ISOLATION AND PROPERTIES OF MINB, A COMPLEX GENETIC-LOCUS INVOLVED IN CORRECT PLACEMENT OF THE DIVISION SITE IN ESCHERICHIA-COLI
ISOLATION AND PROPERTIES OF MINB, A COMPLEX GENETIC-LOCUS INVOLVED IN CORRECT PLACEMENT OF THE DIVISION SITE IN ESCHERICHIA-COLI
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DOI：
10.1128/jb.170.5.2106-2112.1988
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发表时间：
1988-05-01
影响因子：
3.2
通讯作者：
ROTHFIELD, LI
中科院分区：
文献类型：
--
作者：
DEBOER, PAJ;CROSSLEY, RE;ROTHFIELD, LI
大肠杆菌小细胞基因座 (minB) 的突变导致分裂隔膜的异常位置。在本文中，我们报告了 minB 基因座的分离和表征。用含有转座子插入的克隆 minB 序列替换染色体 minB+ 等位基因，产生了小细胞表型，表明需要 minB+ 功能来维持正常的分裂模式。矛盾的是，该位点的过度表达也导致了小细胞表型。该基因座编码几种肽，其表达受到转座子突变的协同影响，这些突变也消除了 minB+ 功能。 minB 肽的一个子集足以防止 minB1 突变体中小细胞的形成，或在野生型菌株中过量产生时诱导小细胞形成，这表明这些肽参与了分裂位点定位的正常过程。结果表明，minB 是一个复杂的基因座，其表达必须维持在一定限度内，以维持分裂隔膜定位的正常模式。
Mutation of Escherichia coli minicell locus (minB) results in aberrant placement of the division septum. In this paper we report the isolation and characterization of the minB locus. Replacement of the chromosomal minB+ allele by cloned minB sequences containing transposon insertions resulted in the minicell phenotype, indicating that minB+ function is required to maintain the normal division pattern. Paradoxically, overexpression of the locus also resulted in the minicell phenotype. The locus codes for several peptides whose expression is coordinately affected by transposon mutations that also eliminate minB+ function. A subset of the minB peptides is sufficient to prevent minicell formation in minB1 mutants or to induce minicell formation when overproduced in wild-type strains, implicating these peptides in the normal process of localization of the division site. The results indicate that minB is a complex locus whose expression must be maintained within certain limits to maintain the normal pattern of localization of the division septum.