MUTATION(from lat. mutatio-change, change). This term in genetics is currently understood as any hereditary change that occurs in the body again. However, different researchers give this word not exactly the same meaning. M. as a genetic concept should be distinguished from the paleontological concept introduced by Waagen (Waagen) in 1869. In 1901, the Dutch botanist de Vries published a book called Mutation Theory. In it, he clearly distinguished modifications or fluctuations(see), representing small deviations from the average, to-rye are non-hereditary in nature and arise due to the diverse influences of external conditions, from M. --- sharp deviations from the norm, inherited. At present, the criterion for distinguishing between modifications and M. is only the non-hereditary nature of the former and hereditary-the latter, and not the degree of change. De Vries pointed to the importance of M. as a material for the evolutionary process and on the basis of Ch. arr. studying M. in the plant Oenothera lamarckiana expressed a number (8) of the provisions of his mutational theory: the sudden appearance of new elementary species, their constancy and nature, the periodicity of M., etc. De Vries' observations were not absolutely new. Animal breeders and plant-"waters" knew that sometimes individuals with extremely deviating properties appear in completely pure breeds and that such new characters are hereditary from the very beginning. variability (Ancon and Moshan sheep, black-shouldered peacocks, etc.) Betson wrote about discontinuous variability in 1894. De Vries’ immediate predecessor was the Russian botanist Korzhinsky (“Heterogenesis and Evolution”, 1899). on a large number of facts from the plant world, he established the existence of the so-called "heterogeneous" variations - variations that appear sharply in one single specimen due to some internal changes in germ cells - and subsequently turn out to be and 32? hereditary. Korzhinsky's views are a typical example of an autogenetic point of view, since the author emphasizes the complete independence of the occurrence of hereditary changes from the external environment. “In order to explain the origin of higher forms from lower ones, it is necessary to accept that organisms have a special tendency towards progress,” Korzhinsky writes, revealing an idealistic attitude on the question of the factors of evolution. Although the donkey (Oenothera), the study of which allowed de Vries to develop the mutation theory, turned out to be characterized by very complex and intricate phenomena that gave rise to and now generate rich literature (the so-called “controversy about evening primroses”), the existence of M. was subsequently absolutely proved, and now many M. are known in a huge number of species of animals and plants. After 1901, according to M., the works of Baur (snapdragon-Antirrhinum "ta ^ uB), Correns (night beauty - Mirabilis jalapa), East, Jones, Emerson (corn), Blaxley (datura), Nilson-Ele (oats), and many others. Of fundamental importance was also the discovery by Johansen M. in pure bean lines. M. were also found in animals, and the palm in terms of the number of found and studied M. belongs to the now extremely popular genetic object - the fruit fly Drosophila (Drosophila melanogaster).Since 1911, the study of Drosophila genetics began in the laboratory of the American scientist Morgan, and since then many hundreds of M. have been obtained, including in the USSR. come closer to understanding the patterns in their appearance.The usual term "mutation", used by Morgan in the broad sense of the word to refer to any newly emerging hereditary change, in fact, combines very different types of phenomena occurring in hereditary elements. Hereditary changes in the genotype may firstly be due to changes in the number of chromosomes and various rearrangements of their individual parts. This group of M. can be called chromosomal aberrations (deviations from the usual type). The second category of M. covers changes in individual, single hereditary factors or genes located along the length of the chromosome. Such are local M. (locus is usually understood as the place where the mutated gene is located), or otherwise "point" mutations or transgenerations (Americans use different terminology - point mutations, gene-mutations, etc.). Chromosomal abnormalities can also be very different: multiple multiplications of the number of chromosomes of the haploid set - polyploidy (triploidy, tetraploidy, etc.). d.); addition to the normal set or loss of one, two, three, etc. chromosomes-polysomy (monosomy, disomy, etc.) and heteroploidy; movement of individual sections from one chromosome to another - trans location; doubling of individual duplication sites; loss or inactivation of areas of different sizes - deletions and deficiencies; reversal of chromosomes - inversions, etc. If at first the term M. referred primarily to the emergence of new hereditary traits, now the name M. refers to changes in the gene or chromosome structure. Therefore, the term proposed by Chetverikov, genovariation = mutations in the sense of Morgan, is quite legal and is beginning to spread. According to the place of origin, M. can be classified into gametic, if they occur in the rudimentary pathway or gamete, and somatic, if any of the cells of the developing organism mutates (for example, mosaics in animals and kidney M. in plants are obtained). The change that appeared as a result of M. will be inherited in different ways depending on where and what kind of M. occurred (sex-linked and autosomal, dominant and recessive, etc.). M. are very different both in the number and degree of external signs affected by them, and in viability. Here we meet all the transitions from low specific changes, very diverse in their external expression, to highly specific ones, from those with quite normal viability to almost or completely lethal ones. The same M., both transgenations and chromosomal aberrations, can be repeated many times. Morgan v. a 1925 report (Genetics of Drosophila) indicates, for example, that about 25 changes appeared in the locus occupied by the “white eye” gene (“white”), of which 11 are different, and all of them influenced the color of the eye; M. "Notch" arose at the same time (cuttings on the wings), etc. In fact, all these numbers can be significantly increased, especially after applying the action of X-rays, rays, with the help of which it is possible to obtain both chromosomal disorders and local M in an almost unlimited number. It is characteristic that, along with points that mutate many times, there are also those in which M. were observed only 1-2 times. This seems to indicate a different degree of stability and ability to change individual points of chromosomes , but other explanations of these facts are also possible.On average, under normal laboratory conditions of breeding in Drosophila, one M. occurs in 8-10 thousand studied individuals.But if we take into account that, according to the external expression of M. can be very different - from strong and clearly visible to extremely small, the appearance of which can sometimes be judged only in a roundabout way (for example, Zeleny's data on the selection of the number of facets, proving the appearance of small M., affecting the number of facets), - the real frequency of M. is much higher. The calculations of Altenburg and Meller (Altenburg, Muller) showed that lethal M. occurs in approximately 1% of the f-chromosomes of Drosophila. Local M. (transgeneration) of the same gene can occur in different directions, i.e. M. of any gene can mutate back to its original position (reverse M.) according to the scheme A-* Aj-> A. In this sense, the mutation process is reversible. Data on certain Drosophila genes make it possible to judge the comparative rate of "direct" and "reverse" mutations (Timofeev-Resovsky). When we talk about the re-emergence of the same M., it should be borne in mind that the criterion of M.'s identity is very arbitrary. M. white (“white eyes”) appeared many times in Drosophila, but we have no sufficient reason to consider all whites the same. Analysis of many allelomorphs of the scute gene (Dubinin et al.) showed that they all differ to some extent in their action. The same applies to reverse M. Reverse M. is not always (and maybe even never) an exact return of the gene to its original normal state. The vast majority of M., in particular in Drosophila, arose under conditions of breeding in the laboratory, which previously gave reason to point to laboratory conditions as the cause of mutational phenomena in Drosophila. However, in nature, inside an outwardly homogeneous species, M. all the time arise, to-rye for a long time are in a latent (heterozygous) state and saturate this species (Chetverikov). For a long time it was not possible either to cause M. by artificial influences or even to increase the frequency of their appearance. The old materials of the Lamarckists had to be discarded as unsatisfactory in terms of methodology and built on the wrong fundamental foundations (cf. Lamarckism, Heredity and others), while exact experiments on hydrosophila gave negative results. In 1927, Meller reported that he was able to obtain from Drosophila by X-ray exposure. M.'s rays of various types, and the frequency of M.'s appearance in the experiment turned out to be 150 times greater than under ordinary conditions. From that moment on, M.'s problem entered a new phase. The following years brought complete confirmation and deepening of Meller's data on various animal and plant objects. With regard to chromosomal aberrations, many effects are already known, physical. and chem. application to-rykh causes emergence of many chromosomal abnormalities. But what other factors, besides such a specific type of radiant energy as X-rays, rays, are capable of causing transgenerations, it is difficult to say, although they are quite possible. There were only attempts to show the role of radioactive radiation from the earth, cosmic radiation, and finally high t ° (Goldschmidt, Jollos). This is directly related to the fundamental question of the causes of M. Genetics in this matter are divided into two areas: autogenetics, who recognize that the cause of the appearance of M. lies in the mutating genes themselves, and ectogenetics, who believe that M. is the result of the action on the genes of some environmental factors. One of the brightest representatives of the autogenetic trend is Korzhinsky, similar views were developed until recently by Morgan and a number of other American women. geneticists, in the USSR Filipchenko spoke out in favor of autogenesis (“The Evolutionary Idea in Biology”). Ectogenesis was clearly formulated by Geoffroy Saint-Hilaire, partly by Haeckel and Spencer. A number of Soviet geneticists who worked on the issue of artificial production of M. by the action of X-rays, rays (Agol, Levit, Serebrovsky), essentially remain on the idealistic position of autogeneticists, arguing that external conditions only cause an acceleration of the process of the emergence of M., which proceeds even without experimental impact. “Mutations naturally arise in any environment, largely autonomously from the latter. The environment surrounding the body can naturally, transforming inside the body and its germ cells, only accelerate, intensify (or, conversely, slow down) the spontaneously flowing process ”(S. G. Levit). When studying the essence of the mutation process, it is necessary to keep in mind both the properties of the germ cells themselves and their constituent parts (chromosomes, genes), and the specific (and nonspecific) effects of the external environment. to say with certainty what has happened in a chromosome or a chromosome complex. The addition or loss of whole chromosomes is usually immediately proved by cytology. But even such changes as the movement of pieces from one chromosome to another or the loss of sections of chromosomes, proved by genetic analysis, were often brilliantly confirmed by cytological pictures (Painter, Meller). Not so with transgenerations. The point of view based on the Betsonian theory of "presence-absence" that a chromosome segment is lost during transgeneration cannot be recognized as proven to any extent, although it is tempting to accept it, since it allows you to outline a single scheme M., covering as if it were different types, such as the loss of whole chromosomes or their pieces, on the one hand, and local M. - on the other (Serebrovsky). Considering that genes are parts (maybe radicals) of a giant protein molecule (Rings), one must think that the slightest chem. changes in them, the detachment of some atoms, their replacement by others, should be the sources of new M. It is not surprising that so far we reliably have X-rays, rays and temperature effects as a source of mutational changes, since, all gross chem. or mechanical influences irrevocably disrupt the complex protein structure of the chromosome. M., unlike modifications, are an important link in the evolutionary process, creating new traits that serve as material for artificial and natural selection. The doctrine of hereditary variability (mutations), together with the Darwinian idea of ​​selection, basically exhausts the content of evolutionary theory. The next task of studying M. is to elucidate the patterns of the mutation process under experimental conditions and to resolve the issue of the factors that cause M. in nature. Currently, work is underway to study the influence of the temperature of ultraviolet rays and other factors on the mutation process. Serious attention also requires the nature of the system that reacts to external influences, which is the germ cell, the bearer of hereditary, rudiments. M. in humans. Although there is no doubt that numerous hereditary diseases or deformities known to us appeared due to M., the number of such cases when M.'s appearance was actually traced is few. The main explanation, of course, is that the researcher can trace only a very small number of generations. Most often (practically, and this is extremely rare), one can trace the appearance of a dominant M. If for one or more generations not a single member of the family has had a corresponding change, and if in subsequent generations it appears and behaves as a dominant, we are undoubtedly dealing with what has happened M. Such is the case of heterohemophilia in one family described by S. G. Levit. Rokitsky considers it indisputable; if so, then this is perhaps one of the few accurately recorded cases of mutation. Koltsov described a case of dominant six-fingeredness, and Patlis - a claw-like limb, where the first generation also did not have this feature. But even in the case of dominance of change, errors are possible in determining the moment of M., t. j. 1) dominance may be incomplete, and due to some reasons that influenced the degree of dominance, the feature will “jump” the generation; 2) if the sign or b-n are such that, due to everyday conditions, they tried to hide it, the children may remain unaware of its presence in the paternal or grandfather generation. This circumstance will be more and more pronounced the further you have to climb up the pedigree. Recessive, but sex-linked M. is found not much more difficult than dominant. If M. arose in the germ cells of the mother, then her sons will already show a new feature. When M. appears in his father, his daughters will be “carriers” of the new gene, but only their sons will show it, that is, only one generation will not show the feature. An opportunity to trace recessive autosomal M. is much less. A recessive change, once having arisen, can be indefinitely latent for a long time until a marriage occurs between two heterozygotes. Therefore, observing the visible appearance of any recessive trait, in the vast majority of cases we must look for that M., the result of which it is, in the depths of centuries. An illustrative example of the length of time a recessive gene is in a heterozygous state can be the case of Friedreich's ataxia described by Ryutimeyer and Frey in 20 b-s of one Swiss village. It turned out that their common ancestor lived in the 16th century. and is separated from the surveyed families by 11-12 generations. But with all the difficulties of finding M. in humans, their search is undoubtedly necessary and is of great importance in the study of human heredity (see also somatic mutation). Lit.: Vavilov N., The law of homological series in hereditary variability, Saratov, 1920; Koltsov N., On the experimental production of mutations, J. exp. biology, vol. VI, c. 4, 1930; Korzhi n with to and y S, Heterogenesis and evolution, Zap. Ross, Academy of Sciences, Volume IX, Vol. 2, 1899; The latest experimental work on the artificial induction of mutations, Usp. exp. biol., v. VIII, c. 4, 1929; Serebrovsky A., Chromosomes and mechanisms of evolution, J. exc. biology, ser. B, vol. V, c. 1, 1926; Filipchenko Yu., Variability and methods of its study, Moscow-Leningrad, 1927 (literature is given); Chetverikov S., About some moments of the evolutionary process from the point of view of modern genetics, Zhurn. experimental biology, ser. A, vol. II, c. 1, 1926; Muller H., Artificial transmutation of the gene, Science, v. LXVI, p. 84, 1927; d e Vri e s H., Die Mutationstheorie, B. I-II, Lpz., 1901-03. See also lit. to articles Genetics, Variation and Heredity. P. Rokitsky.

Mutation is understood change in the amount and structure of DNA in a cell or in an organism. In other words, mutation is a change in the genotype. A feature of the genotype change is that this change as a result of mitosis or meiosis can be transferred to the next generations of cells.

Most often, mutations are understood as a small change in the sequence of DNA nucleotides (changes in one gene). These are the so-called. However, in addition to them, there are also when changes affect large sections of DNA, or the number of chromosomes changes.

As a result of a mutation, a new trait may suddenly appear in an organism.

The idea that it is mutation that is the cause of the appearance of new traits transmitted through generations was first expressed by Hugh de Vries in 1901. Later, mutations in Drosophila were studied by T. Morgan and the staff of his school.

Mutation - harm or benefit?

Mutations that occur in "insignificant" ("silent") sections of DNA do not change the characteristics of the organism and can be easily passed on from generation to generation (natural selection will not act on them). Such mutations can be considered neutral. Mutations are also neutral when a gene segment is replaced with a synonymous one. In this case, although the nucleotide sequence in a certain area will be different, the same protein will be synthesized (with the same amino acid sequence).

However, a mutation can affect a significant gene, change the amino acid sequence of the synthesized protein, and, consequently, cause a change in the characteristics of the organism. Subsequently, if the concentration of a mutation in a population reaches a certain level, this will lead to a change in the characteristic feature of the entire population.

In wildlife, mutations occur as errors in DNA, so all of them are a priori harmful. Most mutations reduce the viability of the organism, cause various diseases. Mutations that occur in somatic cells are not transmitted to the next generation, but as a result of mitosis, daughter cells are formed that make up a particular tissue. Often, somatic mutations lead to the formation of various tumors and other diseases.

Mutations that occur in germ cells can be passed on to the next generation. In stable environmental conditions, almost all changes in the genotype are harmful. But if environmental conditions change, it may turn out that a previously harmful mutation will become beneficial.

For example, a mutation that causes short wings in an insect is likely to be harmful in a population that lives in places where there is no strong wind. This mutation will be akin to deformity, disease. Insects with it will have difficulty finding mating partners. But if stronger winds begin to blow on the terrain (for example, as a result of a fire, a forest area was destroyed), then insects with long wings will be blown away by the wind, it will be harder for them to move. Under such conditions, short-winged individuals can gain an advantage. They will find partners and food more often than long-winged ones. After some time, there will be more short-winged mutants in the population. Thus, the mutation will be fixed and become the norm.

Mutations underlie natural selection and this is their main benefit. For the body, the overwhelming number of mutations is harmful.

Why do mutations occur?

In nature, mutations occur randomly and spontaneously. That is, any gene can mutate at any time. However, the frequency of mutations in different organisms and cells is different. For example, it is related to the duration of the life cycle: the shorter it is, the more often mutations occur. Thus, mutations occur much more frequently in bacteria than in eukaryotic organisms.

Besides spontaneous mutations(happening naturally) are induced(by a person in laboratory conditions or adverse environmental conditions) mutations.

Basically, mutations occur as a result of errors in DNA replication (doubling), repair (restoration) of DNA, with unequal crossing over, improper chromosome segregation in meiosis, etc.

So in cells, the restoration (repair) of damaged DNA sections is constantly taking place. However, if, due to various reasons, the repair mechanisms are violated, then errors in DNA will remain and accumulate.

The result of a replication error is the replacement of one nucleotide in the DNA chain with another.

What causes mutations?

Increased levels of mutations cause x-rays, ultraviolet and gamma rays. Also, mutagens include α- and β-particles, neutrons, cosmic radiation (all these are high-energy particles).

Mutagen is something that can cause mutation.

In addition to various radiations, many chemicals have a mutagenic effect: formaldehyde, colchicine, tobacco components, pesticides, preservatives, some drugs, etc.

The body of a living being consists of organs (liver, legs, eyes, etc.).

Organs are made up of tissues: bones, muscles, nerves. Tissues are made up of cells. Cells contain nuclei. The nuclei contain the chromosomes. Chromosomes carry genes. Mutations are changes in chromosomes and genes.

The cell and nucleus can be seen under a microscope, but the chromosomes are not always visible. They become visible only at certain stages of the cell's life, namely when the cell divides and forms two daughter cells. At this time, the chromosomes are rod-shaped or dot-shaped structures that stain on thin tissue sections with certain dyes more easily than the rest of the cell. Genes are too small to be seen even with a very powerful microscope, but their existence can be judged on the basis of crosses, just as the existence of atoms can be judged on the basis of chemical experiments. Genes are arranged linearly along chromosomes. In some, especially large, chromosomes, it can be seen that they consist of smaller parts, so that they look like a string of beads or a ribbon with transverse stripes. These beads and stripes are too large to represent the genes themselves, but they mark the position of the genes on the chromosomes.

Each species has a specific number of chromosomes in the nucleus. Humans have 46, mice 40, fava beans 12, and corn 20 chromosomes. Each chromosome carries hundreds or thousands of genes. It has been calculated that the chromosomes of a human cell carry at least 40,000 genes, perhaps twice as many. This is a huge number, but it doesn't seem like much when you imagine that genes are responsible for everything that is innate and hereditary in us Genes determine whether we belong to blood type A or 0, whether we were born with normal vision or suffer from one of the many types of hereditary blindness, whether we have brown, light brown, or blue eyes, whether we get fat when we eat a lot of food or stay thin, whether musical education turns us into virtuosos, or whether we continue to be unable to distinguish one sound from another, and so with thousands other features that together make up our physical and mental being.

Before cell division, each chromosome always makes an exact copy of itself, carrying the same genes in the same order. As a result, when two cells arise from one cell, the old chromosomes are separated from their newly formed counterparts and both daughter cells receive exactly the same number and type of chromosomes and genes.

The human body develops from a single cell - a fertilized egg containing 46 chromosomes. The ovum divides and forms two cells, which divide again to form four cells, and so on until the whole body with its billions of cells is formed. Before each cell division, chromosomes and genes are duplicated. Thus, each cell always contains the same 46 chromosomes carrying the same genes.

The process by which the duplication of chromosomes and genes occurs is extremely precise. It leads to the appearance of millions and billions of cells with exactly the same genes. However, sometimes, perhaps once in a million, something in this process is disturbed. A gene undergoes a chemical change, or a new gene is not exactly similar to the old one, or the order of the genes in the chromosome changes. This process of change in a gene or chromosome is called a mutation. Its result, i.e., the altered gene or chromosome itself, is also often called a mutation, but in order to avoid confusion, it is better to speak of a mutated gene or rearranged chromosome, and keep the term "mutation" for the process that caused them. An individual who exhibits the effect of a mutated gene or rearranged chromosome is called a mutant.

When a mutated chromosome doubles in preparation for the next division, it reproduces just as exactly a copy of the mutated gene or new order of genes as it does of the unchanged regions. In this way, the mutated gene is inherited and reproduced in exactly the same way as the original gene from which it originated is inherited. The vast variety of genes found in every species of organism in existence is the result of mutations, many of which occurred millions of years ago.

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What is a mutation? This, contrary to erroneous ideas, is not always something terrible or life-threatening. The term refers to a change in the genetic material that occurs under the influence of external mutagens or the body's own environment. Such changes can be beneficial, not affect the functions of internal systems, or, on the contrary, lead to serious pathologies.

Varieties of mutations

It is customary to subdivide mutations into genomic, chromosomal and gene mutations. Let's talk about them in more detail. Genomic mutations are changes in the structure of hereditary material that radically affect the genome. These include, first of all, an increase or decrease in the number of chromosomes. Genomic mutations are pathologies that are often found in the plant and animal world. Only three varieties have been found in humans.

Chromosomal mutations are persistent abrupt changes. They are associated with the structure of the nucleoprotein unit. These include: deletion - the loss of a section of a chromosome, translocation - the movement of a group of genes from one chromosome to another, inversion - a complete rotation of a small fragment. Gene mutations- this is the most common type of change in genetic material. It is much more common than chromosomal.

Beneficial and neutral mutations

Harmless mutations that occur in humans include heterochromia (irises of different colors), transposition of internal organs, and abnormally high bone density. There are also useful modifications. For example, immunity to AIDS, malaria, tetrachromatic vision, hyposomnia (reduced need for sleep).

Consequences of genomic mutations

Genomic mutations are the causes of the most serious genetic pathologies. Due to a change in the number of chromosomes, the body cannot develop normally. Genomic mutations almost always lead to mental retardation. These include trisomy of the 21st chromosome - the presence of three copies instead of the normal two. She is cause Down syndrome. Children with this disease experience learning difficulties, lag behind in mental and emotional development. The prospects for their full life depend, first of all, on the degree of mental retardation and the effectiveness of training with the patient.

Another terrible deviation is the monosomy of the X chromosome (the presence of one copy instead of two). Leads to another severe pathology - Shereshevsky-Turner syndrome. Only girls suffer from this disease. The main symptoms include short stature, sexual underdevelopment. Often there is a mild form of oligophrenia. Steroids and sex hormones are used for treatment. As you can see, genomic mutation is the cause of severe developmental pathologies.

Some chromosomal pathologies

Hereditary diseases caused by a mutation of several genes at once or any violation of the chromosome structure are called chromosomal diseases. The most common of these is Angelman syndrome. This hereditary disease is caused by the absence of several genes on the maternal chromosome 15. The disease manifests itself at an early age. The first signs are a decrease in appetite, the absence or poverty of speech, a constant unreasonable smile. Children with this pathology experience difficulties with learning and communication. The type of inheritance of the disease is still being studied.

A disease similar to Angelman's syndrome is Prader-Willi syndrome. Here, too, there is a lack of genes on the 15th chromosome, only not maternal, but paternal. Main symptoms: obesity, hypersomnia, strabismus, short stature, impaired mental function. This disease is difficult to diagnose without genetic analysis. As with many hereditary diseases, a complete therapy has not been developed.

Some gene diseases

Genetic disorders include metabolism, caused by a monogenic mutation. These are violations of the metabolism of carbohydrates, proteins, lipids, amino acid synthesis. A disease familiar to many, phenylketonuria, is caused by a mutation in one of the many genes on the 12th chromosome. As a result of the change, one of the essential amino acids phenylalanine is not converted into tyrosine. sick of it genetic disease you have to avoid any food containing even a small amount of phenylalanine.

One of the most serious connective tissue diseases, fibrodysplasia, is also caused by a monogenic mutation on the 2nd chromosome. In patients, muscles and ligaments stiffen over time. The course of the disease is very severe. A complete treatment has not been developed. The type of inheritance is autosomal dominant. Another dangerous disease is Wilson's disease - a rare pathology, which is manifested by a violation of copper metabolism. The disease is caused by a gene mutation on the 13th chromosome. The disease is manifested by the accumulation of copper in the nervous tissue, kidneys, liver, cornea of ​​the eyes. At the edges of the iris, you can see the so-called Kaiser-Fleischner rings - an important symptom in diagnosis. Usually the first sign of the presence of Wilson's syndrome is a violation in the liver, its pathological increase (hepatomegaly), cirrhosis.

As can be seen from these examples, gene mutation is often the cause of serious and currently incurable diseases.