XI.7.2.4 Introns could facilitate detection or even reparation of mutations in exons

This hypothesis assumes that introns are a sort of control orcorrection apparatus for elimination of mutations in genes, whose functioning cannot be maintained by natural selection alone (Forsdyke 1981; Rzeszowska-Wolny 1983).These genes include most of the genes of the somatic cells of multicellular organisms.If mutation occurs in a single-cell organism, putting a certain gene out of action, the mutated line is sooner or later eliminated from the population by natural selection.If a similar mutation occurs in a somatic cell of a multicellular organism, a similar correction mechanism can frequently not be very efficient.The large number of genes that the cell expresses and the large number of functions that they perform are not of direct significance for the survival of the cell itself but rather for the proper functioning of the entire multicellular organism.Because the individual tissues of a multicellular organism are formed of entire populations of identical cells, there is no sufficiently effective mechanism that would be capable of preventing accumulation of mutations in the individual cells.The quality of the tissues gradually deteriorates through the accumulation of mutations without there being any way of discovering and potentially eliminating the individual mutated cells.

            It is known from informatics that a system of encoding information can be created that permits detecting errors arising in the course of transfer of information.There are even self-repairing codes that permit an error to be not only detected, but also repaired.The best-known mechanism of detecting errors is control of the parity of transmitted characters in communication between two computers.The individual characters are usually encoded by seven bits, a combination of seven ones and zeros.If the sum of ones is even, then one is added as the seventh bit; if it is odd, then zero is added.Thus, all the characters obtain an odd sum of ones, odd parity.If an error occurs in the transmission of a character, the odd parity is changed to even parity, which is readily recognized by the receiving equipment and it requests that the given character be sent again.The probability of the occurrence of 2 errors in the same character that would not be manifested in a change in parity is negligibly small compared to the probability of one error.

            It is undoubtedly attractive to imagine that introns could act as a control sequence, with which sequences of exons could be compared to verify that the exons do not contain mutations.The actual molecular mechanism through which this comparison could take place is not entirely clear and the authors of the hypothesis do not much concern themselves with this.As it is not known that introns and exons would contain mutually complementary sections, it cannot be assumed that comparison could occur through simple association of complementary sequences.However, it can be readily imagined that comparison could occur at the level of secondary DNA structures or that only the length of the exons would be compared, so that introns would assist in detection of deletion and insertion.

            From the standpoint of the theory of information transfer, the existence of such a mechanism is certainly possible; however, it is rather doubtful whether it would be “worthwhile” for evolution to reconstruct the simple genetic code to an error-detecting code or even an error-repairing code.It appears in general that the creation of the relevant mechanisms and rearrangement of the existing genetic information would entail such fundamental interventions in the logics of storage and processing of genetic information that the origin of such a code seems highly improbable from the viewpoint of contemporary knowledge of molecular and evolutionary biology.  Simultaneously, it must be admitted that the massive occurrence of introns in the genes of multicellular organisms and also the presence of introns in the genes for tRNA and rRNA prokaryotes is highly compatible with this hypothesis.The genes for tRNA and rRNA are present in the prokaryotic cell in several copies and thus, if mutation of one copy occurs, natural selection is capable of eliminating the mutated cell from the population.

 

 

 

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The classical Darwinian theory of evolution can explain the evolution of adaptive traits only in asexual organisms. The frozen plasticity theory is much more general: It can also explain the origin and evolution of adaptive traits in both asexual and sexual organisms Read more
Draft translation from: Evoluční biologie, 2. vydání (Evolutionary biology, 2nd edition), J. Flegr, Academia Prague 2009. The translation was not done by biologist, therefore any suggestion concerning proper scientific terminology and language usage are highly welcomed. You can send your comments to flegratcesnet [dot] cz. Thank you.