Parma D H, Snyder M, Sobolevski S, Nawroz M, Brody E, Gold L
Department of Molecular, Cellular, and Development Biology, University of Colorado, Boulder 80309-0347.
Genes Dev. 1992 Mar;6(3):497-510. doi: 10.1101/gad.6.3.497.
The rexA and rexB genes of bacteriophage lambda encode a two-component system that aborts lytic growth of bacterial viruses. Rex exclusion is characterized by termination of macromolecular synthesis, loss of active transport, the hydrolysis of ATP, and cell death. By analogy to colicins E1 and K, these results can be explained by depolarization of the cytoplasmic membrane. We have fractionated cells to determine the intracellular location of the RexB protein and made RexB-alkaline phosphatase fusions to analyze its membrane topology. The RexB protein appears to be a polytopic transmembrane protein. We suggest that RexB proteins form ion channels that, in response to lytic growth of bacteriophages, depolarize the cytoplasmic membrane. The Rex system requires a mechanism to prevent lambda itself from being excluded during lytic growth. We have determined that overexpression of RexB in lambda lysogens prevents the exclusion of both T4 rII mutants and lambda ren mutants. We suspect that overexpression of RexB is the basis for preventing self-exclusion following the induction of a lambda lysogen and that RexB overexpression is accomplished through transcriptional regulation.
噬菌体λ的rexA和rexB基因编码一种双组分系统,该系统可阻止细菌病毒的裂解生长。Rex排除的特征是大分子合成终止、主动运输丧失、ATP水解以及细胞死亡。与大肠杆菌素E1和K类似,这些结果可以通过细胞质膜的去极化来解释。我们对细胞进行了分级分离,以确定RexB蛋白在细胞内的位置,并构建了RexB-碱性磷酸酶融合蛋白来分析其膜拓扑结构。RexB蛋白似乎是一种多跨膜蛋白。我们认为,RexB蛋白形成离子通道,响应噬菌体的裂解生长,使细胞质膜去极化。Rex系统需要一种机制来防止λ自身在裂解生长过程中被排除。我们已经确定,在λ溶原菌中过表达RexB可防止T4 rII突变体和λ ren突变体被排除。我们怀疑,RexB的过表达是防止λ溶原菌诱导后自我排除的基础,并且RexB的过表达是通过转录调控实现的。