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Chargaff’s second parity rule lies at the origin of additive genetic interactions in quantitative traits to make omnigenic selection possible

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dc.contributor.author Matkarimov, Bakhyt T.
dc.contributor.author Saparbaev, Murat K.
dc.date.accessioned 2024-09-09T07:46:29Z
dc.date.available 2024-09-09T07:46:29Z
dc.date.issued 2023
dc.identifier.citation Matkarimov BT, Saparbaev MK. 2023. Chargaff’s second parity rule lies at the origin of additive genetic interactions in quantitative traits to make omnigenic selection possible. PeerJ 11:e16671 http://doi.org/10.7717/peerj.16671 ru
dc.identifier.issn DOI 10.7717/peerj.16671
dc.identifier.issn 2691-6657
dc.identifier.uri http://rep.enu.kz/handle/enu/16096
dc.description.abstract Background. Francis Crick’s central dogma provides a residue-by-residue mechanistic explanation of the flow of genetic information in living systems. However, this principle may not be sufficient for explaining how random mutations cause continuous variation of quantitative highly polygenic complex traits. Chargaff’s second parity rule (CSPR), also referred to as intrastrand DNA symmetry, defined as near-exact equalities G ≈ C and A ≈ T within a single DNA strand, is a statistical property of cellular genomes. The phenomenon of intrastrand DNA symmetry was discovered more than 50 years ago; at present, it remains unclear what its biological role is, what the mechanisms are that force cellular genomes to comply strictly with CSPR, and why genomes of certain noncellular organisms have broken intrastrand DNA symmetry. The present work is aimed at studying a possible link between intrastrand DNA symmetry and the origin of genetic interactions in quantitative traits. Methods. Computational analysis of single-nucleotide polymorphisms in human and mouse populations and of nucleotide composition biases at different codon positions in bacterial and human proteomes. Results. The analysis of mutation spectra inferred from single-nucleotide polymorphisms observed in murine and human populations revealed near-exact equalities of numbers of reverse complementary mutations, indicating that random genetic variations obey CSPR. Furthermore, nucleotide compositions of coding sequences proved to be statistically interwoven via CSPR because pyrimidine bias at the 3rd codon position compensates purine bias at the 1st and 2nd positions. Conclusions. According to Fisher’s infinitesimal model, we propose that accumulation of reverse complementary mutations results in a continuous phenotypic variation due to small additive effects of statistically interwoven genetic variations. Therefore, additive genetic interactions can be inferred as a statistical entanglement of nucleotide compositions of separate genetic loci. CSPR challenges the neutral theory of molecular evolution—because all random mutations participate in variation of a trait—and provides an alternative solution to Haldane’s dilemma by making a gene function diffuse. We propose that CSPR is symmetry of Fisher’s infinitesimal model and that genetic information can be transferred in an implicit contactless manner. ru
dc.language.iso en ru
dc.publisher PeerJ ru
dc.relation.ispartofseries J 11;e16671
dc.subject Intra-strand DNA symmetry ru
dc.subject Single nucleotide polymorphisms ru
dc.subject Quantitative trait ru
dc.subject Infinitesimal model ru
dc.subject Statistical entanglement ru
dc.subject Integral characteristics ru
dc.subject Chargaff’s second parity rule ru
dc.subject Nucleotide composition bias ru
dc.subject Random mutations ru
dc.title Chargaff’s second parity rule lies at the origin of additive genetic interactions in quantitative traits to make omnigenic selection possible ru
dc.type Article ru


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