Abstract
Localization ofoskarmRNA includes two distinct phases: transport from nurse cells to the oocyte, a process typically accompanied by cortical anchoring in the oocyte, followed by posterior localization within the oocyte. Signals within theoskar3’ UTR directing transport are individually weak, a feature previously hypothesized to facilitate exchange between the different localization machineries. We show that alteration of the SL2a stem-loop structure containing theoskartransport and anchoring signal (TAS) removes an inhibitory effect such thatin vitrobinding by the RNA transport factor, Egalitarian, is elevated as isin vivotransport from the nurse cells into the oocyte. Cortical anchoring within the oocyte is also enhanced, interfering with posterior localization. We also show that mutation of Staufen recognized structures (SRSs), predicted binding sites for Staufen, disrupts posterior localization ofoskarmRNA just as instaufenmutants. Two SRSs in SL2a, one overlapping the Egalitarian binding site, are inferred to mediate Staufen-dependent inhibition of TAS anchoring activity, thereby promoting posterior localization. The other three SRSs in theoskar3’ UTR are also required for posterior localization, including two located distant from any known transport signal. Staufen, thus, plays multiple roles in localization ofoskarmRNA.
Funder
National Institute of General Medical Sciences
CIHR
NSERC
Department of Molecular Genetics, University of Toronto
Publisher
Public Library of Science (PLoS)
Subject
Cancer Research,Genetics(clinical),Genetics,Molecular Biology,Ecology, Evolution, Behavior and Systematics
Cited by
12 articles.
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