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Mol. Cell. Biol., 11 1997, 6419-6426, Vol 17, No. 11
CH de Moor and JD Richter
Cytoplasmic polyadenylation controls the translation of several maternal
mRNAs during Xenopus oocyte maturation and requires two sequences in the 3'
untranslated region (UTR), the U-rich cytoplasmic polyadenylation element
(CPE), and the hexanucleotide AAUAAA. c-mos mRNA is polyadenylated and
translated soon after the induction of maturation, and this protein kinase
is necessary for a kinase cascade culminating in cdc2 kinase (MPF)
activation. Other mRNAs are polyadenylated later, around the time of cdc2
kinase activation. To determine whether there is a hierarchy in the
cytoplasmic polyadenylation of maternal mRNAs, we ablated c-mos mRNA with
an antisense oligonucleotide. This prevented histone B4 and cyclin A1 and
B1 mRNA polyadenylation, indicating that the polyadenylation of these mRNAs
is Mos dependent. To investigate a possible role of cdc2 kinase in this
process, cyclin B was injected into oocytes lacking c-mos mRNA. cdc2 kinase
was activated, but mitogen-activated protein kinase was not. However,
polyadenylation of cyclin B1 and histone B4 mRNA was still observed. This
demonstrates that cdc2 kinase can induce cytoplasmic polyadenylation in the
absence of Mos. Our data further indicate that although phosphorylation of
the CPE binding protein may be involved in the induction of Mos-dependent
polyadenylation, it is not required for Mos-independent polyadenylation. We
characterized the elements conferring Mos dependence (Mos response
elements) in the histone B4 and cyclin B1 mRNAs by mutational analysis. For
histone B4 mRNA, the Mos response elements were in the coding region or 5'
UTR. For cyclin B1 mRNA, the main Mos response element was a CPE that
overlaps with the AAUAAA hexanucleotide. This indicates that the position
of the CPE can have a profound influence on the timing of cytoplasmic
polyadenylation.
Copyright © 1997, American Society for Microbiology
The Mos pathway regulates cytoplasmic polyadenylation in Xenopus oocytes
Department of Molecular Genetics and Microbiology, University of Massachusetts Medical Center, Worcester 01655, USA.
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