Translational control by cytoplasmic polyadenylation of c‐mos mRNA is necessary for oocyte maturation in the mouse.

F Gebauer, W Xu, GM Cooper, JD Richter - The EMBO journal, 1994 - embopress.org
F Gebauer, W Xu, GM Cooper, JD Richter
The EMBO journal, 1994embopress.org
The c‐mos proto‐oncogene product is a key element in the cascade of events leading to
meiotic maturation of vertebrate oocytes. We have investigated the role of cytoplasmic
polyadenylation in the translational control of mouse c‐mos mRNA and its contribution to
meiosis. Using an RNase protection assay we show that optimal cytoplasmic
polyadenylation of c‐mos mRNA requires three cis elements in the 3′ UTR: the
polyadenylation hexanucleotide AAUAAA and two U‐rich cytoplasmic polyadenylation …
The c‐mos proto‐oncogene product is a key element in the cascade of events leading to meiotic maturation of vertebrate oocytes. We have investigated the role of cytoplasmic polyadenylation in the translational control of mouse c‐mos mRNA and its contribution to meiosis. Using an RNase protection assay we show that optimal cytoplasmic polyadenylation of c‐mos mRNA requires three cis elements in the 3′ UTR: the polyadenylation hexanucleotide AAUAAA and two U‐rich cytoplasmic polyadenylation elements (CPEs) located 4 and 51 nucleotides upstream of the hexanucleotide. When fused to CAT coding sequences, the wild‐type 3′ UTR of c‐mos mRNA, but not a 3′ UTR containing mutations in both CPEs, confers translational recruitment during maturation. This recruitment coincides with maximum polyadenylation. To assess whether c‐mos mRNA polyadenylation is necessary for maturation of mouse oocytes, we have ablated endogenous c‐mos mRNA by injecting an antisense oligonucleotide, which results in a failure to progress to meiosis II after emission of the first polar body. Such antisense oligonucleotide‐injected oocytes could be efficiently rescued by co‐injection of a c‐mos mRNA carrying a wild‐type 3′ UTR. However, co‐injection of a c‐mos mRNA lacking functional CPEs substantially lowered the rescue activity. These results demonstrate that translational control of c‐mos mRNA by cytoplasmic polyadenylation is necessary for normal development.
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