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一个导致酵母异-2-细胞色素c过量产生的广泛缺失。

An extensive deletion causing overproduction of yeast iso-2-cytochrome c.

作者信息

McKnight G L, Cardillo T S, Sherman F

出版信息

Cell. 1981 Aug;25(2):409-19. doi: 10.1016/0092-8674(81)90059-3.

Abstract

CYC7-H3 is a cis-dominant regulatory mutation that causes a 20-fold overproduction of yeast iso-2-cytochrome c. The CYC7-H3 mutation is an approximately 5 kb deletion with one breakpoint located in the 5' noncoding region of the CYC7 gene, approximately 200 base from the ATG initiation codon. The deletion apparently fuses a new regulatory region to the structural portion of the CYC7 locus. The CYC7-H3 deletion encompasses the RAD23 locus, which controls UV sensitivity and the ANP1 locus, which controls osmotic sensitivity. The gene cluster CYC7-RAD23-ANP1 displays striking similarity to the gene cluster CYC1-OSM1-RAD7, which controls, respectively, iso-1-cytochrome c, osmotic sensitivity and UV sensitivity. We suggest that these gene clusters are related by an ancient transpositional event.

摘要

CYC7-H3是一种顺式显性调控突变,它导致酵母同工酶2-细胞色素c过量产生20倍。CYC7-H3突变是一个约5 kb的缺失,一个断点位于CYC7基因的5'非编码区,距ATG起始密码子约200个碱基。该缺失显然将一个新的调控区域与CYC7基因座的结构部分融合。CYC7-H3缺失包含控制紫外线敏感性的RAD23基因座和控制渗透敏感性的ANP1基因座。基因簇CYC7-RAD23-ANP1与分别控制同工酶1-细胞色素c、渗透敏感性和紫外线敏感性的基因簇CYC1-OSM1-RAD7有显著相似性。我们认为这些基因簇通过一个古老的转座事件相关联。

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