IDENTIFICATION OF A GENETIC-LOCUS REQUIRED FOR BIOSYNTHESIS OF THE LIPOPEPTIDE ANTIBIOTIC SURFACTIN IN BACILLUS-SUBTILIS
IDENTIFICATION OF A GENETIC-LOCUS REQUIRED FOR BIOSYNTHESIS OF THE LIPOPEPTIDE ANTIBIOTIC SURFACTIN IN BACILLUS-SUBTILIS
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DOI：
10.1128/jb.170.12.5662-5668.1988
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发表时间：
1988-12-01
影响因子：
3.2
通讯作者：
ZUBER, P
中科院分区：
文献类型：
--
作者：
NAKANO, MM;MARAHIEL, MA;ZUBER, P
表面活性素是由枯草芽孢杆菌ATCC 21332的细胞产生的脂肽抗生素。通过从ATCC 21332转化至JH 642（标准B的衍生物），将负责表面活性素产生（sfp）的遗传位点转移。subtilis 168.为了在分子水平上研究sfp基因座，分离出了在表面活性素产生（srf）中被阻断的Tn 917插入突变体。发现srf：：Tn 917突变与sfp密切相关，并且通过PBS 1噬菌体转导将这两个位点定位到aro 1和mtlB之间的染色体区域。这些研究表明，JH 642，一种不是表面活性素生产者的菌株（基因型sfp 0），含有至少一些编码表面活性素生产的基因。srf基因的表达在sfp和sfp 0细胞中通过测定β-半乳糖苷酶活性由与srf：：Tn 917插入融合的无启动子lacZ基因编码。在两种菌株的细胞中，srf-定向的β-当细胞进入生长曲线的稳定期时，半乳糖苷酶活性升高，但sfp细胞的活性高于sfp 0细胞。srf-lacZ表达部分受损的突变spo 0A。在sfp 0细胞中，这种对sp 0A基因产物的依赖可以完全被abrB抑制突变绕过。在sfp细胞中，abrB突变不能恢复spo 0A突变所赋予的缺陷。这些数据表明，sfp基因座，这是负责表面活性素的生产，改变转录调控的srf在JH 642细胞。
Surfactin is a lipopeptide antibiotic produced by the cells of Bacillus subtilis ATCC 21332. A genetic locus responsible for surfactin production (sfp) was transferred by transformation from ATCC 21332 to JH642, a derivative of the standard B. subtilis 168. To study the sfp locus at the molecular level, a Tn917 insertion mutant that was blocked in surfactin production (srf) was isolated. The srf::Tn917 mutation was found to be closely linked to sfp, and both loci mapped by PBS1 phage transduction to the chromosomal region between aro1 and mtlB. These studies suggest that JH642, a strain which is not a producer of surfactin (genotypically sfp0), contains at least some of the genes encoding surfactin production. Expression of the srf gene(s) was examined in both sfp and sfp0 cells by assaying .beta.-galactosidase activity encoded by a promoterless lacZ gene that was fused to the srf::Tn917 insertion. In cells of both strains, srf-directed .beta.-galactosidase activity increased when cells entered the stationary phase of the growth curve, but the activity in sfp cells was higher than that in sfp0 cells. srf-lacZ expression was partially impaired by a mutation in spo0A. In sfp0 cells, this dependence on the sp0A gene product could be entirely bypassed by an abrB suppressor mutation. In the sfp cells, the abrB mutation could not restore the defect conferred by the spo0A mutation. These data suggest that the sfp locus, which is responsible for surfactin production, alters the transcriptional regulation of srf in JH642 cells.