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首页> 外文期刊>The Journal of biological chemistry >AccR Is a Master Regulator Involved in Carbon Catabolite Repression of the Anaerobic Catabolism of Aromatic Compounds in Azoarcus sp. CIB
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AccR Is a Master Regulator Involved in Carbon Catabolite Repression of the Anaerobic Catabolism of Aromatic Compounds in Azoarcus sp. CIB

机译:ACCR是一种涉及碳分解代谢物抑制Azoarcus SP中芳香族化合物的碳脱代粘合剂的碳分解代谢物抑制。上限

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摘要

Here we characterized the first known transcriptional regulator that accounts for carbon catabolite repression (CCR) control of the anaerobic catabolism of aromatic compounds in bacteria. The AccR response regulator of Azoarcus sp. CIB controls succinate-responsive CCR of the central pathways for the anaerobic catabolism of aromatics by this strain. Phosphorylation of AccR to AccR-P triggers a monomer-to-dimer transition as well as the ability to bind to the target promoter and causes repression both in vivo and in vitro. Substitution of the Asp60 phosphorylation target residue of the N-terminal receiver motif of AccR to a phosphomimic Glu residue generates a constitutively active derivative that behaves as a superrepressor of the target genes. AccR-P binds in vitro to a conserved inverted repeat (ATGCA-N6-TGCAT) present at two different locations within the PN promoter of the bzd genes for anaerobic benzoate degradation. Because the DNA binding-proficient C-terminal domain of AccR is monomeric, we propose an activation mechanism in which phosphorylation of Asp60 of AccR alleviates interdomain repression mediated by the N-terminal domain. The presence of AccR-like proteins encoded in the genomes of other β-proteobacteria of the Azoarcus/Thauera group further suggests that AccR constitutes a master regulator that controls anaerobic CCR in these bacteria.
机译:在这里,我们的特征是第一已知的转录调节剂,其占碳分解代谢抑制(CCR)对细菌芳族化合物厌氧分解代谢的控制。 Azoarcus SP的ACCR反应调节器。 CIB通过这种菌株控制芳族毒性芳族分解代谢的中央途径的琥珀酸响应性CCR。 ACCR至ACCR-P的磷酸化触发单体至二聚体的转变以及结合目标启动子的能力,并在体内和体外引起抑制。 ASP60磷酸化靶残留物的ASP60磷酸化靶残留物的ACCR到硫酸硫钙残基产生组成型活性衍生物,其表现为靶基因的超级压缩机。 ACCR-P在体外与存在于BZD基因的PN启动子的两个不同位置的保守的倒置重复(ATGCA-N6-TGCAT)结合,用于厌氧苯甲酸苯甲酸盐降解。因为ACCR的DNA结合型C-末端结构域是单体,所以我们提出了一种活化机制,其中ACCR ASP60的磷酸化可缓解由N-末端结构域介导的阶段抑制。编码在氮杂神经组织/ Thauera组的其他β-植物组的基因组中的ACCR样蛋白的存在进一步表明Accr构成了在这些细菌中控制厌氧CCR的母扰剂。

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