Elion E A, Grisafi P L, Fink G R
Whitehead Institute for Biomedical Research, Nine Cambridge Center, Massachusetts 02142.
Cell. 1990 Feb 23;60(4):649-64. doi: 10.1016/0092-8674(90)90668-5.
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 (G alpha 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.
FUS3对于细胞在G1期的停滞和交配都是必需的。暴露于交配信息素时,fus3-1和fus3-2突变体无法在G1期停滞,而是在经历交配细胞典型的转录诱导和形态变化时继续分裂。这些fus3突变体的G1期停滞缺陷被daf1/whi1缺失突变(也称为cln3,一种假定的细胞周期蛋白)所抑制。FUS3在接合过程中起积极作用,因为FUS3的过表达增加了野生型细胞对信息素的敏感性,而FUS3的缺失则导致不育。fus3缺失对gpa1缺失(Gα亚基)的抑制也表明FUS3处于信号转导途径中。预测的FUS3蛋白与cdc2+/CDC28激酶有35%的同一性,与预测的KSS1激酶有52%的同一性。