FUS3 ENCODES A CDC2+/CDC28-RELATED KINASE REQUIRED FOR THE TRANSITION FROM MITOSIS INTO CONJUGATION

被引：388

作者：

ELION, EA ^{[1
]}

GRISAFI, PL ^{[1
]}

FINK, GR ^{[1
]}

机构：

[1] MIT,DEPT BIOL,CAMBRIDGE,MA 02142

来源：

CELL | 1990年 / 60卷 / 04期

关键词：

D O I：

10.1016/0092-8674(90)90668-5

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

FUS3 is required for both the arrest of cells in G1 and mating. Upon exposure to mating pheromone, fus3-1 and fus3-2 mutants fail to arrest in G1 and continue to divide while undergoing the transcription induction and morphological changes typical of mating cells. The G1 arrest defect of these fus3 mutants is suppressed by a daf1/whi1 null mutation (also called cln3, a putative cyclin). FUS3 has a positive role in conjugation, because overexpression of FUS3 increases the pheromone sensitivity of wild-type cells, while the absence of FUS3 causes sterility. The suppression of a gpa1 null (Gα subunit) by a fus3 null also suggests FUS3 is in the signal transduction pathway. The predicted FUS3 protein is 35% identical to the cdc2+/CDC28 kinases and 52% identical to the KSS1 predicted kinase. © 1990.

引用

页码：649 / 664

页数：16

共 83 条

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