Frozen Evolution. Or, that’s not the way it is, Mr. Darwin. A Farewell to Selfish Gene.

According to this hypothesis, introns are genome parasites, do not provide any benefit for the cell and their only manifestation is that they are copied into various, more or less randomly selected parts of the DNA.They differ from some viruses, which are basically capable of the same, in that they do not encode their own viral capsid which would allow them horizontal transfer between cells and between organisms in the population.Introns can thus propagate only within a single genome and only vertically in the population, i.e. from parents to their progeny.In order for introns not to kill the cell into whose genes they are inserted (and thus inactivate them), they must be capable of splicing prior to commencement of translation from these genes.

            Some introns are capable of self-splicing - they are self-catalytically spliced at the level of the RNA, while others require a complicated molecular apparatus for this purpose – the enormous supermolecular complex spliceosome, whose components are encoded at various sites of the eukaryotic genome.Some types of introns directly encode enzymes for their horizontal propagation within the genome (for insertion into new loci in the DNA or into alleles that the particular intron does not contain), while others do not bear the relevant genes and, for their functioning, use enzymes encoded in other parts of the genome (Belfort 1993).Even in the case of introns for whose splicing special enzymes or even spliceosome is required in modern cells, we cannot with any certainty exclude that they originally did not function as completely autonomous genome parasites of the viral type or transposons and that only in the course of evolution did they not pass on most of the genes required for their survival in the cell to the genome of their host.

            It is probable that a great many genome parasites, including introns, begin in time to fulfill a function that is advantageous for their host.For example, in humans, about 1000 protein-coding genes are known that contain sections derived from transposons [12260].When the exons in vertebrates were divided into 5 categories according to age, it was found that the youngest do not encode anything, contain repetitions and their sequences in humans are frequently similar to ALU transposomes.Forty percent of these young exons participate in alternative splicing and are mostly spliced off together with introns rather than becoming part of the RNA.During evolution, these exons accumulate nonsynonymous mutations and gradually evolve into normal exons encoding a meaningful protein.It is thus possible that new genes are formed by accumulation and evolution of originally parasitic introns.