Disruptive natural selection by male reproductive potential prevents underexpression of protein-coding genes on the huma
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RESEARCH
Open Access
Disruptive natural selection by male reproductive potential prevents underexpression of protein-coding genes on the human Y chromosome as a selfdomestication syndrome Mikhail Ponomarenko1,2* , Maxim Kleshchev1, Petr Ponomarenko1, Irina Chadaeva1, Ekaterina Sharypova1, Dmitry Rasskazov1, Semyon Kolmykov1, Irina Drachkova1, Gennady Vasiliev1, Natalia Gutorova1, Elena Ignatieva1, Ludmila Savinkova1, Anton Bogomolov1, Ludmila Osadchuk1, Alexandr Osadchuk1 and Dmitry Oshchepkov1 From 11th International Young Scientists School “Systems Biology and Bioinformatics” – SBB-2019 Novosibirsk, Russia. 24-28 June 2019
Abstract Background: In population ecology, the concept of reproductive potential denotes the most vital indicator of chances to produce and sustain a healthy descendant until his/her reproductive maturity under the best conditions. This concept links quality of life and longevity of an individual with disease susceptibilities encoded by his/her genome. Female reproductive potential has been investigated deeply, widely, and comprehensively in the past, but the male one has not received an equal amount of attention. Therefore, here we focused on the human Y chromosome and found candidate single-nucleotide polymorphism (SNP) markers of male reproductive potential. Results: Examining in silico (i.e., using our earlier created Web-service SNP_TATA_Z-tester) all 1206 unannotated SNPs within 70 bp proximal promoters of all 63 Y-linked genes, we found 261 possible male-reproductive-potential SNP markers that can significantly alter the binding affinity of TATA-binding protein (TBP) for these promoters. Among them, there are candidate SNP markers of spermatogenesis disorders (e.g., rs1402972626), pediatric cancer (e.g., rs1483581212) as well as male anxiety damaging family relationships and mother’s and children’s health (e.g., rs187456378). First of all, we selectively verified in vitro both absolute and relative values of the analyzed TBP– promoter affinity, whose Pearson’s coefficients of correlation between predicted and measured values were r = 0.84 (significance p < 0.025) and r = 0.98 (p < 0.025), respectively. Next, we found that there are twofold fewer candidate SNP markers decreasing TBP–promoter affinity relative to those increasing it, whereas in the genome-wide norm, SNP-induced damage to TBP–promoter complexes is fourfold more frequent than SNP-induced improvement (Continued on next page)
* Correspondence: [email protected] 1 Institute of Cytology and Genetics, Siberian Branch of Russian Academy of Sciences, 10 Lavrentyev Ave, Novosibirsk 630090, Russia 2 Novosibirsk State University, 1, Pirogova str., Novosibirsk 630090, Russia © The Author(s). 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if
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