THE CHL1(CTF1) GENE-PRODUCT OF SACCHAROMYCES-CEREVISIAE IS IMPORTANT FOR CHROMOSOME TRANSMISSION AND NORMAL-CELL CYCLE PROGRESSION IN G2/M
THE CHL1(CTF1) GENE-PRODUCT OF SACCHAROMYCES-CEREVISIAE IS IMPORTANT FOR CHROMOSOME TRANSMISSION AND NORMAL-CELL CYCLE PROGRESSION IN G2/M
复制标题
DOI：
10.1002/j.1460-2075.1990.tb07884.x
复制
发表时间：
1990-12-01
期刊：
影响因子：
11.4
通讯作者：
HIETER, P
中科院分区：
文献类型：
--
作者：
GERRING, SL;SPENCER, F;HIETER, P
我们已经分析了CTF1基因，该基因在染色体传递保真度降低的突变体中被鉴定出来，并被证明与之前发现的CHL1突变相对应。CHL1缺失突变体的细胞分裂错配率增加了200倍，通过有丝分裂重组，染色体上标记纯合率接近野生型。对标记染色体的分离分析表明，姐妹染色单体丢失(1：0分离)和姐妹染色单体不分离(2：0分离)是造成染色体错误分离的主要原因。分离了CHL1的一个基因组克隆，并将其定位在第16号染色体上。核苷酸序列分析表明，CHL1有2.6kb的开放阅读框和99kd的预测蛋白序列，含有两个害虫序列，与核苷酸切除修复基因Rad3的编码区有23%的同源性。这两个预测的蛋白质序列之间的同源结构域包括一个螺旋-转角-螺旋基序和一个包含解旋酶Conenus的ATP结合位点。缺乏CHL1基因产物的突变体是活的，并表现出两种显著的、可能相互关联的表型：染色体极端不稳定和G2/M期细胞周期进程延迟。这种延迟与细胞周期检查点无关，而细胞周期检查点需要RAD9基因的功能。
We have analyzed the CTF1 gene, identified in a screen for mutants with decreased chromosome transmission fidelity and shown to correspond to the previously identified chl1 mutation. chl1 null mutants exhibited a 200-fold increase in the rate of chromosome III missegregation per cell division, and near wild-type rates of marker homozygosis on the chromosome by mitotic recombination. Analysis of the segregation of a marker chromosome indicated that sister chromatid loss (1:0 segregation) and sister chromatid non-disjunction (2:0 segregation) contributed equally to chromosome missegregation. A genomic clone of CHL1 was isolated and used to map its physical position on chromosome XVI. Nucleotide sequence analysis of CHL1 revealed a 2.6 kb open reading frame with a 99 kd predicted protein sequence that contained two PEST sequences and was 23% identical to the coding region of nucleotide excision repair gene, RAD3. Domains of homology between these two predicted protein sequences included a helix-turn-helix motif and an ATP binding site containing a helicase consenus. Mutants lacking the CHL1 gene product are viable and display two striking, and perhaps interrelated, phenotypes: extreme chromosome instability and a delay in cell cycle progression in G2/M. This delay is independent of the cell cycle checkpoint that requires the function of the RAD9 gene.