Study of the genetic code. Universal genetic code

GENETIC CODE, a system for recording hereditary information in the form of a sequence of nucleotide bases in DNA molecules (in some viruses - RNA), which determines the primary structure (location of amino acid residues) in protein molecules (polypeptides). The problem of the genetic code was formulated after proving the genetic role of DNA (American microbiologists O. Avery, K. McLeod, M. McCarthy, 1944) and deciphering its structure (J. Watson, F. Crick, 1953), after establishing that genes determine the structure and functions of enzymes (the principle of "one gene - one enzyme" by J. Beadle and E. Tatema, 1941) and that there is a dependence of the spatial structure and activity of a protein on its primary structure (F. Senger, 1955). The question of how combinations of 4 bases of nucleic acids determine the alternation of 20 common amino acid residues in polypeptides was first raised by G. Gamow in 1954.

Based on an experiment in which the interactions of insertions and deletions of a pair of nucleotides were studied, in one of the genes of the bacteriophage T4, F. Crick and other scientists in 1961 determined the general properties of the genetic code: triplet, i.e., each amino acid residue in the polypeptide chain corresponds to a set of three bases (triplet, or codon) in the DNA of a gene; reading of codons within a gene goes from a fixed point, in one direction and "without commas", that is, codons are not separated by any signs from each other; degeneracy, or redundancy, - the same amino acid residue can encode several codons (synonymous codons). The authors suggested that codons do not overlap (each base belongs to only one codon). Direct study of the coding ability of triplets was continued using a cell-free protein synthesis system under the control of synthetic messenger RNA (mRNA). By 1965, the genetic code was completely deciphered in the works of S. Ochoa, M. Nirenberg and H. G. Korana. The discovery of the secret of the genetic code was one of the outstanding achievements of biology in the 20th century.

The implementation of the genetic code in the cell occurs in the course of two matrix processes - transcription and translation. The mediator between a gene and a protein is mRNA, which is formed during transcription on one of the DNA strands. In this case, the DNA base sequence, which carries information about the primary structure of the protein, is "rewritten" in the form of an mRNA base sequence. Then, during translation on the ribosomes, the nucleotide sequence of the mRNA is read by transfer RNA (tRNA). The latter have an acceptor end, to which an amino acid residue is attached, and an adapter end, or triplet anticodon, which recognizes the corresponding mRNA codon. The interaction of codon and anti-codon occurs on the basis of complementary base pairing: Adenine (A) - Uracil (U), Guanine (G) - Cytosine (C); in this case, the mRNA base sequence is translated into the amino acid sequence of the synthesized protein. Different organisms use different synonymous codons for the same amino acid at different frequencies. Reading of the mRNA encoding the polypeptide chain starts (initiates) from the AUG codon corresponding to the amino acid methionine. Less commonly in prokaryotes, the initiating codons are GUG (valine), UUG (leucine), AUU (isoleucine), in eukaryotes - UUG (leucine), AUA (isoleucine), ACG (threonine), CUG (leucine). This sets the so-called frame, or phase, of reading during translation, that is, then the entire nucleotide sequence of mRNA is read triple by triplet of tRNA until any of the three terminator codons, often called stop codons, is found on the mRNA: UAA, UAG , UGA (table). The reading of these triplets leads to the completion of the synthesis of the polypeptide chain.

The AUG and stop codons are located at the beginning and end of the mRNA regions encoding polypeptides, respectively.

The genetic code is quasi-universal. This means that there are small variations in the meaning of some codons in different objects, and this concerns, first of all, terminator codons, which can be significant; for example, in the mitochondria of some eukaryotes and in mycoplasmas, UGA codes for tryptophan. In addition, in some mRNAs of bacteria and eukaryotes, UGA encodes an unusual amino acid, selenocysteine, and UAG, in one of the archaebacteria, encodes pyrrolysine.

There is a point of view according to which the genetic code arose by chance (the “frozen case” hypothesis). It is more likely that he has evolved. This assumption is supported by the existence of a simpler and, apparently, more ancient version of the code, which is read in mitochondria according to the “two out of three” rule, when only two of the three bases in the triplet determine the amino acid.

Lit .: Crick F. N. a. about. General nature of the genetic code for proteins // Nature. 1961 Vol. 192; The genetic code. N.Y., 1966; Ichas M. Biological code. M., 1971; Inge-Vechtomov S. G. How the genetic code is read: rules and exceptions // Modern natural science. M., 2000. T. 8; Ratner V. A. Genetic code as a system // Soros Educational Journal. 2000. V. 6. No. 3.

S. G. Inge-Vechtomov.

1. The code is triplet.

2. The code is degenerate.

3. The code is unambiguous.

4. The code is collinear.

5. The code is non-overlapping.

6. The code is universal.

1) triplet code. 3 adjacent nucleotides carry information about one protein. There can be 64 such triplets (this shows the redundancy of the genetic code), but only 61 of them carry information about the protein (codons). 3 triplets are called anticodons, they are stop signals at which protein synthesis stops.

2) The code is degenerate. One amino acid can be coded for by several codons.

3) The code is unambiguous. Each codon codes for only one amino acid.

4) The code is collinear. The sequence of nucleotides in a gene corresponds to the sequence of amino acids in a protein.

5) The code is non-overlapping. the same nucleotide cannot be part of two different codons, the reading goes on continuously, in a row, up to the stop codon. There are no "punctuation marks" in the code.

6) The code is universal. It is the same for all living beings, i.e. the same triplet codes for the same amino acid.

61. In what cases does a change in the nucleotide sequence in a gene not affect the structure and functions of the coding protein?

1) if, as a result of a nucleotide substitution, another codon appears that codes for the same amino acid;

2) if the codon formed as a result of a nucleotide substitution encodes another amino acid, but with similar chemical properties that does not change the structure of the protein;

3) if nucleotide changes occur in intergenetic or non-functioning DNA regions.

№62. DNA replication.

Short review:

replication- the process of synthesis of the daughter molecule of deoxyribonucleic acid on the matrix of the parent DNA molecule. During the subsequent division of the mother cell, each daughter cell receives one copy of a DNA molecule that is identical to the DNA of the original mother cell. This process ensures the accurate transmission of genetic information from generation to generation. DNA replication is carried out by a complex enzyme complex, consisting of 15-20 different proteins, called the replisome.

By the time of division, the DNA must be replicated completely and only once. Replication takes place in three stages:

1. Initiation of replication (DNA polymerase begins DNA replication by binding to a segment of a chain of nucleotides. At a certain site (the start point of replication), local DNA denaturation occurs, the chains diverge and two replication forks are formed, moving in opposite directions.).

2. Elongation (a stage in the biosynthesis of nucleic acid molecules, which consists in the sequential addition of monomers (nucleotides) to a growing DNA chain).

3. Termination of replication (the final stage occurs at the moment when empty areas are filled with nucleotides between Okazaki fragments).

Main part:

Since DNA is a molecule of heredity, in order to realize this quality, it must exactly copy itself and thus preserve all the information available in the original DNA molecule in the form of a certain sequence of nucleotides. This is ensured by a special process that precedes the division of any cell in the body, which is called DNA replication - the process of synthesizing a daughter molecule of deoxyribonucleic acid on the template of the parent DNA molecule.

DNA replication occurs in three steps:

1. Initiation. It consists in the fact that special enzymes -DNA helicases, which unwind the double-stranded DNA helix, break the weak hydrogen bonds that connect the nucleotides of the two chains. As a result, the DNA strands are disconnected, and free nitrogenous bases “stick out” from each strand (the appearance of the so-called replication fork).

2. Elongation(a stage in the biosynthesis of nucleic acid molecules, which consists in the sequential attachment of monomers (nucleotides) to a growing DNA chain). Each of the two strands of DNA serves as a template for the synthesis of a new strand. Since the parental strands are antiparallel, continuous DNA replication occurs only on one strand, which is called the leader (leading). A special enzyme, DNA polymerase, begins to move along the free DNA chain from the 5 "to the 3" end, helping to attach the free nucleotides constantly synthesized in the cell to the 3 "end of the newly synthesized DNA strand. The synthesis of a new strand on a lagging strand requires constant formation new seeds (the so-called primers - short fragments of nucleic acid used by DNA - polymerases to initiate DNA synthesis) to start replication and is carried out in small segments of 1000-2000 nucleotides each (Okazaki fragments). The seeds degrade after the completion of the synthesis of the next Okazaki fragment. The resulting adjacent DNA fragments are connected by DNA ligase. Topoisomerase removes helix supercoils, helicase unwinds the double helix, and SSB protein ensures the stability of single-stranded DNA.

3. Termination (completion) of replication occurs when the gaps between Okazaki fragments are filled with nucleotides (with the participation of DNA ligase) with the formation of two continuous double strands of DNA and when two replication forks meet. Then the synthesized DNA is twisted to form supercoils.

63. Describe the sequence of processes occurring during DNA replication in eukaryotes

The DNA replication mechanisms of prokaryotes and eukaryotes differ significantly in that in the second case, the synthesis of the leading and lagging DNA strands is carried out by different DNA polymerases (alpha and delta, respectively), while in E. coli both DNA strands are synthesized by the DNA polymerase III dimer. DNA polymerase alpha initiates the synthesis of the leading strand at the points of replication origin, and DNA polymerase delta performs cyclic reinitiation of the synthesis of Okazaki fragments, apparently recognizing the presence of the 5'-terminal nucleotide of the next primer, followed by dissociation from template DNA and attachment to it for reinitiation of the synthesis of the next Okazaki fragment.

The maturation of Okazaki fragments in eukaryotes requires the removal of RNA primers with the help of 5'->3'-exonuclease (protein factors FEN-1 or MF-1) and RNase H1, as well as the covalent connection of the fragments to each other under the action of DNA ligase I.

At present, it is not known what exactly serves as a starting signal for the start of DNA replication in the S phase. The initiating event, after which DNA synthesis begins, occurs at specific sites called "replication forks". During the S phase, clusters of replication forks are activated simultaneously on all chromosomes.

The position of origins of replication in genes can be of great biological importance. The fact that a number of animal viruses begin replication at specific genome sites suggests that replication origins are specialized sequences in chromosomal DNA. The average distance between replication origins is comparable to the average distance between neighboring chromatin loops. Thus, it is possible that there is only one origin of replication in each loop.

When two replication forks diverge from one replication start point on opposite sides of this point, parental nucleosomes will fall into different child DNA helices. In this case, the distribution of preexisting parental histones between the two daughter genes will depend on the exact location of the origin of replication in the transcription unit. Not all nucleosomes are exactly the same - in different areas of the genetic material, the structure of chromatin is different. The precise position of the origin of replication in a gene could therefore be of great biological importance, since it would determine the chromatin structure of that gene in the next generation of cells.

The DNA replication trigger clearly works on an all-or-nothing basis, since DNA replication, which began in the S phase, continues until this process is completed. The all-or-nothing control of the replication process can be done in at least two different ways:

1) a certain general system can specifically recognize each chromosome band, decondense it, and thereby make all replication origins simultaneously accessible to proteins responsible for the formation of replication bubbles;

2) replicative proteins can recognize only a few origins of replication from a given set, after which the local replication that has begun will change the structure of the rest of the chromatin of the replication unit in such a way that replication at all other origins becomes possible.

It is possible that the critical moment in the chain of events initiating DNA replication is the achievement of a certain stage in the process of centriole doubling, which acts both as part of an important microtubule organizing center closely associated with the interphase nucleus and as a component of each of the spindle poles during mitosis. Apparently, the centriole doubles by a matrix process once per cell cycle (Fig. 11-19).

It is also not yet known what determines the fixed replication sequence of chromosome bands. Two hypotheses have been proposed to explain this sequence. According to one of them, various replicative proteins, each of which is specific for a certain type of chromosome bands, are synthesized in the S phase at different times. According to another hypothesis, which now seems more plausible, replicative proteins simply act on those parts of DNA that are more accessible to them; for example, during the S phase, continuous decondensation of chromosomes can occur, and chromosome bands one by one become available to replicative proteins.

Leading scientific journal Nature announced the discovery of a second genetic code - a kind of "code within a code", which was recently cracked by molecular biologists and computer programmers. Moreover, in order to reveal it, they did not use evolutionary theory, but information technology.

The new code is called the Splicing Code. It is within the DNA. This code controls the underlying genetic code in a very complex yet predictable way. The splicing code controls how and when genes and regulatory elements are assembled. Revealing this code within a code helps shed light on some of the long-standing mysteries of genetics that have surfaced since the Complete Human Genome Sequencing Project. One such mystery was why there are only 20,000 genes in an organism as complex as the human being? (Scientists expected to find a lot more.) Why are genes broken into segments (exons) that are separated by non-coding elements (introns) and then joined together (i.e., spliced) after transcription? And why are genes turned on in some cells and tissues and not in others? For two decades, molecular biologists have tried to elucidate the mechanisms of genetic regulation. This article points to a very important point in understanding what is really going on. It doesn't answer every question, but it does demonstrate that the internal code exists. This code is a communication system that can be deciphered so clearly that scientists could predict how a genome might behave in certain situations and with inexplicable accuracy.

Imagine that you hear an orchestra in the next room. You open the door, look inside and see three or four musicians playing musical instruments in the room. This is what Brandon Frey, who helped break the code, says the human genome looks like. He says: “We were only able to detect 20,000 genes, but we knew that they form a huge number of protein products and regulatory elements. How? One of the methods is called alternative splicing". Different exons (parts of genes) can be assembled in different ways. “For example, three genes for the neurexin protein can create over 3,000 genetic messages that help control the brain’s wiring system.” Frey says. Right there in the article, it says that scientists know that 95% of our genes have alternative splicing, and in most cases, transcripts (RNA molecules resulting from transcription) are expressed differently in different types of cells and tissues. There must be something that controls how these thousands of combinations are assembled and expressed. This is the task of the Splicing Code.

Readers who want a quick overview of the discovery can read the article at Science Daily entitled "Researchers who cracked the 'Splicing Code' unravel the mystery behind biological complexity". The article says: “Scientists at the University of Toronto have gained a fundamental new understanding of how living cells use a limited number of genes to form incredibly complex organs like the brain.”. Nature magazine itself begins with Heidi Ledford's "Code Within Code." This was followed by a paper by Tejedor and Valcarcel titled “Gene Regulation: Breaking the Second Genetic Code. Finally, a paper by a group of researchers from the University of Toronto led by Benjamin D. Blencoe and Brandon D. Frey, "Deciphering the Splicing Code," was decisive.

This article is an information science victory that reminds us of codebreakers from World War II. Their methods included algebra, geometry, probability theory, vector calculus, information theory, program code optimization, and other advanced techniques. What they didn't need was evolutionary theory, which has never been mentioned in scientific articles. Reading this article, you can see how much tension the authors of this overture are under:

“We describe a ‘splicing code’ scheme that uses combinations of hundreds of RNA properties to predict tissue-mediated changes in alternative splicing of thousands of exons. The code establishes new classes of splicing patterns, recognizes different regulatory programs in different tissues, and establishes mutation-controlled regulatory sequences. We have uncovered widely used regulatory strategies, including: using unexpectedly large property pools; detection of low levels of exon inclusion, which are attenuated by the properties of specific tissues; the manifestation of properties in introns is deeper than previously thought; and modulation of the levels of the splice variant by the structural characteristics of the transcript. The code helped establish a class of exons whose inclusion mutes expression in adult tissues, activating mRNA degradation, and whose exclusion promotes expression during embryogenesis. The code facilitates the disclosure and detailed description of genome-wide regulated events of alternative splicing.”

The team that cracked the code included specialists from the Department of Electronics and Computer Engineering, as well as from the Department of Molecular Genetics. (Frey himself works for Microsoft Research, a division of Microsoft Corporation) Like the decoders of the past, Frey and Barash developed "a new computer-assisted biological analysis that detects 'code words' hidden within the genome". With the help of a huge amount of data created by molecular geneticists, a group of researchers carried out "reverse engineering" of the splicing code until they could predict how he would act. Once the researchers got the hang of it, they tested the code for mutations and saw how exons were inserted or removed. They found that the code could even cause tissue-specific changes or act differently depending on whether it was an adult mouse or an embryo. One gene, Xpo4, is associated with cancer; The researchers noted: “These data support the conclusion that Xpo4 gene expression must be tightly controlled to avoid potential detrimental effects, including oncogenesis (cancer), since it is active during embryogenesis but is reduced in adult tissues. It turns out that they were absolutely surprised by the level of control they saw. Intentionally or not, Frey did not use random variation and selection as a clue, but the language of intelligent design. He noted: "Understanding a complex biological system is like understanding a complex electronic circuit."

Heidi Ledford said that the apparent simplicity of Watson-Crick's genetic code, with its four bases, triplet codons, 20 amino acids, and 64 DNA "characters" - hides a whole world of complexity. Encapsulated within this simpler code, the splicing code is much more complex.

But between DNA and proteins lies RNA, a separate world of complexity. RNA is a transformer that sometimes carries genetic messages, and sometimes controls them, while using many structures that can influence its function. In an article published in the same issue, a team of researchers led by Benjamin D. Blencoe and Brandon D. Frey at the University of Toronto in Ontario, Canada, report attempts to unravel a second genetic code that can predict how messenger RNA segments are transcribed from a particular genes can mix and match to form a variety of products in different tissues. This process is known as alternative splicing. This time there is no simple table - instead, algorithms that combine more than 200 different properties of DNA with definitions of the structure of RNA.

The work of these researchers indicates the rapid progress that computational methods have made in modeling RNA. In addition to understanding alternative splicing, computer science is helping scientists predict RNA structures and identify small regulatory fragments of RNA that do not code for proteins. "It's a wonderful time", says Christopher Berg, a computer biologist at the Massachusetts Institute of Technology in Cambridge. "In the future, we will have a huge success".

Computer science, computer biology, algorithms, and codes were not part of Darwin's vocabulary when he developed his theory. Mendel had a very simplified model of how traits are distributed during inheritance. In addition, the idea that features are encoded was only introduced in 1953. We see that the original genetic code is regulated by an even more complex code included in it. These are revolutionary ideas.. Moreover, there are all indications that this level of control is not the last. Ledford reminds us that, for example, RNA and proteins have a three-dimensional structure. The function of molecules can change when their shape changes. There must be something that controls folding so that the three-dimensional structure does what the function requires. In addition, access to genes appears to be controlled another code, histone code. This code is encoded by molecular markers or "tails" on histone proteins that serve as centers for DNA coiling and supercoiling. Describing our time, Ledford speaks of "permanent renaissance in RNC informatics".

Tejedor and Valcarcel agree that complexity lies behind simplicity. “In theory, everything looks very simple: DNA forms RNA, which then creates a protein”, - they begin their article. “But the reality is much more complicated.”. In the 1950s, we learned that all living organisms, from bacteria to humans, have a basic genetic code. But we soon realized that complex organisms (eukaryotes) have some unnatural and difficult to understand property: their genomes have peculiar sections, introns, that must be removed so that exons can join together. Why? The fog is clearing today "The main advantage of this mechanism is that it allows different cells to choose alternative ways of splicing the precursor messenger RNA (pre-mRNA) and thus one gene forms different messages," they explain, "and then different mRNAs can code for different proteins with different functions". From less code, you get more information, as long as there is this other code inside the code that knows how to do it.

What makes cracking the splicing code so difficult is that the factors that control exon assembly are set by many other factors: sequences near exon boundaries, intron sequences, and regulatory factors that either aid or inhibit the splicing mechanism. Besides, "the effects of a certain sequence or factor may vary depending on its location relative to the boundaries of the intron-exon or other regulatory motifs", - Tejedor and Valcarcel explain. “Therefore, the most difficult task in predicting tissue-specific splicing is to compute the algebra of the myriad of motifs and the relationships between the regulatory factors that recognize them.”.

To solve this problem, a team of researchers entered into the computer a huge amount of data about the RNA sequences and the conditions under which they were formed. "The computer was then given the task of identifying the combination of properties that would best explain the experimentally established tissue-specific exon selection.". In other words, the researchers reverse engineered the code. Like World War II codebreakers, once scientists know the algorithm, they can make predictions: "It correctly and accurately identified alternative exons and predicted their differential regulation between pairs of tissue types." And just like any good scientific theory, the discovery provided new insights: “This allowed us to re-explain previously established regulatory motivations and pointed to previously unknown properties of known regulators, as well as unexpected functional relationships between them.”, the researchers noted. “For example, the code implies that the inclusion of exons leading to processed proteins is a general mechanism for controlling the process of gene expression during the transition from embryonic tissue to adult tissue.”.

Tejedor and Valcarcel consider the publication of their paper an important first step: "The work... is better seen as the discovery of the first fragment of the much larger Rosetta Stone needed to decipher the alternative messages of our genome." According to these scientists, future research will undoubtedly improve their knowledge of this new code. At the end of their article, they mention evolution in passing, and they do it in a very unusual way. They say, “That doesn't mean that evolution created these codes. This means that progress will require an understanding of how the codes interact. Another surprise was that the degree of conservation observed to date raises the question of the possible existence of "species-specific codes".

The code probably works in every single cell, and therefore must be responsible for more than 200 types of mammalian cells. It also has to handle a huge variety of alternative splicing patterns, not to mention simple decisions to include or skip a single exon. The limited evolutionary retention of regulation of alternative splicing (estimated to be about 20% between humans and mice) raises the question of the existence of species-specific codes. Moreover, the relationship between DNA processing and gene transcription influences alternative splicing, and recent evidence points to DNA packaging by histone proteins and histone covalent modifications (the so-called epigenetic code) in the regulation of splicing. Therefore, future methods will have to establish the exact interaction between the histone code and the splicing code. The same applies to the still little understood influence of complex RNA structures on alternative splicing.

Codes, codes and more codes. The fact that scientists say almost nothing about Darwinism in these papers indicates that evolutionary theorists, adherents of old ideas and traditions, have a lot to think about after they read these papers. But those who are enthusiastic about the biology of codes will be at the forefront. They have a great opportunity to take advantage of the exciting web application that the codebreakers have created to encourage further exploration. It can be found on the University of Toronto website called "Alternative Splicing Prediction Website". Visitors will look in vain for mention of evolution here, despite the old axiom that nothing in biology makes sense without it. The new 2010 version of this expression might sound like this: "Nothing in biology makes sense unless viewed in the light of computer science" .

Links and notes

We're glad we were able to tell you about this story on the day it was published. Perhaps this is one of the most significant scientific articles of the year. (Of course, every big discovery made by other groups of scientists, like the discovery of Watson and Crick, is significant.) The only thing we can say to this is: “Wow!” This discovery is a remarkable confirmation of Designed Creation and a huge challenge to the Darwinian empire. It is interesting how evolutionists will try to correct their simplified history of random mutations and natural selection, which was invented back in the 19th century, in light of these new data.

Do you understand what Tejedor and Valcarcel are talking about? Views can have their own code specific to those views. “Therefore, future methods will have to establish the exact interaction between the histone [epigenetic] code and the splicing code,” they note. In translation, this means: “Darwinists have nothing to do with it. They just can't handle it." If the simple genetic code of Watson-Crick was a problem for the Darwinists, then what do they say now about the splicing code, which creates thousands of transcripts from the same genes? And how will they deal with the epigenetic code that controls gene expression? And who knows, maybe in this incredible "interaction" that we are just beginning to learn about, other codes are involved, reminiscent of the Rosetta Stone, just beginning to emerge from the sand?

Now that we're thinking about codes and computer science, we're starting to think about different paradigms for new research. What if the genome partially acts as a storage network? What if cryptography takes place in it or compression algorithms occur? We should remember about modern information systems and information storage technologies. Maybe we will even find elements of steganography. Undoubtedly, there are additional resistance mechanisms, such as duplications and corrections, that may help explain the existence of pseudogenes. Whole genome copying may be a response to stress. Some of these phenomena may prove to be useful indicators of historical events that have nothing to do with a universal common ancestor, but help explore comparative genomics within informatics and resistance design, and help understand the cause of a disease.

Evolutionists find themselves in a severe quandary. The researchers tried to modify the code, but got only cancer and mutations. How are they going to navigate the field of fitness when it's all mined with catastrophes waiting in the wings as soon as someone starts tampering with these inextricably linked codes? We know that there is some built-in resilience and portability, but the whole picture is an incredibly complex, designed, optimized information system, not a jumble of pieces that can be played around endlessly. The whole idea of ​​code is the concept of intelligent design.

A.E. Wilder-Smith emphasized this. The code assumes an agreement between the two parts. An agreement is an agreement in advance. It implies planning and purpose. The SOS symbol, as Wilder-Smith would say, we use by convention as a distress signal. SOS does not look like a disaster. It doesn't smell like a disaster. It doesn't feel like a disaster. People would not understand that these letters stand for disaster if they did not understand the essence of the agreement itself. Similarly, an alanine codon, HCC, does not look, smell, or feel like alanine. A codon would have nothing to do with alanine unless there was a pre-established agreement between the two coding systems (protein code and DNA code) that "GCC should stand for alanine." To convey this agreement, a family of transducers, aminoacyl-tRNA synthetases, are used, which translate one code into another.

This was to strengthen the theory of design in the 1950s, and many creationists preached it effectively. But evolutionists are like eloquent salesmen. They made up their tales about the Tinker Bell fairy, who deciphers the code and creates new species through mutation and selection, and convinced many people that miracles can still happen today. Well, well, today is the 21st century outside the window and we know the epigenetic code and the splicing code - two codes that are much more complex and dynamic than the simple code of DNA. We know about codes within codes, about codes above codes and below codes - we know a whole hierarchy of codes. This time around, evolutionists can't just put their finger in the gun and bluff us with their beautiful speeches, when guns are placed on both sides - a whole arsenal aimed at their main structural elements. All this is a game. A whole era of computer science has grown around them, they have long gone out of fashion and look like the Greeks, who are trying to climb modern tanks and helicopters with spears.

Sad to admit, evolutionists don't understand this, or even if they do, they're not going to give up. Incidentally, this week, just as the article on the Splicing Code was published, the most vicious and hateful anti-creation and intelligent design rhetoric in recent memory has been pouring from the pages of pro-Darwinian magazines and newspapers. We are yet to hear of many more such examples. And as long as they hold the microphones in their hands and control the institutions, many people will fall for them, thinking that science continues to give them a good reason. We are telling you all this so that you will read this material, study it, understand it and stock up on the information you need in order to combat this fanatical, misleading nonsense with the truth. Now, go ahead!

They line up in chains and, thus, sequences of genetic letters are obtained.

Genetic code

The proteins of almost all living organisms are built from only 20 types of amino acids. These amino acids are called canonical. Each protein is a chain or several chains of amino acids connected in a strictly defined sequence. This sequence determines the structure of the protein, and therefore all its biological properties.

CUU (Leu/L) Leucine
CUC (Leu/L)Leucine
CUA (Leu/L) Leucine
CUG (Leu/L) Leucine

In some proteins, non-standard amino acids such as selenocysteine ​​and pyrrolysine are inserted by the stop codon-reading ribosome, which depends on the sequences in the mRNA. Selenocysteine ​​is now considered as the 21st, and pyrrolysine as the 22nd amino acid that makes up proteins.

Despite these exceptions, the genetic code of all living organisms has common features: a codon consists of three nucleotides, where the first two are defining, codons are translated by tRNA and ribosomes into a sequence of amino acids.

The history of ideas about the genetic code

Nevertheless, in the early 1960s, new data revealed the failure of the “comma-free code” hypothesis. Then experiments showed that codons, considered by Crick to be meaningless, can provoke protein synthesis in a test tube, and by 1965 the meaning of all 64 triplets was established. It turned out that some codons are simply redundant, that is, a number of amino acids are encoded by two, four or even six triplets.

see also

Notes

1. Genetic code supports targeted insertion of two amino acids by one codon. Turanov AA, Lobanov AV, Fomenko DE, Morrison HG, Sogin ML, Klobutcher LA, Hatfield DL, Gladyshev VN. Science. 2009 Jan 9;323(5911):259-61.
2. The AUG codon encodes methionine, but also serves as a start codon - as a rule, translation begins from the first AUG codon of mRNA.
3. NCBI: "The Genetic Codes", Compiled by Andrzej (Anjay) Elzanowski and Jim Ostell
4. Jukes TH, Osawa S, The genetic code in mitochondria and chloroplasts., Experientia. 1990 Dec 1;46(11-12):1117-26.
5. Osawa S, Jukes TH, Watanabe K, Muto A (March 1992). "Recent evidence for evolution of the genetic code". microbiol. Rev. 56 (1): 229–64. PMID 1579111.
6. SANGER F. (1952). "The arrangement of amino acids in proteins.". Adv Protein Chem. 7 : 1-67. PMID 14933251 .
7. M. Ichas biological code. - Mir, 1971.
8. WATSON JD, CRICK FH. (April 1953). «Molecular structure of nucleic acids; a structure for deoxyribose nucleic acid.". Nature 171 : 737-738. PMID 13054692 .
9. WATSON JD, CRICK FH. (May 1953). "Genetical implications of the structure of deoxyribonucleic acid.". Nature 171 : 964-967. PMID 13063483 .
10. Crick F.H. (April 1966). "The genetic code - yesterday, today, and tomorrow." Cold Spring Harb Symp Quant Biol.: 1-9. PMID 5237190.
11. G. GAMOW (February 1954). "Possible Relationship between Deoxyribonucleic Acid and Protein Structures.". Nature 173 : 318. DOI: 10.1038/173318a0 . PMID 13882203.
12. GAMOW G, RICH A, YCAS M. (1956). "The problem of information transfer from the nucleic acids to proteins.". Adv Biol Med Phys. 4 : 23-68. PMID 13354508 .
13. Gamow G, Ycas M. (1955). STATISTICAL CORRELATION OF PROTEIN AND RIBONUCLEIC ACID COMPOSITION. ". Proc Natl Acad Sci U S A. 41 : 1011-1019. PMID 16589789 .
14. Crick FH, Griffith JS, Orgel LE. (1957). CODES WITHOUT COMMAS. ". Proc Natl Acad Sci U S A. 43 : 416-421. PMID 16590032.
15. Hayes B. (1998). "The Invention of the Genetic Code." (PDF reprint). American scientist 86 : 8-14.

Literature

• Azimov A. Genetic code. From the theory of evolution to the decoding of DNA. - M.: Tsentrpoligraf, 2006. - 208 s - ISBN 5-9524-2230-6.
• Ratner V. A. Genetic code as a system - Soros Educational Journal, 2000, 6, No. 3, pp. 17-22.
• Crick FH, Barnett L, Brenner S, Watts-Tobin RJ. General nature of the genetic code for proteins - Nature, 1961 (192), pp. 1227-32

Links

• Genetic code- article from the Great Soviet Encyclopedia

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