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dc.contributor.authorHain, Danielen_US
dc.contributor.authorBettencourt, Brian R.en_US
dc.contributor.authorOkamura, Katsutomoen_US
dc.contributor.authorCsorba, Tiboren_US
dc.contributor.authorMeyer, Wibkeen_US
dc.contributor.authorJin, Zhigangen_US
dc.contributor.authorBiggerstaff, Jasonen_US
dc.contributor.authorSiomi, Haruhikoen_US
dc.contributor.authorHutvagner, Gyorgyen_US
dc.contributor.authorLai, Eric C.en_US
dc.contributor.authorWelte, Michaelen_US
dc.contributor.authorMüller, H.-Arno J.en_US
dc.date.accessioned2012-01-09T21:00:20Z
dc.date.available2012-01-09T21:00:20Z
dc.date.issued2010-12-17
dc.identifier.citationHain, Daniel, Brian R. Bettencourt, Katsutomo Okamura, Tibor Csorba, Wibke Meyer, Zhigang Jin, Jason Biggerstaff, Haruhiko Siomi, Gyorgy Hutvagner, Eric C. Lai, Michael Welte, H.-Arno J. Müller. "Natural Variation of the Amino-Terminal Glutamine-Rich Domain in Drosophila Argonaute2 Is Not Associated with Developmental Defects" PLoS ONE 5(12): e15264. (2010)
dc.identifier.issn1932-6203
dc.identifier.urihttps://hdl.handle.net/2144/2975
dc.description.abstractThe Drosophila argonaute2 (ago2) gene plays a major role in siRNA mediated RNA silencing pathways. Unlike mammalian Argonaute proteins, the Drosophila protein has an unusual amino-terminal domain made up largely of multiple copies of glutamine-rich repeats (GRRs). We report here that the ago2 locus produces an alternative transcript that encodes a putative short isoform without this amino-terminal domain. Several ago2 mutations previously reported to be null alleles only abolish expression of the long, GRR-containing isoform. Analysis of drop out (dop) mutations had previously suggested that variations in GRR copy number result in defects in RNAi and embryonic development. However, we find that dop mutations genetically complement transcript-null alleles of ago2 and that ago2 alleles with variant GRR copy numbers support normal development. In addition, we show that the assembly of the central RNAi machinery, the RISC (RNA induced silencing complex), is unimpaired in embryos when GRR copy number is altered. In fact, we find that GRR copy number is highly variable in natural D. melanogaster populations as well as in laboratory strains. Finally, while many other insects share an extensive, glutamine-rich Ago2 amino-terminal domain, its primary sequence varies drastically between species. Our data indicate that GRR variation does not modulate an essential function of Ago2 and that the amino-terminal domain of Ago2 is subject to rapid evolution.en_US
dc.description.sponsorshipEuropean Molecular Biology Organisation; the Commonwealth of Massachusetts; Wellcome Trust Career Development Fellowship; European Union Framework 6 programme SIROCCO (Silencing RNAs: organisers and coordinators of complexity in eukaryotic organisms); the Burroughs Wellcome Fund; the Alfred Bressler Scholars Fund; the National Institutes of Health (R01-GM083300); National Institute of General Medical Sciences (GM64687); the Biotechnological and Biological Sciences Research Council; Deutsche Forschungsgemeinshaften_US
dc.language.isoen
dc.publisherPublic Library of Scienceen_US
dc.rightsHain et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en_US
dc.titleNatural Variation of the Amino-Terminal Glutamine-Rich Domain in Drosophila Argonaute2 Is Not Associated with Developmental Defectsen_US
dc.typeArticleen_US
dc.identifier.doi10.1371/journal.pone.0015264
dc.identifier.pmid21253006
dc.identifier.pmcid3002974


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