Zalieckas J M, Wray L V, Fisher S H
Department of Microbiology, Boston University School of Medicine, Boston, Massachusetts 02118, USA.
J Bacteriol. 1998 Dec;180(24):6649-54. doi: 10.1128/JB.180.24.6649-6654.1998.
In Bacillus subtilis, carbon catabolite repression (CCR) of many genes is mediated at cis-acting carbon repression elements (cre) by the catabolite repressor protein CcpA. Mutations in transcription-repair coupling factor (mfd) partially relieve CCR at cre sites located downstream of transcriptional start sites by abolishing the Mfd-mediated displacement of RNA polymerase stalled at cre sites which act as transcriptional roadblocks. Although the acsA cre is centered 44.5 bp downstream of the acsA transcriptional start site, CCR of acsA expression is not affected by an mfd mutation. When the acsA cre is centered 161.5 bp downstream of the transcriptional start site for the unregulated tms promoter, CCR is partially relieved by the mfd mutation. Since CCR mediated at an acsA cre centered 44.5 bp downstream of the tms start site is not affected by the mfd mutation, the inability of Mfd to modulate CCR of acsA expression most likely results from the location of the acsA cre. Higher levels of CCR were found to occur at cre sites flanked by A+T-rich sequences than at cre sites bordered by G and C nucleotides. This suggests that nucleotides adjacent to the proposed 14-bp cre consensus sequence participate in the formation of the CcpA catabolite repression complex at cre sites. Examination of CCR of acsA expression revealed that this regulation required the Crh and seryl-phosphorylated form of the HPr proteins but not glucose kinase.
在枯草芽孢杆菌中，许多基因的碳分解代谢物阻遏（CCR）由分解代谢物阻遏蛋白CcpA在顺式作用碳阻遏元件（cre）处介导。转录修复偶联因子（mfd）中的突变通过消除Mfd介导的在作为转录障碍的cre位点处停滞的RNA聚合酶的置换，部分缓解了转录起始位点下游cre位点处的CCR。尽管acsA cre位于acsA转录起始位点下游44.5 bp处的中心位置，但acsA表达的CCR不受mfd突变的影响。当acsA cre位于未调控的tms启动子转录起始位点下游161.5 bp处的中心位置时，CCR被mfd突变部分缓解。由于位于tms起始位点下游44.5 bp处中心位置的acsA cre介导的CCR不受mfd突变的影响，Mfd无法调节acsA表达的CCR很可能是由acsA cre的位置导致的。发现富含A+T序列侧翼的cre位点处的CCR水平高于由G和C核苷酸边界的cre位点处的CCR水平。这表明与提议的14 bp cre共有序列相邻的核苷酸参与了cre位点处CcpA分解代谢物阻遏复合物的形成。对acsA表达的CCR检查表明，这种调控需要Crh和丝氨酸磷酸化形式的HPr蛋白，但不需要葡萄糖激酶。
