A1 Refereed original research article in a scientific journal

Widespread formation of double-stranded RNAs in testis




AuthorsWerner Andreas, Clark James E, Samaranayake Calum, Casement John, Zinad Hany S, Sadeq Shaymaa, Al-Hashimi Surar, Smith Martin, Kotaja Noora, Mattick John S

PublisherCOLD SPRING HARBOR LAB PRESS

Publication year2021

JournalGenome Research

Journal name in sourceGENOME RESEARCH

Journal acronymGENOME RES

Volume31

Issue9

First page 1174

Last page1186

Number of pages14

ISSN1088-9051

eISSN1549-5469

DOIhttps://doi.org/10.1101/gr.265603.120(external)

Self-archived copy’s web addresshttps://research.utu.fi/converis/portal/detail/Publication/66669136(external)


Abstract

The testis transcriptome is highly complex and includes RNAs that potentially hybridize to form double-stranded RNA (dsRNA). We isolated dsRNA using the monoclonal J2 antibody and deep-sequenced the enriched samples from testes of juvenile Dicer1 knockout mice, age-matched controls, and adult animals. Comparison of our data set with recently published data from mouse liver revealed that the dsRNA transcriptome in testis is markedly different from liver: In testis, dsRNA-forming transcripts derive from mRNAs including promoters and immediate downstream regions, whereas in somatic cells they originate more often from introns and intergenic transcription. The genes that generate dsRNA are significantly expressed in isolated male germ cells with particular enrichment in pachytene spermatocytes. dsRNA formation is lower on the sex (X and Y) chromosomes. The dsRNA transcriptome is significantly less complex in juvenile mice as compared to adult controls and, possibly as a consequence, the knockout of Dicer1 has only a minor effect on the total number of transcript peaks associated with dsRNA. The comparison between dsRNA-associated genes in testis and liver with a reported set of genes that produce endogenous siRNAs reveals a significant overlap in testis but not in liver. Testis dsRNAs also significantly associate with natural antisense genes-again, this feature is not observed in liver. These findings point to a testis-specific mechanism involving natural antisense transcripts and the formation of dsRNAs that feed into the RNA interference pathway, possibly to mitigate the mutagenic impacts of recombination and transposon mobilization.


Downloadable publication

This is an electronic reprint of the original article.
This reprint may differ from the original in pagination and typographic detail. Please cite the original version.





Last updated on 2024-26-11 at 21:18