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起始蛋白中的单个氨基酸改变导致了质粒R6K拷贝数突变体的DNA过量产生表型。

A single amino acid alteration in the initiation protein is responsible for the DNA overproduction phenotype of copy number mutants of plasmid R6K.

作者信息

Inuzuka M, Wada Y

出版信息

EMBO J. 1985 Sep;4(9):2301-7. doi: 10.1002/j.1460-2075.1985.tb03930.x.

Abstract

A novel type of high copy-number (cop) mutants of a mini-R6K plasmid were isolated. The mutations were mapped in the pir gene which encodes the pi initiation protein for plasmid R6K DNA replication. They resulted in an alteration by substitution of a single amino acid: threonine to isoleucine at the 108th position for the cop41, and proline to serine at the 113th position for the cop50, of the 305 amino acid pi protein. The cop41 mutation in the pi protein was found to be trans-dominant over the wild-type allele in the copy control of plasmid R6K. Moreover, it was shown that the altered pi protein was not overproduced in maxicells carrying this mutant plasmid and had a higher affinity to the repeated sequence which is present in the pir promoter region. Most likely the mutated pi protein also interacts more efficiently with the same repeated sequences, a target of pi, in the replication origin region and increases the frequency of the initiation event per cell division.

摘要

分离出了一种新型的微小R6K质粒高拷贝数(cop)突变体。这些突变定位在pir基因中,该基因编码质粒R6K DNA复制的π起始蛋白。它们导致了单个氨基酸的替换改变:cop41在305个氨基酸的π蛋白的第108位由苏氨酸替换为异亮氨酸,cop50在第113位由脯氨酸替换为丝氨酸。发现π蛋白中的cop41突变在质粒R6K的拷贝控制中对野生型等位基因具有反式显性。此外,研究表明,携带这种突变体质粒的大细胞中,改变后的π蛋白并未过量产生,并且对pir启动子区域中存在的重复序列具有更高的亲和力。最有可能的是,突变的π蛋白在复制起始区域也能更有效地与作为π靶点的相同重复序列相互作用,并增加每个细胞分裂起始事件的频率。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d64/554501/92ebf39a78c9/emboj00274-0152-a.jpg

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