C. elegans ADARs antagonize silencing of cellular dsRNAs by the antiviral RNAi pathway.
C. elegans ADARs antagonize silencing of cellular dsRNAs by the antiviral RNAi pathway.
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DOI:
10.1101/gad.310672.117
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发表时间:
2018-02-01
影响因子:
10.5
通讯作者:
Bass BL
中科院分区:
文献类型:
--
作者:
Reich DP;Tyc KM;Bass BL
In this study, Reich et al. researched the functions of Caenorhabditis elegans adenosine deaminases that act on RNA (ADARs), which catalyze A-to-I RNA editing in dsRNA. Using dsRNA immunoprecipitation (dsRIP) and RNA-seq, they identified 1523 regions of clustered A-to-I editing, termed editing-enriched regions (EERs), in four stages of C. elegans development, often with highest expression in embryos. Cellular dsRNAs are edited by adenosine deaminases that act on RNA (ADARs). While editing can alter mRNA-coding potential, most editing occurs in noncoding sequences, the function of which is poorly understood. Using dsRNA immunoprecipitation (dsRIP) and RNA sequencing (RNA-seq), we identified 1523 regions of clustered A-to-I editing, termed editing-enriched regions (EERs), in four stages of Caenorhabditis elegans development, often with highest expression in embryos. Analyses of small RNA-seq data revealed 22- to 23-nucleotide (nt) siRNAs, reminiscent of viral siRNAs, that mapped to EERs and were abundant in adr-1;adr-2 mutant animals. Consistent with roles for these siRNAs in silencing, EER-associated genes (EAGs) were down-regulated in adr-1;adr-2 embryos, and this was dependent on associated EERs and the RNAi factor RDE-4. We observed that ADARs genetically interact with the 26G endogenous siRNA (endo-siRNA) pathway, which likely competes for RNAi components; deletion of factors required for this pathway (rrf-3 or ergo-1) in adr-1;adr-2 mutant strains caused a synthetic phenotype that was rescued by deleting antiviral RNAi factors. Poly(A)+ RNA-seq revealed EAG down-regulation and antiviral gene induction in adr-1;adr-2;rrf-3 embryos, and these expression changes were dependent on rde-1 and rde-4. Our data suggest that ADARs restrict antiviral silencing of cellular dsRNAs.
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DOI:
10.1073/pnas.76.3.1333
发表时间:
1979-01-01
影响因子:
11.1
作者:
EMMONS, SW;KLASS, MR;HIRSH, D
通讯作者:
HIRSH, D
影响因子:
7.7
作者:
Ashe A;Bélicard T;Le Pen J;Sarkies P;Frézal L;Lehrbach NJ;Félix MA;Miska EA
通讯作者:
Miska EA
DOI:
10.1126/science.1157647
发表时间:
2008-07-25
期刊:
Science (New York, N.Y.)
影响因子:
--
作者:
Guang S;Bochner AF;Pavelec DM;Burkhart KB;Harding S;Lachowiec J;Kennedy S
通讯作者:
Kennedy S
影响因子:
8.8
作者:
Mannion NM;Greenwood SM;Young R;Cox S;Brindle J;Read D;Nellåker C;Vesely C;Ponting CP;McLaughlin PJ;Jantsch MF;Dorin J;Adams IR;Scadden AD;Ohman M;Keegan LP;O'Connell MA
通讯作者:
O'Connell MA
影响因子:
3.3
作者:
Cho SW;Lee J;Carroll D;Kim JS;Lee J
通讯作者:
Lee J