Overexpression of the cytoplasmic retention signal region of cyclin B2, but not of cyclin B1, inhibits bipolar spindle formation in Xenopus oocytes
Overexpression of the cytoplasmic retention signal region of cyclin B2, but not of cyclin B1, inhibits bipolar spindle formation in Xenopus oocytes
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细胞周期蛋白 B2 的细胞质保留信号区域的过表达(而非细胞周期蛋白 B1 的细胞质保留信号区域)抑制非洲爪蟾卵母细胞中双极纺锤体的形成
DOI:
10.1111/j.1768-322x.1998.tb01060.x
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发表时间:
1998
影响因子:
2.7
通讯作者:
N. Sagata
中科院分区:
文献类型:
--
作者:
Satoshi Yoshitome;N. Furuno;N. Sagata
Cyclin B, a regulatory subunit of maturation/M‐phase promoting factor (MPF), has several subtypes in many vertebrate species. However, it is not known whether the different B‐type cyclins have any different functions in vertebrate cells, although their subcellular localizations seem to differ largely from each other. To examine the roles of two major B‐type cyclins, B1 and B2, in spindle formation in M phase, we overexpressed their N‐termini in Xenopus oocytes; the N‐termini of cyclins B1 and B2 contained a cytoplasmic retention signal (CRS), and hence their overexpressions were expected to competitively inhibit the subcellular localizations of the endogenous cyclins B1 and B2, respectively. Upon entry into meiosis I, oocytes overexpressing the cyclin B1 N‐terminus formed an apparently normal bipolar spindle, but those oocytes overexpressing the cyclin B1 N‐terminus formed a monopolar (or monoastral) spindle. This defect in bipolar spindle formation was observed only when the cyclin B2 N‐terminus contained its own CRS sequence, and was able to be rescued by overexpression of full‐length cyclin B2. These results suggest, for the first time, that the correct subcellular localization of cyclin B2, but not of cyclin B1, is essential for (the initiation of) bipolar spindle formation in Xenopus oocytes.
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影响因子:
7.5
作者:
AULT, JG;RIEDER, CL
通讯作者:
RIEDER, CL
DOI:
10.1073/pnas.85.9.3009
发表时间:
1988-05-01
影响因子:
11.1
作者:
LOHKA, MJ;HAYES, MK;MALLER, JL
通讯作者:
MALLER, JL
影响因子:
56.9
作者:
HARTWELL, LH;WEINERT, TA
通讯作者:
WEINERT, TA
影响因子:
11.4
作者:
PINES, J;HUNTER, T
通讯作者:
HUNTER, T