variants of unknown significance in cancer.
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Because so many chronic illnesses dont manifest until later in life, unusually healthy elderly are one good place to start searching for protective mutations. There have been few hypotheses about why some people live such long, healthy lives, says Nir Barzilai of Albert Einstein College of Medicine. One was that these guys have perfect genome; they just do have any of the mutations that are associated with disease, he say. Another was that theyre all lean, nonsmoking vegetarians. Recent studies quash both these theories. Last year, Barzilais group analyzed 44 full genome sequences from centenarians. In total, group had 250 mutations linked to Parkinsons, Alzheimers, cardiovascular Disease, and other chronic conditions, scientists report in Molecular Genetics and Genomic Medicine. Moreover, some hundred - year - olds were obese, others had been lifelong smokers, and many had never regularly exercise. However, they all lived century, and none had developed signs of chronic disease. That leaves us with the fact that they must have some genomic reasonsother than lack of disease genesfor their longevity, says Barzilai. Shortly after Barzilais Study was publish, NHGRI researchers led by Biesecker analyzed protein - coding genes, or exomes, of 951 healthy adults and found that 1 in 10 had mutations linked to Parkinsons, heart defects, and blood disorders, among other things. These are gene variants that do just increase disease risk but are thought to always cause disease. But half of those people were not ill. Despite such tantalizing clues, searches for protective mutations that could be offsetting effects of disease - link genes and lifestyle factors have been hit and miss so far. In 2007, Eric Topol of Scripps Institute and his colleagues, eager to look at concentrated collection of healthy genomes, began recruiting people over the age of 80 who didnt have chronic diseases and were on medications, as part of the Scripps Wellderly Project. Over the next 7 years, they will develop a cohort of 1 400 so - called Wellderly. In 2014, they published full genomes of 454 participants in an open - access database for researchers anywhere in the world to use. So far, no protective mutations have been turned up. But the hunt is on, Topol say. Over a similar period, Barzilai, keen to focus on relatively homogeneous population to facilitate discovery of genetic variants, Study Ashkenazi Jews over the age of 95. Barzilais LonGenity Project has collected genetic and health information from over 500 of these extreme elderly as well as 700 of their offspring. Even before theyd completed full genomes of their centenarians, Barzilai and his colleagues had turned up two promising gene variants. Deletion in adiponectin gene ADIPOQ, they find, appears to protect against inflammation of arteries. And mutation in cholesteryl ester transfer - protein gene CETP was seen more often in older cohort, and was linked to protection against both high cholesterol levels and cognitive disorders.
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|Name||Disease||Molecular Defect||Donor Cell||Age||Sex|
|ADA||ADA-SCID||GGG > AGG, exon 7 and Del(GAAGA) exon 10, ADA gene||Fibroblast||3M||Male|
|GD||Gaucher's disease type III||AAC > AGC, exon 9, G-insertion, nucleotide 84 of cDNA, GBA gene||Fibroblast||20Y||Male|
|DMD||Duchenne muscular dystrophy||Deletion of exons 45-52, dystrophin gene||Fibroblast||6Y||Male|
|BMD||Becker muscular dystrophy||Unidentified mutation in dystrophin gene||Fibroblast||38Y||Male|
|DS1||Down syndrome||Trisomy 21||Fibroblast||1Y,1M||Male|
|JDM||Juvenile diabetes mellitus||Multifactorial||Fibroblast||42Y||Female|
|SBDS||Shwachman-Bodian-Diamond syndrome||IV2 + 2T > C and IV3 - 1G > A, SBDS gene||Bone marrow mesenchymal cells||4M||Male|
|HD||Huntington's disease||72 CAG repeats, huntingtin gene||Fibroblast||20Y||Female|
|LNSc||Lesch-Nyhan syndrome (carrier)||Heterozygosity of HPRT1||Fibroblast||34Y||Female|
Kathiresans experiment depends on the huge NHLBI exome database because beneficial mutations are both hard to find and hard to prove. For his plan to predict drugs performance in trials, as with any efforts to hunt down protective mutations, researchers need very large pools of people and loads of data on their health. If a few people with rare disease also all share rare genetic mutation, there is a good bet that the mutation is related to their disease. But if a handful of healthy people have the same genetic mutation, it is more likely to be coincidence, and more difficultfrom statistical standpointto demonstrate causation. Risk and protection are really just flip sides of the same coin, says Kathiresan. If you have a mutation that increases risk in 5 percent of people, you could really say that 95 percent of people have a protective version of gene. When he and his team looked for mutations linked to low blood triglycerides, they decided their quarry had to both knock out or impede protein function and lower risk below norm. Amid 100 000 exomes, they managed to find four variants in APOC3, each of which occur in only around 1 in 1 000 people. The Bieseckers ClinSeq study, with under 1 000 participants, was even designed to seek out protective mutations, only to document examples of people with disease - causing gene variants but no disease. That is because getting enough people to search for disease - preventing genes is such a challenge, Biesecker say. Complicating matters, vast networks of related genes might contribute to giving disease or set of symptoms. We 've long known that you can have genegene interactions and that one gene variant can compensate for another. But these things are statistically and mathematically challenging to study because combinatorial possibilities here are enormous, he say. It is a numbers and power issue. Wed need millions of people in cohort to be able to statistically tease those things out. Efforts are underway to construct enormous databases that can be mined for protective mutations. Perhaps most ambitious is the Resilience Project, lead by researchers at Icahn School of Medicine at Mount Sinai in New York and Sage Bionetworks in Seattle. They are attempting to solicit 1 million volunteers to donate DNA samples. Projects focus on finding people in this huge random sample who harbor gene mutations known to cause rare and severe disorders when a single gene copy is present, such as Costello Syndrome and Cardiofaciocutaneous Syndrome, yet who may not even know they have disease. The potential value of such a database, especially the prospect of including detailed health histories to detect presence or absence of illness, is illustrated by lucky break that led Altschulers group at Broad group to zero in on one variant of SLC30A8 gene. Team had data suggesting that SLC30A8 might be protective, but they could quite come up with the statistical power they needed to prove gene effect.
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|Gene Variant||Environmental Exposure||Relative Risk (XP)||Relative Risk (PKU)||Relative Risk (emphysema)|
|Present||Present||Very High||Very High||High|
Wellderly, there is only one harboring potential genetic gems; examining infectious disease survivors offers another promising avenue. Wherever there is a profound infectious disease infecting the community, looking at survivors enables you to look for resistance genes which may cast enormous light on the etiology of disease and potentially lead to new treatment, says neurologist John Collinge of University College London. Researchers, for example, are investigating drugs to fight the Ebola virus that target protein known as Niemann Pick Type C. Genes that encode it, when mutate, cause rare version of Niemann Pick Disease that is usually fatal in childhood to people with two copies. But in animal studies, individuals with only one mutated copy of gene resist Ebola infection because the virus needs a working version of protein to infect host cells. In other recent research, investigators have looked for gene mutations that protect against infection, or severe illness from influenza and other pathogens. In October, researchers with MalariaGEN international consortium identified a gene variant that affects blood cell surface receptor and protects against severe cases of malaria. Collinge and his colleagues have been studying survivors of more exotic epidemic: kuru, deadly neurological illness similar to Creutzfeld Jakob Disease. Like CJD, kuru is transmitted by misshapen proteins called prions, and, in the 1950s and 1960s, it spread rapidly among members of cannibalistic tribe in Papa New Guinea. When someone dies of kuru, ritualistic consumption of their body means that those participating in the ceremony would contract the disease too. In some villages, almost all women of childbearing age perish. But decades later, there were also survivorspeople who partaken in feasts and never got sick. In the early 1990s, Collinge began sequencing their genomes. Over the past two decades, hes revealed mutations in their prion protein gene, PRNP, that protect them from kuru. In those families with polymorphism, there is hardly any kuru despite very high levels of exposure, says Collinge. This year, Collinge and his colleagues report in Nature that mice with one of the mutations were protected from 18 different kinds of prion disease. This particular finding is incredibly powerful, says Collinge. We go from 100 percent of mice dying to 0 percent. Now, researchers are working on determining the structure of protective prion proteins, which could shed light on how to mimic mutations in the rest of the human population, possibly leading to treatments for not just kuru but a variety of prion diseases. Ideally, discovery of protective mutation could inform development of drugs that mimic its molecular effects in the body. Inhibitors of CETP, studied by Barzilai, have been explored as cholesterol drugs, although none has reached the market.
Since Allison and Haldane's work, action of natural selection on genetic resistance to malaria has been shown in a multitude of contexts. Indeed, Sickle - Cell variant has been identified in four distinct genetic backgrounds in different African populations, suggesting that the same mutation arise independently several times through convergent evolution. Beyond HbS, other distinct mutations in HBB gene have generated HbC and HbE alleles, which arose and spread in Africa and in Southeast Asia, respectively. Various HBB alleles aren't alone in offering protection against malaria, however. Geographic distributions of several other red blood cell disorders, including - thalassemia, G6PD deficiency, and ovalocytosis, correlate to malaria endemicity, and diseases are also linked to malaria resistance. An even more striking worldwide geographical difference exists for mutation in Duffy antigen gene, which encodes membrane protein used by Plasmodium vivax malaria parasite to enter red blood cells. This mutation disrupts protein, thus conferring protection against P. Vivax malaria, and it occurs at a prevalence of 100% throughout most of sub - Saharan Africa yet is virtually absent outside of Africa. Moreover, through convergent evolution, independent mutation in FY that decreases this gene's expression has also become prevalent in Southeast Asia. So, why has malaria exerted such strong selective pressure? Scientists now know the answer. Malaria is arguably one of the human population's oldest diseases and the greatest causes of morbidity and mortality. Research indicates that the malaria - causing parasite Plasmodium falciparum has occurred in human populations for approximately 100 000 years, with LARGE population expansion in the last 10 000 years AS human populations begin to move into settlements. P. Falciparum, together with other malaria species, P. Vivax, P. Malariae, and P. Ovale, infect hundreds of millions of people worldwide each year, and kill more than 1 million children annually. Because this disease is so devastating, humans have had to evolve adaptive traits to survive in the face of this infectious condition over the past few millennia. While malaria is the best - understood example of an infectious disease that has driven human evolution, numerous other infectious diseases have also acted on human populations over generations, thus allowing resistance alleles to emerge and spread over time. Base on historical records from the last millennium, these diseases might include smallpox in ancient Europe and in Native American populations, AS well AS cholera, tuberculosis, and bubonic plague in Europe. Many diseases in Africa have likely been endemic for even longer, such AS numerous diarrheal diseases, yellow fever, and Lassa hemorrhagic fever. Today, with access to heretofore unprecedented data sets for the study of human genetic variation, researchers can exploit genetic signatures of natural selection using novel analytical methods. In this way, they can identify genetic variants conferring resistance to infectious diseases that have spread through human populations over time. These studies will help elucidate natural mechanisms of defense and perhaps uncover novel evolutionary pressures. Moreover, same tools that have revolutionized study of natural selection in humans will also make unprecedented studies of pathogens possible.
Beneficial mutations are often assumed to be rare, and adaptation therefore to be mutation limit. This is the basis for the picture of successional selective sweeps and the conclusion that mutations arise and fix at a rate proportional to NU B S. This picture of successional sweeps underlies the strong - selection weak - mutation assumption that is essential to many conclusions in population genetics and evolutionary theory. This assumption is likely to be correct for evolution of some strongly selected characters in complex multicellular organisms. But most unicellular organisms and viruses tend to live in much larger population sizes and can have larger mutation rates. For such populations, much of one's intuition from rare - mutations picture will often be wrong. This makes it important to go beyond successional - mutations regime and to develop understanding of evolutionary dynamics when beneficial mutations are common. This is a very broad subject. In this article, we have focus on concurrent - mutations regime in which there is strong selection and strong mutation. By strong mutation, we mean that total beneficial mutation production rate NU B is sufficiently large that the time to establish a mutant population is less than the time it will take to sweep to fixation. As establishment time is 1 / and sweep time is, condition to be in concurrent mutations regime is, so that multiple beneficial mutations are present in the population and tend to interfere. By strong selection, we mean both and. The former condition is what is commonly meant by strong selection and is required to ensure that selection is strong compared to drift except when subpopulations are rare. The latter constraint makes analysis simpler, because it ensure that only one population at a time needs to be treated stochastically, but is not essential for the general picture. The concurrent - mutations regime that we analyze is likely to be quite common in nature. Even if there are only 10 or so beneficial point mutations available to a population that has a per base pair mutation rate of order 10 9, this gives U B 10 8. To have, we therefore need only population sizes of order 10 7. In other words, if there are even a few mutations of effect available, population as small as 10 7 individuals will experience multiple - concurrent - mutation effects. These sizes are well within normal ranges for many populations, including, for example, Escherichia coli in single human gut, cells in evolving cancer, pathogens within a single host, and many others. Moreover, this is a very conservative estimate. Viral and certain bacterial populations, or mutator strains in any organism, often have much higher overall mutation rates. Organisms with more beneficial mutations available will also have much larger U B. In recent experiments in Saccharomyces cerevisiae adapting to low glucose, we have inferred a beneficial mutation rate of U B = 10 5. 5 in nonmutator strains and order of magnitude higher in mutators. Such values are not atypical.
Mutation, alteration in genetic material of cell of living organism or of virus that is more or less permanent and that can be transmitted to cells or virus descendants. Mutations in DNA of body cell of a multicellular organism may be transmitted to descendant cells by DNA replication and hence result in sectors or patches of cells having abnormal function, example being cancer. Mutations in egg or sperm cells may result in individual offspring, all of whose cells carry mutation,ss which often cause some serious malfunction, as in the case of human genetic disease such as cystic fibrosis. Mutations result either from accidents during normal chemical transactions of DNA, often during replication, or from exposure to high - energy electromagnetic radiation or particle radiation or to highly reactive chemicals in the environment. Because mutations are random changes, they are expected to be mostly deleterious, but some may be beneficial in certain environments. In general, mutation is the main source of genetic variation, which is raw material for evolution by natural selection. The genome is composed of one to several long molecules of DNA, and mutation can occur potentially anywhere on these molecules at any time. Most serious changes take place in functional units of DNA, genes. A mutated form of gene is called mutant allele. Genes are typically composed of the regulatory region, which is responsible for turning gene transcription on and off at appropriate times during development, and the coding region, which carries genetic code for the structure of functional molecule, generally protein. Protein is a chain of several hundred amino acids. Cells make 20 common amino acids, and it is the unique number and sequence of these that give protein its specific function. Each amino acid is encoded by a unique sequence, or codon, of three of four possible base pairs in DNA. Hence, mutations that change DNA sequence can change amino acid sequence and, in this way, potentially reduce or inactivate protein function. Change in DNA sequence of gene regulatory region can adversely affect timing and availability of gene proteins and also lead to serious cellular malfunction. On the other hand, many mutations are silent, showing no obvious effect at functional level. Some silent mutations are in DNA between genes, or they are of the type that results in no significant amino acid changes. Mutations are of several types. Changes within genes are called point mutations. The simplest kinds are changes to single base pairs, called base - pair substitutions. Many of these substitute incorrect amino acids in corresponding position in encoded protein, and of these large proportion result in altered protein function. Some base - pair substitutions produce stop codon.
Imagine making random changes in a complicated machine such as a car engine. The chance that random change would improve the functioning of a car is very small. Change is far more likely to result in cars that do not run well or perhaps do not run at all. By same token, any random change in a gene's DNA is likely to result in proteins that do not function normally or may not function at all. Such mutations are likely to be harmful. Harmful mutations may cause genetic disorders or cancer. A Genetic disorder is a disease caused by mutation in one or few genes. Human example is cystic fibrosis. A Mutations in a single gene causes the body to produce thick, sticky mucus that clogs lungs and blocks ducts in digestive organs. You can watch a video about cystic fibrosis and other genetic disorders at this link: http: / www. Youtube. Com / watch? V = 8s4he3wLgkM. Cancer is a disease in which cells grow out of control and form abnormal masses of cells. It is generally caused by mutations in genes that regulate cell cycle. Because of mutations, cells with damaged DNA are allowed to divide without limits. Cancer genes can be inherit. You can learn more about hereditary cancer by watching the video at the following link: http: / www. Youtube.
Genetic mutation is permanent alteration in DNA sequence that make up gene, such that sequence differs from what is found in most people. Mutations range in size; they can affect anywhere from single DNA building block to large segments of the chromosome that include multiple genes. Evolution would have been possible without mutations. For example, about 12 000 years ago, single human had mutation that granted them incredible power to digest milk from cow. Today, this mutation is a common trait, and weve get entire industries devoted to producing and selling cow milk in various forms. Scientists have estimated that every time the human genome replicates itself, there are roughly 100 new mutations. Most of them are negligible, but so often mutation expresses itself in the form of superhuman ability. Here are eight such bizarre mutations:
Sickle - cell anemia is a hereditary disease which is characterized by a mutated form of hemoglobin that causes red blood cells to take on a distorted shape, which reduces their ability to carry oxygen. Even though this is obviously a disadvantage, there is a bright side as sickle cells have proven to be resistant to malaria. People with sickle - cell anemia carry two copies of mutation, but individuals with only a single copy can maintain malaria resistance without exhibiting any sickle - cell symptoms. It is because they still have normal enough shaped red blood cells to nullify the effects of misshapen ones. Research indicates that certain variations in genes are responsible for sickle - cell anemia that could offer up to 93% higher resistance to malaria with only mild anemic symptoms associate. A Mutations like this would have the potential to spread very quickly throughout the human population since it unmistakably beneficial to survival.
But we also know that categorising mutations as good or bad can sometimes be very difficult. Often it depends on context,. For example, whether mutation helps organism use particular food source or fight off disease present during its lifetime. And some mutations can be beneficial if just one copy is inherit, but harmful if two copies are inherit. One example of gene mutation subject to this kind of balancing selection is sickle cell disease. People with sickle - cell disease have gene mutation that produce an altered form of haemoglobin, protein in red blood cells that carry oxygen around the body. Altered haemoglobin produces long sickle - shaped blood cells that can get stuck in small blood vessels. This causes pain in the chest and joints, as well as anaemia, increasing the risk of infections and other problems. Yet despite these potentially devastating health effects, disease is relatively common in certain countries. An estimated 300 000 infants who inherit two copies of sickle - cell gene mutation are born with the disease every year, mostly in Nigeria, Democratic Republic of Congo, and India. This is because people with one copy of mutation are resistant to malaria, and so are more likely to survive to adulthood and pass mutated gene on to their children. So, even though having sickle disease is an evolutionary disadvantage, unaffected carriers of gene mutation have survival advantage in countries where malaria was rife. A recent US study suggests that all people living with the condition today descended from a single ancestor who lived around 7 300 years ago in either Sahara or west - central Africa. This shows how a single mutation can spread to many, many individuals in the population if it bestows significant benefit, even if it also has potential to do harm. Similarly, there is evidence that a single copy of cystic fibrosis gene mutation may have provided our ancestors with resistance to cholera, and that carriers of Tay - Sachs disease have tuberculosis resistance. Better understanding of the effects of mutations could play a big role in treating disease. For example, studying mutation rates in different cell types could shed light on how cancer arises in different body tissues. And understanding bacterial mutation rates could help scientists fight microbes that have evolved resistance to antibiotics. This will eventually help usher in a new era of Medicine, in which many diseases will be diagnosed and treated with the help of genetic information. And that get to be good.
Important questions to be addrest include predicting fate of individual mutations such as their fixation probability P fix and times to loss T loss or fixation T fix in population, how flux of mutations will impact properties of the population such as nucleotide diversity, divergence, survival or rate of evolution of quantitative traits, how fates of different mutations will affect each other, how quantitative genetic variation is maintain, and estimation of evolutionary parameters of populations and species from DNA sequence patterns theories to investigate some of these questions can be categorize by complexity of models assume and by their general approach: those restrict to single sites, in which all mutations are treat as completely independent of each other; those invoking linkage, in which changes in frequency of mutations are no longer independent, even if their effects are independent; and those invoking epistasis in which effects of mutations depend on which others are present. In each case, overall effects of mutations can be studied in two ways. Analysis may focus on individuals and their mutations explicitly, track their fate and later summarize behaviour of many mutations in the population to compute quantities like DNA sequence diversity. Alternatively, it may focus directly on quantitative traits in which mutations are not individually identified but considered more implicitly as components of total effect on either individual or population mean phenotype.
Mutations are one of the fundamental forces of evolution because they fuel variability in populations and thus enable evolutionary change. Base on their effects on fitness, mutations can be divided into three broad categories: good or advantageous that increase fitness, bad or deleterious that decrease it and indifferent or neutral that are not affected by selection because their effects are too small. While this simplistic view serves well as the first rule of thumb for understanding the fate of mutations, research in recent decades has uncovered a complex web of interactions. For example, effects of mutations often depend on the presence or absence of other mutations, Their effects can also depend on the environment, fate of mutations may depend on the size and structure of the population, which can severely limit the ability of selection to discriminate among three types, and mutations fate can also depend on fate of others that have more pronounced effects and are in close proximity on same chromosome. Major theoretical goal in the study of population genetics of mutations is to understand how mutations change populations in the long term. To this end, we have to consider many features of evolution and extant populations at both phenotypic and molecular level, and ask how these can be explained in terms of rates and kinds of mutations and how they are affected by forces that influence their fates. We have increasing amounts of information at our disposal to help us answer these questions. Continuous improvement of DNA sequencing technology is providing more detailed genotypes on more species and observations of more phenomena at genomic level. We are also gaining more understanding of processes that lead from changes in level of genotypes through various intermediate molecular changes in individuals to new visible phenotypes. Use of this new knowledge presents both opportunities and challenges to our understanding, and new methods have been developed to address them. Brian Charlesworth has been at the forefront of many developments in population genetics of mutations, both in collection and analysis of new data and in providing new models to explain observations he and others have make. This themed issue of Phil. Trans. R. Soc. B is dedicated to him to mark his 65 birthday. Authors of accompanying papers have individually made important contributions to the field and have been directly associated with or indirectly influenced by their work. In this collection of papers, various aspects are considered in detail, and in this introduction, we aim to provide an overview as the basis for in - depth treatments that follow. We outline some of theories that serve as quantitative basis for more applied questions and have been developed with main aims of: measuring rates at which different types of mutations occur in nature, predicting quantitatively their subsequent fate in populations, and assessing how they affect some properties of populations and therefore could be use for inference.
Heredity is the passing of genes from one generation to the next. You inherit your parents ' genes. Heredity helps to make you the person you are today: short or tall, with black hair or blond, with brown eyes or blue. Can your genes determine whether you 'll be a straight - student or a great athlete? Heredity plays an important role, but your environment also influences your abilities and interests. People can have changes in genes that can cause many problems for them. Sometimes changes cause little differences, like hair color. Other changes in genes can cause health problems. Mutations in gene usually end up causing that particular gene copy to not do its job the way it normally should. Since we have two copies of every gene, typically there's still a normal working copy of gene. In these cases, usually nothing out of ordinary happens since the body can still do the jobs it needs to do. This is an example of autosomal recessive trait. For someone to have recessive disease or characteristic, person must have gene mutation in both copies of gene pair, causing the body to not have working copies of that particular gene. Genes can be either dominant or recessive. Dominant genes show their effect even if there is just one mutation in one copy of that gene pair; one mutation dominates the normal back - up copy of the gene, and the characteristic shows itself. People can be born with gene mutations, or they can happen over their lifetime. Mutations can occur when cells are aging or have been exposed to certain chemicals or radiation. Fortunately, cells usually recognize these types of mutations and repair them by themselves. Other times, however, they can cause illnesses, such as some types of cancer. If gene mutations exist in egg or sperm cells, children can inherit gene mutations from their parents. When mutation is in every cell of the body, body is not able to repair gene change.
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