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Enforcing temporal control of maternal mRNA translation during oocyte cell-cycle progression.


ABSTRACT: Meiotic cell-cycle progression in progesterone-stimulated Xenopus oocytes requires that the translation of pre-existing maternal mRNAs occur in a strict temporal order. Timing of translation is regulated through elements within the mRNA 3' untranslated region (3' UTR), which respond to cell cycle-dependant signalling. One element that has been previously implicated in the temporal control of mRNA translation is the cytoplasmic polyadenylation element (CPE). In this study, we show that the CPE does not direct early mRNA translation. Rather, early translation is directed through specific early factors, including the Musashi-binding element (MBE) and the MBE-binding protein, Musashi. Our findings indicate that although the cyclin B5 3' UTR contains both CPEs and an MBE, the MBE is the critical regulator of early translation. The cyclin B2 3' UTR contains CPEs, but lacks an MBE and is translationally activated late in maturation. Finally, utilizing antisense oligonucleotides to attenuate endogenous Musashi synthesis, we show that Musashi is critical for the initiation of early class mRNA translation and for the subsequent activation of CPE-dependant mRNA translation.

SUBMITTER: Arumugam K 

PROVIDER: S-EPMC2824450 | biostudies-literature | 2010 Jan

REPOSITORIES: biostudies-literature

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Enforcing temporal control of maternal mRNA translation during oocyte cell-cycle progression.

Arumugam Karthik K   Wang Yiying Y   Hardy Linda L LL   MacNicol Melanie C MC   MacNicol Angus M AM  

The EMBO journal 20091203 2


Meiotic cell-cycle progression in progesterone-stimulated Xenopus oocytes requires that the translation of pre-existing maternal mRNAs occur in a strict temporal order. Timing of translation is regulated through elements within the mRNA 3' untranslated region (3' UTR), which respond to cell cycle-dependant signalling. One element that has been previously implicated in the temporal control of mRNA translation is the cytoplasmic polyadenylation element (CPE). In this study, we show that the CPE do  ...[more]

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