CALMODULIN-DEPENDENT PROTEIN KINASE-II MEDIATES INACTIVATION OF MPF AND CSF UPON FERTILIZATION OF XENOPUS EGGS

被引:403
作者
LORCA, T
CRUZALEGUI, FH
FESQUET, D
CAVADORE, JC
MERY, J
MEANS, A
DOREE, M
机构
[1] INSERM, F-34100 MONTPELLIER, FRANCE
[2] BAYLOR COLL MED, DEPT CELL BIOL, HOUSTON, TX 77030 USA
[3] DUKE UNIV, MED CTR, DEPT PHARMACOL, DURHAM, NC 27710 USA
关键词
D O I
10.1038/366270a0
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
IN vertebrates, unfertilized eggs are arrested at second meiotic metaphase by a cytostatic factor (CSF)1, an essential component of which is the product of the c-mos proto-oncogene2. CSF prevents ubiquitin-dependent degradation of mitotic cyclins and thus inactivation of the M phase-promoting factor (MPF)3,4. Fertilization or parthenogenetic activation triggers a transient increase in the cytoplasmic free Ca2+ (reviewed in refs 5 and 6), inactivates both CSF and MPF, and releases eggs from meiotic metaphase arrest7-10. A calmodulin-dependent process is required for cyclin degradation to occur in cell-free extracts prepared from metaphase II-arrested eggs (CSF extracts) when the free Ca2+ concentration is transiently raised in the physiological micromolar range10. Here we show that when a constitutively active mutant of calmodulin-dependent protein kinase II (CaM K(II)) is added to a CSF extract, cyclin degradation and Cdc2 kinase inactivation occur even in the absence of Ca2+, and the extract loses its ability to cause metaphase arrest when transferred into embryos. Furthermore, specific inhibitors of CaM K(II) prevent cyclin degradation after calcium addition. Finally, the direct microinjection of constitutively active CaM K(II) into unfertilized eggs inactivates Cdc2 kinase and CSF, even in the absence of a Ca2+ transient. The target for Ca2+-calmodulin is thus CaM K(II).
引用
收藏
页码:270 / 273
页数:4
相关论文
共 29 条
[1]   INOSITOL TRISPHOSPHATE AND CALCIUM SIGNALING [J].
BERRIDGE, MJ .
NATURE, 1993, 361 (6410) :315-325
[2]   IDENTIFICATION OF THE CALMODULIN-BINDING DOMAIN OF SKELETAL-MUSCLE MYOSIN LIGHT CHAIN KINASE [J].
BLUMENTHAL, DK ;
TAKIO, K ;
EDELMAN, AM ;
CHARBONNEAU, H ;
TITANI, K ;
WALSH, KA ;
KREBS, EG .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1985, 82 (10) :3187-3191
[3]  
CHEUNG WY, 1971, J BIOL CHEM, V246, P2859
[4]  
COLBRAN RJ, 1988, J BIOL CHEM, V263, P18145
[5]   REGULATION OF INTRASTERIC INHIBITION OF THE MULTIFUNCTIONAL CALCIUM CALMODULIN-DEPENDENT PROTEIN-KINASE [J].
CRUZALEGUI, FH ;
KAPILOFF, MS ;
MORFIN, JP ;
KEMP, BE ;
ROSENFELD, MG ;
MEANS, AR .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (24) :12127-12131
[6]   CALCIUM AND CALMODULIN ACTIVATION OF MUSCLE PHOSPHORYLASE-KINASE - EFFECT OF TRYPTIC PROTEOLYSIS [J].
DEPAOLIROACH, AA ;
GIBBS, JB ;
ROACH, PJ .
FEBS LETTERS, 1979, 105 (02) :321-324
[7]  
GLOTZER M, 1991, NATURE, V349, P132, DOI 10.1038/349132a0
[8]   SOURCES OF CALCIUM IN EGG ACTIVATION - A REVIEW AND HYPOTHESIS [J].
JAFFE, LF .
DEVELOPMENTAL BIOLOGY, 1983, 99 (02) :265-276
[9]  
LABBE JC, 1991, METHOD ENZYMOL, V200, P291
[10]   DEGRADATION OF THE PROTOONCOGENE PRODUCT P39MOS IS NOT NECESSARY FOR CYCLIN PROTEOLYSIS AND EXIT FROM MEIOTIC METAPHASE - REQUIREMENT FOR A CA2+ CALMODULIN DEPENDENT EVENT [J].
LORCA, T ;
GALAS, S ;
FESQUET, D ;
DEVAULT, A ;
CAVADORE, JC ;
DOREE, M .
EMBO JOURNAL, 1991, 10 (08) :2087-2093