Gutenberg Open Science: piRNAs from pig testis provide evidence for a conserved role of the Piwi pathway in post-transcriptional gene regulation in mammals

Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-8009

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DC Field	Value	Language
dc.contributor.author	Gebert, Daniel	-
dc.contributor.author	Ketting, René F.	-
dc.contributor.author	Zischler, Hans	-
dc.contributor.author	Rosenkranz, David	-
dc.date.accessioned	2022-10-14T08:18:03Z	-
dc.date.available	2022-10-14T08:18:03Z	-
dc.date.issued	2015
dc.identifier.uri	https://openscience.ub.uni-mainz.de/handle/20.500.12030/8024	-
dc.description.abstract	Piwi-interacting (pi-) RNAs guide germline-expressed Piwi proteins in order to suppress the activity of transposable elements (TEs). But notably, the majority of pachytene piRNAs in mammalian testes is not related to TEs. This raises the question of whether the Piwi/piRNA pathway exerts functions beyond TE silencing. Although gene-derived piRNAs were described many times, a possible gene-regulatory function was doubted due to the absence of antisense piRNAs. Here we sequenced and analyzed piRNAs expressed in the adult testis of the pig, as this taxon possesses the full set of mammalian Piwi paralogs while their spermatozoa are marked by an extreme fitness due to selective breeding. We provide an exhaustive characterization of porcine piRNAs and genomic piRNA clusters. Moreover, we reveal that both sense and antisense piRNAs derive from protein-coding genes, while exhibiting features that clearly show that they originate from the Piwi/piRNA-mediated post-transcriptional silencing pathway, commonly referred to as ping-pong cycle. We further show that the majority of identified piRNA clusters in the porcine genome spans exonic sequences of protein-coding genes or pseudogenes, which reveals a mechanism by which primary antisense piRNAs directed against mRNA can be generated. Our data provide evidence that spliced mRNAs, derived from such loci, are not only targeted by piRNAs but are also subject to ping-pong cycle processing. Finally, we demonstrate that homologous genes are targeted and processed by piRNAs in pig, mouse and human. Altogether, this strongly suggests a conserved role for the mammalian Piwi/piRNA pathway in post-transcriptional regulation of protein-coding genes, which did not receive much attention so far.	en_GB
dc.description.sponsorship	DFG, Open Access-Publizieren Universität Mainz / Universitätsmedizin	de
dc.language.iso	eng	de
dc.rights	CC BY	*
dc.rights.uri	https://creativecommons.org/licenses/by/4.0/	*
dc.subject.ddc	570 Biowissenschaften	de_DE
dc.subject.ddc	570 Life sciences	en_GB
dc.title	piRNAs from pig testis provide evidence for a conserved role of the Piwi pathway in post-transcriptional gene regulation in mammals	en_GB
dc.type	Zeitschriftenaufsatz	de
dc.identifier.doi	http://doi.org/10.25358/openscience-8009	-
jgu.type.dinitype	article	en_GB
jgu.type.version	Published version	de
jgu.type.resource	Text	de
jgu.organisation.department	FB 10 Biologie	de
jgu.organisation.number	7970	-
jgu.organisation.name	Johannes Gutenberg-Universität Mainz	-
jgu.rights.accessrights	openAccess	-
jgu.journal.title	PLoS one	de
jgu.journal.volume	10	de
jgu.journal.issue	5	de
jgu.pages.alternative	e0124860	de
jgu.publisher.year	2015	-
jgu.publisher.name	PLoS	de
jgu.publisher.place	Lawrence, Kan.	de
jgu.publisher.uri	http://dx.doi.org/10.1371/journal.pone.0124860	de
jgu.publisher.issn	1932-6203	de
jgu.organisation.place	Mainz	-
jgu.identifier.pmid	25950437
jgu.subject.ddccode	570	de
opus.date.modified	2018-09-05T09:08:22Z
opus.subject.dfgcode	00-000
opus.organisation.string	FB 10: Biologie: Institut für Anthropologie	de_DE
opus.identifier.opusid	51337
opus.importsource	pubmed
opus.institute.number	1007
opus.metadataonly	false
opus.type.contenttype	Keine	de_DE
opus.type.contenttype	None	en_EN
opus.affiliated	Zischler, Hans
opus.affiliated	Rosenkranz, David
jgu.publisher.doi	10.1371/journal.pone.0124860	de
jgu.organisation.ror	https://ror.org/023b0x485	-
Appears in collections:	DFG-OA-Publizieren (2012 - 2017)

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