de Boer P A, Crossley R E, Rothfield L I
Department of Microbiology, University of Connecticut Health Center, Farmington 06032.
J Bacteriol. 1988 May;170(5):2106-12. doi: 10.1128/jb.170.5.2106-2112.1988.
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.
大肠杆菌小细胞位点（minB）的突变会导致分裂隔膜定位异常。在本文中，我们报告了minB位点的分离与表征。用含有转座子插入的克隆minB序列取代染色体上的minB⁺等位基因会导致小细胞表型，这表明维持正常分裂模式需要minB⁺功能。矛盾的是，该位点的过表达也会导致小细胞表型。该位点编码几种肽，其表达受转座子突变的协同影响，这些突变也会消除minB⁺功能。minB肽的一个子集足以防止minB1突变体中形成小细胞，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是一个复杂的位点，其表达必须维持在一定范围内，以维持分裂隔膜定位的正常模式。
