Nickas M E, Yaffe M P
Department of Biology, University of California, San Diego, La Jolla 92093, USA.
Mol Cell Biol. 1996 Jun;16(6):2585-93. doi: 10.1128/MCB.16.6.2585.
Yeast cells with mutations in BRO1 display phenotypes similar to those caused by deletion of BCK1, a gene encoding a MEK kinase that functions in a mitogen-activated protein kinase pathway mediating maintenance of cell integrity. bro1 cells exhibit a temperature-sensitive growth defect that is suppressed by the addition of osmotic stabilizers or Ca2+ to the growth medium or by additional copies of the BCK1 gene. At permissive temperatures, bro1 mutants are sensitive to caffeine and respond abnormally to nutrient limitation. A null mutation in BRO1 is synthetically lethal with null mutations in BCK1, MPK1, which encodes a mitogen-activated protein kinase that functions downstream of Bck1p, or PKC1, a gene encoding a protein kinase C homolog that activates Bck1p. Analysis of the isolated BRO1 gene revealed that it encodes a novel, 97-kDa polypeptide which contains a putative SH3 domain-binding motif and is homologous to a protein of unknown function in Caenorhabditis elegans.
在BRO1中发生突变的酵母细胞表现出与BCK1缺失所导致的表型相似的表型,BCK1是一个编码MEK激酶的基因,该激酶在介导细胞完整性维持的丝裂原活化蛋白激酶途径中发挥作用。bro1细胞表现出温度敏感型生长缺陷,在生长培养基中添加渗透稳定剂或Ca2+,或通过额外拷贝的BCK1基因可抑制该缺陷。在允许温度下,bro1突变体对咖啡因敏感,并且对营养限制反应异常。BRO1的无效突变与BCK1、MPK1(编码在Bck1p下游发挥作用的丝裂原活化蛋白激酶)或PKC1(编码激活Bck1p的蛋白激酶C同源物的基因)的无效突变具有合成致死性。对分离出的BRO1基因的分析表明,它编码一种新的97 kDa多肽,该多肽包含一个假定的SH3结构域结合基序,并且与秀丽隐杆线虫中一个功能未知的蛋白质同源。