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Tytuł pozycji:

Tertiary siRNAs mediate paramutation in C. elegans.

Tytuł:
Tertiary siRNAs mediate paramutation in C. elegans.
Autorzy:
Sapetschnig A; Wellcome Trust Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge, United Kingdom; Department of Biochemistry and Department of Genetics, University of Cambridge, Cambridge, United Kingdom.
Sarkies P; Wellcome Trust Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge, United Kingdom; Department of Biochemistry and Department of Genetics, University of Cambridge, Cambridge, United Kingdom.
Lehrbach NJ; Wellcome Trust Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge, United Kingdom; Department of Biochemistry and Department of Genetics, University of Cambridge, Cambridge, United Kingdom.
Miska EA; Wellcome Trust Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge, United Kingdom; Department of Biochemistry and Department of Genetics, University of Cambridge, Cambridge, United Kingdom.
Źródło:
PLoS genetics [PLoS Genet] 2015 Mar 26; Vol. 11 (3), pp. e1005078. Date of Electronic Publication: 2015 Mar 26 (Print Publication: 2015).
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Original Publication: San Francisco, CA : Public Library of Science, c2005-
MeSH Terms:
Epigenesis, Genetic*
RNA Interference*
Argonaute Proteins/*genetics
Caenorhabditis elegans Proteins/*genetics
Nuclear Proteins/*genetics
RNA, Small Interfering/*genetics
Animals ; Caenorhabditis elegans/genetics ; Germ-Line Mutation/genetics
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Grant Information:
11832 United Kingdom CRUK_ Cancer Research UK; MC_UP_1102/13 United Kingdom MRC_ Medical Research Council; P40 OD010440 United States OD NIH HHS; RG57329 United Kingdom CRUK_ Cancer Research UK
Molecular Sequence:
GEO GSE49220; GSE66344
Substance Nomenclature:
0 (Argonaute Proteins)
0 (Caenorhabditis elegans Proteins)
0 (HRDE-1 protein, C elegans)
0 (Nuclear Proteins)
0 (RNA, Small Interfering)
Entry Date(s):
Date Created: 20150327 Date Completed: 20151228 Latest Revision: 20210109
Update Code:
20240104
PubMed Central ID:
PMC4374809
DOI:
10.1371/journal.pgen.1005078
PMID:
25811365
Czasopismo naukowe
In the nematode Caenorhabditis elegans, different small RNA-dependent gene silencing mechanisms act in the germline to initiate transgenerational gene silencing. Piwi-interacting RNAs (piRNAs) can initiate transposon and gene silencing by acting upstream of endogenous short interfering RNAs (siRNAs), which engage a nuclear RNA interference (RNAi) pathway to trigger transcriptional gene silencing. Once gene silencing has been established, it can be stably maintained over multiple generations without the requirement of the initial trigger and is also referred to as RNAe or paramutation. This heritable silencing depends on the integrity of the nuclear RNAi pathway. However, the exact mechanism by which silencing is maintained across generations is not understood. Here we demonstrate that silencing of piRNA targets involves the production of two distinct classes of small RNAs with different genetic requirements. The first class, secondary siRNAs, are localized close to the direct target site for piRNAs. Nuclear import of the secondary siRNAs by the Argonaute HRDE-1 leads to the production of a distinct class of small RNAs that map throughout the transcript, which we term tertiary siRNAs. Both classes of small RNAs are necessary for full repression of the target gene and can be maintained independently of the initial piRNA trigger. Consistently, we observed a form of paramutation associated with tertiary siRNAs. Once paramutated, a tertiary siRNA generating allele confers dominant silencing in the progeny regardless of its own transmission, suggesting germline-transmitted siRNAs are sufficient for multigenerational silencing. This work uncovers a multi-step siRNA amplification pathway that promotes germline integrity via epigenetic silencing of endogenous and invading genetic elements. In addition, the same pathway can be engaged in environmentally induced heritable gene silencing and could therefore promote the inheritance of acquired traits.

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