Disruptive natural selection by male reproductive potential prevents underexpression of the genes encoding proteins on the human Y chromosome as a self-domestication syndrome

Poster (download) Mikhail Ponomarenko1, Irina Chadaeva2, Dmitry Oshchepkov3, Dmitry Rasskazov4, Alexander Osadchuk5, Ludmila Osadchuk61Systems Biology Department Institute of Cytology and Genetics, ICG SB RAS Novosibirsk, Russia, pon@bionen.nsc.ru2Systems Biology Department Institute of Cytology and Genetics, ICG SB RAS Novosibirsk, Russia, ichadaeva@bionet.nsc.ru3Systems Biology Department Institute of Cytology and Genetics, ICG SB RAS Novosibirsk, Russia, diman@bionet.nsc.ru4Systems Biology Department Institute of Cytology and Genetics, ICG SB RAS Novosibirsk, Russia, rassk@bionen.nsc.ru5Animal Genetics Department Institute of Cytology and Genetics, ICG SB RAS Novosibirsk, Russia, osadchuk@bionet.nsc.ru6Animal Genetics Department Institute of Cytology and Genetics, ICG SB RAS Novosibirsk, Russia, losadch@bionet.nsc.ru We performed an in silico genome-wide analysis of all SNPs located within 70 bp proximal promoters in front of the all experimentally knowns starts of protein-coding transcripts from human Y chromosome within the framework of the current release #151 of the dbSNP database and GRCh38/hg38 assembly of the human reference genome, which are publicly available using the UCSC Genome Browser. As a result, we first found disruptive natural selection by male reproductive potential preventing underexpression of the Y-linked proteins under this study as if self-domestication would have happened during the human origing and evolution that could cause male fertility disorders as self-domestication syndrome.

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Candidate SNP markers of atherosclerosis reliably altering the affinity of TATA-binding protein for human gene promoters point to stabilizing natural selection as sum of neutral drift spuring atherogenesis and directional natural selection preventing it

Poster (download) Dmitry Rasskazov1, Irina Chadaeva2, Mikhail Ponomarenko3, Ekaterina Sharypova4, Irina Drachkova5, Maria Nazarenko61Systems Biology Department, Institute of Cytology and Genetics (ICG SB RAS), Novosibirsk, Russia, rassk@bionen.nsc.ru2Systems Biology Department, Institute of Cytology and Genetics (ICG SB RAS), Novosibirsk, Russia, ichadaeva@bionet.nsc.ru3Systems Biology Department, Institute of Cytology and Genetics (ICG SB RAS), Novosibirsk, Russia, pon@bionen.nsc.ru4Molecular Genetics Department, Institute of Cytology and Genetics (ICG SB RAS), Novosibirsk, Russia, sharypova@bionet.nsc.ru5Molecular Genetics Department, Institute of Cytology and Genetics (ICG SB RAS), Novosibirsk, Russia, drachkova@bionet.nsc.ru6Population Genetics Laboratory, Institute of Medical Genetics (IMG TNRMC RAS), Tomsk, Russia, maria.nazarenko@medgenetics.ru In this work we carried out a computer-based whole-genome search for all variants of single-nucleotide polymorphism (SNP) within 70 bp regions upstream the all experimentally proven transcription start sites of the human genes associated with atherogenesis according to the current release #151 of the dbSNP database and GRCh38/hg38 assembly of the human reference genome, both of which are publicly available due to the UCSC Genome Browser. In the end, we first found atherosclerosis-related candidate SNP markers signoficantly changing the affinity of TATA-binding protein for promoters of these human gene, frequencies of which differes from the commonly accepted genome-wide norm as if they were under pressure of stabilizing natural selection, which summing up neutral drift accelerating atherogenesis and directional natural selection slowing it down

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Candidate SNP markers of rheumatoid arthritis changing the affinity of TATA-binding protein for the human gene promoters expo disruptive selection of immunoactivative and immunosuppressive genenets that provoke and prevent this disorder, respectively, as if it could be a self-domestication syndrome

Poster (download) Natalya Klimova1, Dmitry Oshchepkov2, Irina Chadaeva3, Mikhail Ponomarenko4, Evgeniya Oshchepkova5, academician Vladimir Kozlov61Molecular Genetics Department, Institute of Cytology and Genetics, ICG SB RAS, Novosibirsk, Russia, klimova@bionet.nsc.ru2Systems Biology Department, Institute of Cytology and Genetics, ICG SB RAS, Novosibirsk, Russia, diman@bionet.nsc.ru3Systems Biology Department, Institute of Cytology and Genetics, ICG SB RAS, Novosibirsk, Russia, ichadaeva@bionet.nsc.ru4Systems Biology Department, Institute of Cytology and Genetics, ICG SB RAS, Novosibirsk, Russia, pon@bionen.nsc.ru5Systems Biology Department, Institute of Cytology and Genetics, ICG SB RAS, Novosibirsk, Russia, nzhenia@bionet.nsc.ru6Research Institute of Fundamental and Clinical Immunology, RIFCI SB RAS, Novosibirsk, Russia, niiki01@online.nsk.su Here we conducted a computational genome-wide study of the all known single-nucleotide polymorphism (SNP) of 70 bp proximal promoters of 67 human rheumatoid arthritis (RA)-related genes that displayed disruptive natural selections of immunoactivative or immunosuppressive genes raising or reducing risks of RA, respectively, as if it maybe a domestication syndrome. That is why, we confirmed it in vivo using the genome-wide transcriptome profiling (RNA-seq assay) of the differentially expressed genes (DEGs) within hypothalamus of adult male rats (Rattus norvegicus) of two unique outbred lines bred in aggressiveness and tameness as an animal model of human diseases (statistical significance padj < 0.025 at Pearson\’s П‡2 criterion with Bonferroni\’s correction).

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