The discoveries of the exon-intron organization of eukaryotic genes and the possibility of alternative splicing have shown that the same nucleotide sequence of the primary transcript can provide the synthesis of several polypeptide chains with different functions or their modified analogs. For example, yeast mitochondria contain the box (or cob) gene encoding the cytochrome b respiratory enzyme. It can exist in two forms: The “long” gene, consisting of 6400 bp, has 6 exons with a total length of 1155 bp. and 5 introns. The short form of the gene consists of 3300 bp. and has 2 introns. It is actually a "long" gene devoid of the first three introns. Both forms of the gene are equally well expressed.

After the removal of the first intron of the “long” box gene, based on the combined nucleotide sequence of the first two exons and part of the nucleotides of the second intron, a template for an independent protein, RNA maturase, is formed (Fig. 3.43). The function of RNA maturase is to provide the next stage of splicing - the removal of the second intron from the primary transcript and, ultimately, the formation of a template for cytochrome b.

Another example is a change in the splicing pattern of the primary transcript encoding the structure of antibody molecules in lymphocytes. The membrane form of antibodies has a long "tail" of amino acids at the C-terminus, which ensures the fixation of the protein on the membrane. The secreted form of antibodies does not have such a tail, which is explained by the removal of nucleotides encoding this region from the primary transcript during splicing.

In viruses and bacteria, a situation has been described where one gene can simultaneously be part of another gene, or some DNA nucleotide sequence can be part of two different overlapping genes. For example, on the physical map of the phage FX174 genome (Fig. 3.44), it can be seen that the B gene sequence is located inside the A gene, and the E gene is part of the D gene sequence. This feature of the organization of the phage genome managed to explain the existing discrepancy between its relatively small size (it consists of 5386 nucleotides) and the number of amino acid residues in all synthesized proteins, which exceeds the theoretically permissible for a given genome capacity. The possibility of assembling different peptide chains on mRNA synthesized from overlapping genes (A and B or E and D) is ensured by the presence of ribosomal binding sites within this mRNA. This allows translation of another peptide to start from a new point of reference.

The nucleotide sequence of the B gene is also part of the A gene, and the E gene is part of the D gene.

In the λ phage genome, overlapping genes were also found, translated both with a frameshift and in the same reading frame. It is also assumed that two different mRNAs can be transcribed from both complementary strands of the same DNA region. This requires the presence of promoter regions that determine the movement of RNA polymerase in different directions along the DNA molecule.

The described situations, which testify to the admissibility of reading different information from the same DNA sequence, suggest that overlapping genes are a fairly common element in the organization of the genome of viruses and, possibly, prokaryotes. In eukaryotes, gene discontinuity also allows the synthesis of various peptides based on the same DNA sequence.

With all of this in mind, it is necessary to amend the definition of a gene. Obviously, one can no longer speak of a gene as a continuous sequence of DNA that uniquely encodes a specific protein. Apparently, at present, the formula "One gene - one polypeptide" should still be considered the most acceptable, although some authors suggest changing it: "One polypeptide - one gene." In any case, the term gene should be understood as a functional unit of hereditary material, which by its chemical nature is a polynucleotide and determines the possibility of synthesizing a polypeptide chain, tRNA or rRNA.

One gene one enzyme.

In 1940, J. Beadle and Edward Tatum used a new approach to study how genes provide metabolism in a more convenient object of research - the microscopic fungus Neurospora crassa .. They obtained mutations in which; there was no activity of one or another metabolic enzyme. And this led to the fact that the mutant fungus was not able to synthesize a certain metabolite itself (for example, the amino acid leucine) and could live only when leucine was added to the nutrient medium. The theory "one gene - one enzyme" formulated by J. Beadle and E. Tatum quickly gained wide recognition among geneticists, and they themselves were awarded the Nobel Prize.

Methods. selection of the so-called "biochemical mutations" that lead to disruption of the action of enzymes that provide different metabolic pathways, proved to be very fruitful not only for science, but also for practice. First, they led to the emergence of genetics and selection of industrial microorganisms, and then to the microbiological industry, which uses strains of microorganisms that overproduce such strategically important substances as antibiotics, vitamins, amino acids, etc. The principles of selection and genetic engineering of strains of overproducers are based on the notion that "one gene codes for one enzyme". And although this idea is excellent practice brings multi-million dollar profits and saves millions of lives (antibiotics) - it is not final. One gene is not just one enzyme.

First research. After in 1902 Garrod pointed out the connection of a genetic defect in alkaptonuria with the body's inability to break down homogentisic acid, it was important to elucidate the specific mechanism underlying this disorder. Since then it was already known that metabolic reactions are catalyzed by enzymes, it could be assumed that it was the violation of some enzyme that leads to alkaptonuria. Such a hypothesis was discussed by Driesch (in 1896). It was also expressed by Haldane (1920, see) and Garrod (1923). Important stages in the development of biochemical genetics were the work of Kuhn and Butenandt on the study of eye color in the mill moth. Ephesia kuhniella and similar studies by Beadle and Ephrussi on Drosophila(1936). In these pioneering works, insect mutants previously studied by genetic methods were selected to elucidate the mechanisms of action of genes. However, this approach did not lead to success. The problem turned out to be too complicated, and in order to solve it, it was necessary:

1) choose a simple model organism convenient for experimental study;

2) to look for the genetic basis of biochemical traits, and not the biochemical basis of genetically determined traits. Both conditions were met by Beadle and Tatum in 1941 (see also Beadle 1945).

Beadle and Tatum model. Their article began like this:

“From the point of view of physiological genetics, the development and functioning of an organism can be reduced to complex system chemical reactions that are somehow controlled by genes. It is quite logical to assume that these genes ... either act as enzymes themselves, or determine their specificity. It is known that genetic physiologists usually try to investigate the physiological and bio chemical bases already known hereditary traits. This approach made it possible to establish that many biochemical reactions are controlled by specific genes. Such studies have shown that enzymes and genes have the same order of specificity. However, the scope of this approach is limited. The most serious limitation is that, in this case, hereditary traits that do not have a lethal effect and, therefore, are associated with reactions that are not very important for the life of the organism, fall into the field of view of researchers. The second difficulty ... is that the traditional approach to the problem involves the use of outwardly manifest signs. Many of them are morphological variations based on systems of biochemical reactions so complex that their analysis is extremely difficult.

These considerations led us to the following conclusion. The study common problem genetic control of biochemical reactions that determine development and metabolism should be carried out using procedure opposite to the generally accepted: instead of trying to find out the chemical basis of known hereditary traits, it is necessary to establish whether genes control known biochemical reactions and how they do it. The ascomycete neurospore has the properties that make it possible to implement this approach and, at the same time, serves as a convenient object for genetic studies. That is why our program was built on the use of this particular organism. We proceeded from the fact that X-ray exposure causes mutations in the genes that control certain chemical reactions. Suppose that in order to survive in a given environment, the organism must carry out some kind of chemical reaction, then the mutant, deprived of this ability, under these conditions will be unviable. However, it can be maintained and studied if grown in a medium to which the vital product of a genetically blocked reaction has been added.”

4 Action of genes 9

Next, Beadle and Tatum describe the design of the experiment (Figure 4.1). The composition of the complete medium included agar, inorganic salts, malt extract, yeast extract and glucose. The minimal medium contained only agar, salts, biotin, and a carbon source. The mutants that grew on the complete medium and did not grow on the minimal medium were studied in the most detail. In order to establish the compound, the synthesis of which was impaired in each of the mutants, individual components of the complete medium were added to the minimal agar.

In this way, strains were isolated that were unable to synthesize certain growth factors: pyridoxine, thiamine, and para-aminobenzoic acid. These defects have been shown to be due to mutations at specific loci. The work marked the beginning of numerous studies on neurospores, bacteria and yeasts, in which a correspondence was established between the "genetic blocks" responsible for individual metabolic steps and specific enzyme disorders. This approach has rapidly evolved into a tool for researchers to uncover metabolic pathways.

The hypothesis "one gene - one enzyme" has received strong experimental confirmation. As the work of subsequent decades showed, it proved to be surprisingly fruitful. The analysis of defective enzymes and their normal variants soon made it possible to identify a class of genetic disorders that led to a change in the function of the enzyme, although the protein itself was still detectable and retained immunological properties. In other cases, the temperature optimum of enzyme activity changed. Some variants could be explained by a mutation that affects the general regulatory mechanism and, as a result, changes the activity of a whole group of enzymes. Such studies led to the creation of the concept of regulation of gene activity in bacteria, which included the concept of the operon.

10 4. Action of genes

The first examples of enzymatic disorders in humans. The first hereditary human disease for which an enzymatic disorder could be shown was methemoglobinemia with a recessive mode of inheritance (Gibson and Harrison, 1947; Gibson, 1948) (25080). In this case, the damaged enzyme is NADH - dependent methemoglobin reductase. The first attempt to systematically study a group of human diseases associated with metabolic defects was made in 1951. In a study of glycogen storage disease, the Corys showed that in eight out of ten cases of the pathological condition that was diagnosed as Gierke's disease (23220), the structure of liver glycogen was a normal variant, and in two cases it was clearly disturbed. It was also evident that liver glycogen, accumulating in excess, could not be directly converted into sugar, since patients tend to hypoglycemia. Many enzymes are needed to break down glycogen into glucose in the liver. Two of them, amyl-1,6-glucosidase and glucose-6-phosphatase, were chosen for study as possible defective elements of the enzyme system. Phosphate release from glucose-6phosphate was measured in liver homogenates at various pH values. The results are presented in fig. 4.2. In a normal liver, high activity was found with an optimum at pH 6-7. Severe liver dysfunction in cirrhosis correlated with a slight decrease in activity. On the other hand, in the case of Gierke's disease with a fatal outcome, the activity of the enzyme could not be detected at all; the same result was obtained in the examination of the second similar patient. In two patients with less severe symptoms, there was a significant decrease in activity.

It was concluded that in these cases of Gierke's disease with a fatal outcome, there was a defect in glucose-6-phosphatase. However, in most of the milder cases, the activity of this enzyme was not lower than in liver cirrhosis, and only in two patients was it slightly lower (Fig. 4.2).

According to the Corey spouses, the abnormal accumulation of glycogen in muscle tissue cannot be associated with a lack of glucose-6-phosphatase, since this enzyme is absent in the muscles and is normal. As a possible explanation for muscle glycogenosis, they suggested a violation of the activity of amylo-1,6-glucosidase. This prediction was soon confirmed: Forbes discovered such a defect in one of the clinically significant cases of glycogen storage disease involving the heart and skeletal muscles. Now we

4. Action of genes 11

known big number enzymatic defects in glycogen storage disease.

Although the various forms of this disease vary somewhat in degree of manifestation, there is much in common between them clinically. With one exception, they are all inherited in an autosomal recessive manner. If enzymatic defects had not been uncovered, the pathology of glycogen accumulation would be considered as a single disease with characteristic intrafamilial correlations in severity, symptom details, and timing of death. Thus, we have an example where genetic heterogeneity, which could only be assumed on the basis of the study of the phenotype (Sec. 3.3.5), was confirmed by analysis at the biochemical level: the study of enzymatic activity made it possible to identify specific genes.

In subsequent years, the pace of research into enzymatic defects increased, and for the 588 identified recessive autosomal genes that McKusick describes in the sixth edition of his book Mendelian Inheritance in Man (1983), specific enzymatic disorders were found in more than 170 cases. Our progress in this area is directly related to the development of the concepts and methods of molecular genetics.

Some stages of the study of enzymatic disorders in humans. We present only the most important milestones in this ongoing process: 1934 Völling discovered phenylketonuria

1941 Beadle and Tatum formulated the one-gene-one-enzyme hypothesis 1948 Gibson described the first case of an enzymatic disorder in a human disease (recessive methemoglobinemia)

1952 Cory's discovered glucose-6-phosphatase deficiency in Gierke's disease

1953 Jervis demonstrated the absence of phenylalanine hydroxylase in phenylketonuria. Bickel reported the first attempt to alleviate an enzymatic disorder by adopting a diet low in phenylalanine.

1955 Smithies developed the starch gel electrophoresis technique

1956 Carson et al. discovered a defect in glucose-6-phosphate dehydrogenase (G6PD) in a case of induced hemolytic anemia

1957 Kalkar et al. described enzymatic deficiency in galactosemia, showing that humans and bacteria have an identical enzymatic disorder

1961 Krut and Weinberg demonstrated an enzyme defect in galactosemia in vitro in cultured fibroblasts

1967 Sigmiller et al. discovered a hypoxanthine-guanine phosphoribosyltransferase (HPRT) defect in Lesch-Nyhan syndrome

1968 Cleaver described violation of excisional repair in xeroderma pigmentosa

1970 Neufeld identified enzymatic defects in mucopolysaccharidoses, which made it possible to identify the pathways for the breakdown of mucopolysaccharides

1974 Brown and Goldstein showed that the genetically determined overproduction of hydroxymethylglutaryl-CoA reductase in familial hypercholesterolemia is due to a defect in the membrane-located low-density lipoprotein receptor, which modulates the activity of this enzyme (HMG)

1977 Sly et al. demonstrated that mannose-6-phosphate (as a component of lysosomal enzymes) is recognized by fibroblast receptors. A genetic defect in processing prevents the binding of lysosomal enzymes, resulting in impaired release into the cytoplasm and subsequent secretion into the plasma (I-cell disease)

12 4. Action of genes

1980 In pseudohypoparathyroidism, a defect in the protein that provides the coupling of the receptor and cyclase was discovered.

This happened in 1941. The "first geneticist" turned out to be a fungus with a romantic name - neurospore. Does it really sound nice? Moreover, the neurospore is very attractive in appearance. Place the mycelium of the fungus under a strong magnifying glass and admire: a thin transparent lace... You can spend hours looking at a fungus grown in a test tube, admiring the perfect creation of nature. Only American geneticists Beadle and Tatum looked at him as researchers, and not as domestic natural philosophers. Scientists in the subtleties learned the structure of the fungus in order to make it work for genetics. And that's what made me happy. The neurospore is a haploid organism. She only has 7 chromosomes ordinary life there are no cells with a double set in the mycelium of the fungus. This means that if a mutant gene arises in a fungus, the consequences of this will appear very soon - after all, the neurospore does not have a second dominant gene!

But that's not all. In neurospores, you can find ... a sexual stage of development. At some point in life, special, "female" cells appear in the mycelium of the fungus. They, like all mycelial cells, are haploid, but unlike them, they are able to merge with any other cell, which thus plays the role of "male". So there is a diploid cell with a double set of chromosomes. There are now 14 of them.

At first, the nuclei of such a cell do not merge, and it divides mitotically several times, forming an island of diploid cells in the mycelium. By the way, maybe this island is the "draft version" of nature when creating a multicellular diploid organism of animals and plants?

But in one of the diploid cells, the nuclei merge. In this case, the process of crossing over and reduction division takes place in the nucleus. In a word, the cell performs two divisions of meiosis, after which four haploid cells are formed. They are located in the shell exactly in a row, like soldiers in the ranks. Then each cell divides mitotically again, and that's it. As a result, 8 cells are formed (they are called ascospores), which are dressed in a shell.

And now let's imagine that a "trouble" happened to one of the genes of the mother cell - it became mutated. After crossing over, which will occur after the fusion of the nuclei, two hybrid cells will develop, and the mutant gene will fall into one of them. Such a cell will also give offspring - four ascospores. The bag will contain two genetically distinct types of ascospores. How to find out if there are mutants among them? That's what Beadle and Tatum did. They learned how to select ascospores from the bag and plant them one by one on a nutrient medium. From each ascospore, after a whole cycle of mitotic divisions, a mycelium grows - its direct descendant. If we compare the properties of mycelia from different ascospores, we can distinguish mutant and normal ones among them.

Here it is necessary to say about one more wonderful quality of neurospores.

It is extremely unpretentious and grows well on a nutrient-poor, so-called "minimal" or "hungry" environment (several inorganic salts, glucose, ammonium nitrate and the vitamin biotin). From these products, a normal fungus synthesizes all the amino acids, proteins, carbohydrates and vitamins it needs, except for biotin.

But scientists "hit" one of the genes with ultraviolet or X-rays, and it became mutant. If the ability to synthesize any vital amino acid was associated with it, this will immediately be revealed: some ascospores - the descendants of the female cell will stop growing on a starving environment. And do not wait for hundreds of generations of the fungus. After all, the ascospore does not have a second gene that compensates for the impaired function: its offspring, as we have already said, are haploid, that is, it contains only one set of chromosomes.

It remains to find out exactly which vital function is affected. Beadle and Tatum decided to add various amino acids, vitamins, salts, etc. to the starving medium in turn and plant whole herds of ascospores there. Finally! One of the ascospores germinated on a starvation medium with arginine, the other on a medium with tryptophan. This means that the first did not grow because it was not able to create a single molecule of arginine, the second - tryptophan. There is only one reason - on the chromosome of the ascospore, the gene that "manages" the synthesis of tryptophan is affected. In a similar way, Beadle and Tatum found 380 mutants (!) that carried a mutation in 100 separate genes that control vital biochemical reactions.

And here's what's interesting. For each gene, several mutants were found. Thus, the gene responsible for the synthesis of tryptophan accounted for 30 mutants. And are they all the same? Is everyone's ability to synthesize tryptophan impaired at one point in the gene? To answer this question, scientists crossed all 30 mutants with each other.

In these experiments, the mutants were divided into two groups. The mutants of the first group mutually complemented the mutants of the second group during crossing over. As a result, wild-type * recombinants synthesizing tryptophan were found among the ascospores. This means that two genes must be involved in the synthesis of tryptophan: in the mutants of the first group, one gene is affected, in the mutants of the second group, the other. But what do these genes control?

* (This is the name of the type that is not changed by mutations, the most common in natural conditions.)

Mutants of both groups grew if serine and indole were added instead of tryptophan, and tryptophan appeared in the medium. This means that all mutants could convert indole and series into tryptophan. Hence the conclusion: indole and series are precursors of tryptophan in the chain of its biosynthesis in a living cell.

This assumption was confirmed when a mutant was found in which this particular function was blocked. It did not produce the tryptophan synthetase enzyme that wild neurospores have.

The mutants of the first group were also capable of synthesizing the substance that stimulated the growth of the mutants of the second group. This substance turned out to be anthranilic acid, which apparently functions as an indole precursor. This means that in the mutants of the first group, the reaction of the conversion of anthranilic acid into indole is disrupted, while the mutants of the second group cannot synthesize anthranilic acid, but are able to convert it into indole.

Based on these data, a method for the synthesis of tryptophan in living cells was discovered: anthranilic acid is converted into indole. Indole combines with serine and under the influence of the enzyme tryptophan synthetase is converted into tryptophan. At least three genes are involved in the synthesis of tryptophan, each of them is responsible for the production of enzymes. These genes can be mapped on the neurospore chromosome in crossbreeding reactions.

So in 1941, for the first time in the history of natural science, scientists found on the chromosome the genes responsible for the synthesis of proteins - enzymes. Beadle and Tatum formulated the conclusions of their research as follows: "One gene - one enzyme." It is assumed that the cell's genes control the synthesis of all its enzymes that catalyze metabolic reactions, and each gene controls only one enzyme.

If you think about it, you can imagine that the scope of this hypothesis is much wider than its name implies. Indeed. We know that all enzymes are proteins. But in fact, in addition to enzymes, there are non-enzymatic proteins in the body. These are hemoglobin, antibodies and others. Where is the information for their synthesis stored? Also in chromosomal genes. That is why the "One gene - one enzyme" hypothesis now sounds like this: "One gene - one protein", or even: "One gene - one gulipeptid chain".

Until 1941, genetics and biochemistry were separate sciences, and each, by virtue of its capabilities, tried to find the key to the secrets of life: geneticists discovered genes, biochemists discovered enzymes. The experiments of the American scientists Beadle, Tatum and Brenner linked these two units of life together and laid the foundation for the commonwealth of genetics and biochemistry, and at the same time such a progress in knowledge that was not equal in the entire history of biology. The gene appeared as a specific unit that controls the synthesis of a specific protein. It was a qualitatively new level of research.

Experiments with neurospores inspired scientists, but still the questions still needed to be answered: what is a gene? What material is it made from? How does it regulate protein synthesis?

Genetics unraveled these puzzles of nature only after it began to search in the kingdom of bacteria. But before starting a story about the new heroes of genetic experiments, we must finally get to know them better.

one gene - one enzyme theory- the theory of "one gene - one enzyme".

The concept that only one enzyme can be encoded by one gene; this ratio is reflected more strictly in the theory of “one gene - one polypeptide”, since one enzyme may be a heteropolymer and include polypeptide chains encoded by different genes.

(Source: "English-Russian Explanatory Dictionary of Genetic Terms". Arefiev V.A., Lisovenko L.A., Moscow: VNIRO Publishing House, 1995)

• - one gene - one polypeptide hypothesis - the theory of “one gene - one polypeptide”...
• - the theory of “one gene - one protein”. the “one gene, one polypeptide” hypothesis...

  Molecular biology and genetics. Dictionary

• - the theory of “one gene - one polypeptide”. the “one gene, one polypeptide” hypothesis...

  Molecular biology and genetics. Dictionary

• - one enzyme - two genes theory - the theory of “one enzyme - two genes”...

  Molecular biology and genetics. Dictionary

• - Wed. I am alone like a finger in the whole world, I have no wife, no children, no stake, no yard, no one to shelter or take care of me ... Saltykov. Provincial points. 5. Christmas tree. Wed So I live ... exactly like God in a skudelnitsa ...

  Explanatory-phraseological dictionary of Michelson

• - From the poem “Among the flat valley” by the poet Alexei Fedorovich Merzlyakov, which later became the words of a popular song: Among the flat valley, At a smooth height, the mighty oak blossoms, grows In ...

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• - The first speaker does not want to notice the difference in anything. The interlocutor clearly disagrees with this position ...

  Dictionary of folk phraseology

• - One stick, two strings .... - this is most often called primitive music, bad musical instruments. About girls - this is for rhyme ...

  Dictionary of folk phraseology

• - see They live like brother and sister ...
• - Cm....

  IN AND. Dal. Proverbs of the Russian people

• - Cm....

  IN AND. Dal. Proverbs of the Russian people

• - See LIFE -...

  IN AND. Dal. Proverbs of the Russian people

• - One jumps, one cries, and all alone ...

  IN AND. Dal. Proverbs of the Russian people

• - See ROSE -...

  IN AND. Dal. Proverbs of the Russian people

• - One hundred and one brothers, all in one row, stand together connected ...

  IN AND. Dal. Proverbs of the Russian people

• - See Groom -...

  IN AND. Dal. Proverbs of the Russian people

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Genetics- science is by no means young, research in it has been going on for several centuries, starting with Mendel in 1865 and up to the present day. The term "gene" for a unit of hereditary characteristic was first proposed by Johannsen in 1911, and in the 1940s was refined by the concept of "one gene - one enzyme" proposed by Tatum and Beadle.

This position was determined in experiments on Drosophila flies, but equally applies to humans; Ultimately, the life of all beings is determined by their DNA. The DNA molecule in humans is larger than in all other organisms, and it is more complex, but the essence of its functions is the same for all living beings.

Concept " one gene - one enzyme”, which arose on the basis of the ideas of Tatum and Beadle, can be formulated as follows:
1. All biological processes are under genetic control.
2. All biochemical processes occur in the form of phased reactions.
3. Each biochemical reaction is ultimately controlled by different individual genes.
4. A mutation in a certain gene leads to a change in the cell's ability to carry out a certain chemical reaction.

Since then, the concept of "one gene - one enzyme" has expanded somewhat, and now sounds like " one gene - one protein". Besides, latest research indicate that some genes act in collaboration with others, resulting in the formation of unique proteins, i.e., some genes can encode more than one protein.

human genome contains about 3 billion nucleotide pairs; it is believed that it contains from 50,000 to 100,000. After deciphering the genome, it turned out that there were only about 30,000 genes. The interaction of these genes is much more complicated than expected. Genes are encoded in DNA strands, which, in combination with certain nuclear proteins, form chromosomes.

Genes- not just segments of DNA: they are formed by coding sequences - exons, interspersed with non-coding sequences - introns. Exons, as the expressed part of DNA, are only a small part of the most important molecule of the organism; most of it is not expressed, is formed by introns and is often called "silent" DNA.

Approximate size and structure human genome shown in the figure below. The functional length of the human chromosome is expressed in centimorganides. Centimorganide (cm) - the distance over which the probability of crossing over during meiosis is 1%. Gene linkage analysis has shown that the length of the human genome is about 3000 cM.

Medium chromosome contains approximately 1500 genes, encoded in 130 million base pairs. The figure below schematically shows the physical and functional dimensions of the genome: the first one is calculated in nucleotide pairs, and the second one is in cM. Most of the human genome is represented by "silent" DNA and is not expressed.

On the DNA template As a result of the transcription process, RNA is synthesized, and then protein. Therefore, the DNA sequence completely determines the sequence of the functional proteins of the cell. All proteins are synthesized as follows:
DNA => RNA => protein

The genetic apparatus of humans and other mammals is more complex than that of other living organisms, since sections of some genes in mammals can be combined with parts of others genes, resulting in the synthesis of an entirely new protein or the control of a particular cellular function.

Therefore, it is possible for a person to increase the number of genes expressed without actually increasing the amount of genes expressed. DNA or the absolute number of genes.
Overall, about 70% of all genetic material is not expressed.