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Nat Ecol Evol. 2020 Jan;4(1):156-168. doi: 10.1038/s41559-019-1065-1. Epub 2019 Dec 23.

Evolutionarily conserved pachytene piRNA loci are highly divergent among modern humans.

Author information

1
RNA Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA, USA.
2
Program in Bioinformatics and Integrative Biology, University of Massachusetts Medical School, Worcester, MA, USA.
3
Department of Bioinformatics, School of Life Sciences and Technology, Tongji University, Shanghai, People's Republic of China.
4
Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, MA, USA.
5
Program in Bioinformatics and Integrative Biology, University of Massachusetts Medical School, Worcester, MA, USA. zhiping.weng@umassmed.edu.
6
RNA Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA, USA. phillip.zamore@umassmed.edu.
7
Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, MA, USA. phillip.zamore@umassmed.edu.

Abstract

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.

PMID:
31900453
PMCID:
PMC6961462
[Available on 2020-06-23]
DOI:
10.1038/s41559-019-1065-1

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