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J. Biol. Chem., Vol. 277, Issue 36, 33196-33204, September 6, 2002
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From the The docking protein SNT1/FRS2
(fibroblast growth factor receptor substrate 2) is implicated in the
transmission of extracellular signals from the fibroblast growth factor
receptor (FGFR), which plays vital roles during embryogenesis.
Activating FGFR mutations cause several craniosynostoses and dwarfism
syndromes in humans. Here we show that the Xenopus homolog
of mammalian FRS-2 (XFRS2) is essential for the induction of oocyte
maturation by an XFGFR1 harboring an activating mutation (XFGFR1act).
Using a dominant-negative form of kinase suppressor of Ras, we show the
Mek activity is required for germinal vesicle breakdown (GVBD) induced
by co-expression of XFGFR1act and XFRS2, but this activity is not
required for progesterone-induced GVBD. Furthermore, Mek/MAPK activity
is critical for the induction and/or maintenance of H1 kinase activity
at metaphase of meiosis II in progesterone-treated oocytes. An
activated XFGFR1 containing a mutation in the phospholipase C
SNT1/FRS2 Mediates Germinal Vesicle Breakdown Induced by an
Activated FGF Receptor1 in Xenopus Oocytes*
,
Regulation of Cell Growth Laboratory,
NCI-Frederick, National Institutes of Health, Frederick, Maryland 21702 and § Center for Molecular Medicine, Maine Medical Center
Research Institute, South Portland, Maine 04106
binding site (XFGFR1actY672F) displayed a reduced ability to induce
cell-cycle progression in oocytes, suggesting phospholipase C may
not be necessary but that it augments XFGFR signaling in this system. Oocytes co-expressing XFGFR1act and XFRS2 showed substantial H1 kinase
activity, but this activity was blocked when the oocytes were treated
with the phosphatidylinositol 3-kinase inhibitor LY294002. Although
phosphatidylinositol 3-kinase activity is essential for
XFGFR1act/XFRS2-induced oocyte maturation, this activity is not
required for maturation induced by progesterone. Finally, ectopic
expression of Xspry2, a negative regulator of XFGFR signaling, greatly
reduced MAPK activation and GVBD induced by the expression of either
XFGFR1act plus XFRS2 or activated Ras (H-RasV12). In contrast, Xspry2
did not prevent GVBD induced by an activated form of Raf1, suggesting
that Xspry2 exerts its inhibitory function upstream or parallel to Raf
and downstream of Ras.
*
The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Bldg. 560, Rm.
22-3, Regulation of Cell Growth Laboratory, NCI-Frederick, Frederick, MD 21702. Tel.: 301-846-1667; Fax: 301-846-1666; E-mail:
daar@ncifcrf.gov.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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