FUS3 ENCODES A CDC2+/CDC28-RELATED KINASE REQUIRED FOR THE TRANSITION FROM MITOSIS INTO CONJUGATION
FUS3 ENCODES A CDC2+/CDC28-RELATED KINASE REQUIRED FOR THE TRANSITION FROM MITOSIS INTO CONJUGATION
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DOI：
10.1016/0092-8674(90)90668-5
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发表时间：
1990-02-23
期刊：
影响因子：
64.5
通讯作者：
FINK, GR
中科院分区：
文献类型：
--
作者：
ELION, EA;GRISAFI, PL;FINK, GR
FUS 3是细胞在G1期和交配期停滞所必需的。当暴露于交配信息素时，fus 3 -1和fus 3 -2突变体不能在G1期停止，并继续分裂，同时经历交配细胞典型的转录诱导和形态变化。这些fus 3突变体的G1期阻滞缺陷被daf 1/whi 1无效突变（也称为cln 3，一种假定的细胞周期蛋白）抑制。FUS 3在接合中具有积极作用，因为FUS 3的过表达增加了野生型细胞的信息素敏感性，而FUS 3的缺失导致不育。fus 3 null对gpa 1 null（Ga亚基）的抑制也表明FUS 3在信号转导途径中。预测的FUS 3蛋白与cdc 2 + CDC 28激酶35%相同，与KSS 1预测的激酶52%相同。
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 (Ga 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.