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在黄色粘球菌发育过程中对信号缺陷的抑制。

Suppression of a signaling defect during Myxococcus xanthus development.

作者信息

Lee K, Shimkets L J

机构信息

Department of Microbiology, University of Georgia, Athens 30602, USA.

出版信息

J Bacteriol. 1996 Feb;178(4):977-84. doi: 10.1128/jb.178.4.977-984.1996.

Abstract

The csgA gene encodes an extracellular protein that is essential for cell-cell communication (C-signaling) during fruiting body development of Myxococcus xanthus. Two transposon insertions in the socABC operon, soc-560 and socC559, restore development to csgA null mutants. Mixing soc-560 csgA cells or socC559 csgA cells with csgA cells at a ratio of 1:1 stimulated the development of csgA cells, suggesting that soc mutations allow cells to produce the C-signal or a similar molecule via a csgA-independent mechanism. The socABC operon contains the following three genes: socA, a member of the short-chain alcohol dehydrogenase gene family; socB, a gene encoding a putative membrane anchoring protein; and socC, a negative autoregulator of socABC operon expression. Both suppressor mutations inactivate socC, leading to a 30- to 100-fold increase in socA transcription; socA expression in suppressor strains is at least 100-fold higher than csgA expression during all stages of development. The amino acid sequence of SocA has 28% identity and 51% similarity with that of CsgA. We suggest that CsgA suppression is due to overproduction of SocA, which can substitute for CsgA. These results raise the possibility that a cell surface dehydrogenase plays a role in C-signaling.

摘要

csgA基因编码一种细胞外蛋白,该蛋白在黄色黏球菌子实体发育过程中的细胞间通讯(C信号传导)中至关重要。socABC操纵子中的两个转座子插入突变体soc-560和socC559,可恢复csgA基因敲除突变体的发育。将soc-560 csgA细胞或socC559 csgA细胞与csgA细胞以1:1的比例混合,可刺激csgA细胞的发育,这表明soc突变使细胞能够通过一种不依赖csgA的机制产生C信号或类似分子。socABC操纵子包含以下三个基因:socA,短链醇脱氢酶基因家族的成员;socB,一个编码假定膜锚定蛋白的基因;以及socC,socABC操纵子表达的负自调控因子。这两个抑制突变均使socC失活,导致socA转录增加30至100倍;在发育的所有阶段,抑制菌株中socA的表达比csgA的表达至少高100倍。SocA的氨基酸序列与CsgA的氨基酸序列有28%的同一性和51%的相似性。我们认为CsgA的抑制是由于SocA的过量产生,它可以替代CsgA。这些结果增加了细胞表面脱氢酶在C信号传导中起作用的可能性。

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