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The pathway of MAP kinase mediation of CSF arrest in Xenopus oocytes
Author(s) -
Maller James L.,
Schwab Markus S.,
Roberts B.Tibor,
Gross Stefan D.,
Taieb Frédéric E.,
Tunquist Brian J.
Publication year - 2001
Publication title -
biology of the cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.543
H-Index - 85
eISSN - 1768-322X
pISSN - 0248-4900
DOI - 10.1016/s0248-4900(01)01127-3
Subject(s) - biology , microbiology and biotechnology , anaphase promoting complex , mapk/erk pathway , maturation promoting factor , metaphase , xenopus , spindle checkpoint , cyclin b , protein kinase a , anaphase , ask1 , kinase , mitogen activated protein kinase kinase , cyclin dependent kinase 1 , cyclin , cell cycle , genetics , spindle apparatus , cell division , cell , chromosome , gene
Summry— A cytoplasmic activity in mature oocytes responsible for second meiotic metaphase arrest was identified over 30 years ago in amphibian oocytes. In Xenopus oocytes CSF activity is initiated by the progesterone‐dependent synthesis of Mos, a MAPK kinase kinase, which activates the MAPK pathway. CSF arrest is mediated by a sole MAPK target, the protein kinase p90 Rsk which leads to inhibition of cyclin B degradation by the anaphase‐promoting complex. Rsk phosphorylates and activates the Bub1 protein kinase, which may cause metaphase arrest due to inhibition of the anaphase‐promoting complex (APC) by a conserved mechanism defined genetically in yeast and mammalian cells. CSF arrest in vertebrate oocytes by p90 Rsk provides a potential link between the MAPK pathway and the spindle assembly checkpoint in the cell cycle.