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dc.contributor.authorOzata, Deniz M.
dc.contributor.authorYu, Tianxiong
dc.contributor.authorMou, Haiwei
dc.contributor.authorColpan, Cansu
dc.contributor.authorCecchini, Katharine
dc.contributor.authorKaymaz, Yasin
dc.contributor.authorFan, Kaili
dc.contributor.authorKucukural, Alper
dc.contributor.authorWeng, Zhiping
dc.contributor.authorZamore, Phillip D.
dc.date2022-08-11T08:07:59.000
dc.date.accessioned2022-08-23T15:38:07Z
dc.date.available2022-08-23T15:38:07Z
dc.date.issued2020-01-04
dc.date.submitted2020-01-14
dc.identifier.citation<p>Nat Ecol Evol. 2020 Jan;4(1):156-168. doi: 10.1038/s41559-019-1065-1. Epub 2019 Dec 23. <a href="https://doi.org/10.1038/s41559-019-1065-1">Link to article on publisher's site</a></p>
dc.identifier.issn2397-334X (Linking)
dc.identifier.doi10.1038/s41559-019-1065-1
dc.identifier.pmid31900453
dc.identifier.urihttp://hdl.handle.net/20.500.14038/25870
dc.description.abstractIn the fetal mouse testis, PIWI-interacting RNAs (piRNAs) guide PIWI proteins to silence transposons but, after birth, most post-pubertal pachytene piRNAs map to the genome uniquely and are thought to regulate genes required for male fertility. In the human male, the developmental classes, precise genomic origins and transcriptional regulation of postnatal piRNAs remain undefined. Here, we demarcate the genes and transcripts that produce postnatal piRNAs in human juvenile and adult testes. As in the mouse, human A-MYB drives transcription of both pachytene piRNA precursor transcripts and messenger RNAs encoding piRNA biogenesis factors. Although human piRNA genes are syntenic to those in other placental mammals, their sequences are poorly conserved. In fact, pachytene piRNA loci are rapidly diverging even among modern humans. Our findings suggest that, during mammalian evolution, pachytene piRNA genes are under few selective constraints. We speculate that pachytene piRNA diversity may provide a hitherto unrecognized driver of reproductive isolation.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=31900453&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1038/s41559-019-1065-1
dc.subjectBiochemistry, Biophysics, and Structural Biology
dc.subjectBioinformatics
dc.subjectComputational Biology
dc.subjectDevelopmental Biology
dc.subjectEcology and Evolutionary Biology
dc.subjectIntegrative Biology
dc.subjectSystems Biology
dc.titleEvolutionarily conserved pachytene piRNA loci are highly divergent among modern humans
dc.typeArticle
dc.source.journaltitleNature ecology and evolution
dc.source.volume4
dc.source.issue1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/bioinformatics_pubs/162
dc.identifier.contextkey16211940
html.description.abstract<p>In the fetal mouse testis, PIWI-interacting RNAs (piRNAs) guide PIWI proteins to silence transposons but, after birth, most post-pubertal pachytene piRNAs map to the genome uniquely and are thought to regulate genes required for male fertility. In the human male, the developmental classes, precise genomic origins and transcriptional regulation of postnatal piRNAs remain undefined. Here, we demarcate the genes and transcripts that produce postnatal piRNAs in human juvenile and adult testes. As in the mouse, human A-MYB drives transcription of both pachytene piRNA precursor transcripts and messenger RNAs encoding piRNA biogenesis factors. Although human piRNA genes are syntenic to those in other placental mammals, their sequences are poorly conserved. In fact, pachytene piRNA loci are rapidly diverging even among modern humans. Our findings suggest that, during mammalian evolution, pachytene piRNA genes are under few selective constraints. We speculate that pachytene piRNA diversity may provide a hitherto unrecognized driver of reproductive isolation.</p>
dc.identifier.submissionpathbioinformatics_pubs/162
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.contributor.departmentProgram in Bioinformatics and Integrative Biology
dc.contributor.departmentRNA Therapeutics Institute
dc.source.pages156-168


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