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ScoC介导枯草芽孢杆菌中孢子形成的分解代谢物阻遏。

ScoC mediates catabolite repression of sporulation in Bacillus subtilis.

作者信息

Shafikhani Sasha H, Núñez Esperanza, Leighton Terrance

机构信息

Department of Molecular and Cellular Biology, Division of Biochemistry and Molecular Biology, University of California, Berkeley, California 94720, USA.

出版信息

Curr Microbiol. 2003 Oct;47(4):327-36. doi: 10.1007/s00284-002-4013-1.

DOI:10.1007/s00284-002-4013-1
PMID:14629015
Abstract

Sporulation in Bacillus subtilis can be triggered by carbon catabolite limitation. Conversely, carbon source excess can repress the production of extracellular enzymes, motility, and sporulation. Recent studies have implicated a pH-sensing mechanism, involving AbrB, the TCA cycle, Spo0K, and sigmaH in controlling the catabolite repression of sporulation gene expression. In an accompanying paper, we demonstrate that the AbrB-dependent pH-sensing mechanism may not be the only means by which carbon catabolites affect sporulation. In the studies reported here, we have examined the molecular basis underlying the catabolite repression phenotype of mutations in the hpr (scoC), rpoD (crsA47), and spo0A (rvtA11) loci. Loss of function mutations in hpr (scoC) restored sporulation gene expression and sporulation in the presence of excess catabolite(s), suggesting that Hpr (ScoC) has a pivotal role in mediating catabolite repression. Moreover, hpr gene expression increased substantially in the presence of excess catabolite(s), further supporting the involvement of Hpr (ScoC) in the carbon catabolite response system. We suggest that alterations in the phosphorelay response to catabolites may be one mechanism by which catabolite-resistant mutants such as crsA and rvtA are able to sporulate in the presence of excess glucose.

摘要

枯草芽孢杆菌中的孢子形成可由碳分解代谢物限制触发。相反,碳源过量会抑制细胞外酶的产生、运动性和孢子形成。最近的研究表明,一种pH感应机制,涉及AbrB、三羧酸循环、Spo0K和sigmaH,在控制孢子形成基因表达的分解代谢物阻遏中起作用。在一篇配套论文中,我们证明依赖AbrB的pH感应机制可能不是碳分解代谢物影响孢子形成的唯一方式。在此报道的研究中,我们研究了hpr(scoC)、rpoD(crsA47)和spo0A(rvtA11)基因座突变的分解代谢物阻遏表型背后的分子基础。hpr(scoC)功能丧失突变在存在过量分解代谢物的情况下恢复了孢子形成基因表达和孢子形成,这表明Hpr(ScoC)在介导分解代谢物阻遏中起关键作用。此外,在存在过量分解代谢物的情况下,hpr基因表达大幅增加,进一步支持Hpr(ScoC)参与碳分解代谢物反应系统。我们认为,对分解代谢物的磷酸化传递反应的改变可能是诸如crsA和rvtA等抗分解代谢物突变体能够在过量葡萄糖存在下形成孢子的一种机制。

相似文献

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ScoC mediates catabolite repression of sporulation in Bacillus subtilis.ScoC介导枯草芽孢杆菌中孢子形成的分解代谢物阻遏。
Curr Microbiol. 2003 Oct;47(4):327-36. doi: 10.1007/s00284-002-4013-1.
2
Catabolite-induced repression of sporulation in Bacillus subtilis.枯草芽孢杆菌中分解代谢物诱导的芽孢形成抑制作用。
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Proc Natl Acad Sci U S A. 1985 Dec;82(23):8124-8. doi: 10.1073/pnas.82.23.8124.
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Developmental gene expression in Bacillus subtilis crsA47 mutants reveals glucose-activated control of the gene for the minor sigma factor sigma(H).枯草芽孢杆菌crsA47突变体中的发育基因表达揭示了葡萄糖对次要σ因子σ(H)基因的激活控制。
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Genetic mapping of rpoD implicates the major sigma factor of Bacillus subtilis RNA polymerase in sporulation initiation.rpoD的遗传图谱表明枯草芽孢杆菌RNA聚合酶的主要σ因子参与芽孢形成起始过程。
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Suppression of defective-sporulation phenotypes by mutations in transcription factor genes of Bacillus subtilis.枯草芽孢杆菌转录因子基因突变对缺陷芽孢形成表型的抑制作用
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