Identification of Novel Mutations in ACT1 and SLA2 That Suppress the Actin-Cable-Overproducing Phenotype Caused by Overexpression of a Dominant Active Form of Bni1p in Saccharomyces cerevisiae
Identification of Novel Mutations in ACT1 and SLA2 That Suppress the Actin-Cable-Overproducing Phenotype Caused by Overexpression of a Dominant Active Form of Bni1p in Saccharomyces cerevisiae
复制标题
鉴定 ACT1 和 SLA2 中的新突变，这些突变抑制由酿酒酵母中 Bni1p 的显性活性形式过度表达引起的肌动蛋白索过量产生表型
作者：
Shiro Yoshiuchi;Takaharu G. Yamamoto;H. Sakane;J. Kadota;Junko Mochida;M. Asaka;Kazuma Tanaka
一个Bni 1 p成核肌动蛋白组装肌动蛋白电缆，指导极性运输的分泌囊泡在芽殖酵母。我们鉴定了抑制由截短的Bni 1 p（BNI 1 ΔN）过表达引起的致死性和过度肌动蛋白电缆形成的突变。两个隐性突变，act 1 -301的肌动蛋白基因和sla 2 -82的基因参与皮层肌动蛋白补丁组装，被确定。sla 2 -82的分离是出乎意料的，因为内吞作用的内化步骤需要皮层肌动蛋白片。act 1 -301和sla 2 -82都表现出与bni 1 Δ的合成生长缺陷。act 1 -301导致E117 K取代，与profilin（PFY 1）和BUD 6中的突变发生遗传相互作用，表明Act 1 - 301 p在formin介导的聚合中不完全起作用。SLA 2 -82还与参与肌动蛋白缆组装的基因发生遗传相互作用。然而，一些实验表明，sla 2 -82的作用是由肌动蛋白单体的消耗引起的，因为bni 1 Δ sla 2 -82突变体的温度敏感性生长表型被ACT 1表达的增加所抑制。BNI 1 ΔN表型抑制子的分离可能为鉴定肌动蛋白氨基酸残基提供一个有用的系统，这些氨基酸残基对福尔马林介导的肌动蛋白聚合和影响肌动蛋白单体可用性的突变很重要。
A formin Bni1p nucleates actin to assemble actin cables, which guide the polarized transport of secretory vesicles in budding yeast. We identified mutations that suppressed both the lethality and the excessive actin cable formation caused by overexpression of a truncated Bni1p (BNI1ΔN). Two recessive mutations, act1-301 in the actin gene and sla2-82 in a gene involved in cortical actin patch assembly, were identified. The isolation of sla2-82 was unexpected, because cortical actin patches are required for the internalization step of endocytosis. Both act1-301 and sla2-82 exhibited synthetic growth defects with bni1Δ. act1-301, which resulted in an E117K substitution, interacted genetically with mutations in profilin (PFY1) and BUD6, suggesting that Act1-301p was not fully functional in formin-mediated polymerization. sla2-82 also interacted genetically with genes involved in actin cable assembly. Some experiments, however, suggested that the effects of sla2-82 were caused by depletion of actin monomers, because the temperature-sensitive growth phenotype of the bni1Δ sla2-82 mutant was suppressed by increased expression of ACT1. The isolation of suppressors of the BNI1ΔN phenotype may provide a useful system for identification of actin amino-acid residues that are important for formin-mediated actin polymerization and mutations that affect the availability of actin monomers.
登录
查看更多内容
影响因子：
2.7
作者：
R. Elble
通讯作者：
R. Elble
Sla2p 通过冗余定位信号与酵母皮质肌动蛋白细胞骨架相关。
影响因子：
3.3
作者：
Yang,S;Cope,MJ;Drubin,DG
通讯作者：
Drubin,DG
交配酵母中肌动蛋白斑块的生命周期。
影响因子：
4
作者：
Smith,MG;Swamy,SR;Pon,LA
通讯作者：
Pon,LA
酿酒酵母 MRT4、GRC5、SLA2 和 THS1 基因中的温度敏感突变会导致 mRNA 周转缺陷。
影响因子：
3.3
作者：
Zuk,D;Belk,JP;Jacobson,A
通讯作者：
Jacobson,A
影响因子：
7.8
作者：
Pruyne, DW;Schott, DH;Bretscher, A
通讯作者：
Bretscher, A