大肠杆菌SOS反应后呼吸的恢复需要RecA介导的2-酮-4-羟基戊二酸醛缩酶的诱导。
Recovery of respiration following the SOS response of Escherichia coli requires RecA-mediated induction of 2-keto-4-hydroxyglutarate aldolase.
作者信息
Cayrol C, Petit C, Raynaud B, Capdevielle J, Guillemot J C, Defais M
机构信息
Laboratoire de Pharmacologie et Toxicologie Fondamentales du Centre National de la Recherche Scientifique, Toulouse, France.
出版信息
Proc Natl Acad Sci U S A. 1995 Dec 5;92(25):11806-9. doi: 10.1073/pnas.92.25.11806.
Abstract
Agents that damage DNA in Escherichia coli or interfere with its replication induce DNA repair and mutagenesis via the SOS response. This well-known activity is regulated by the RecA protein and the LexA repressor. Following repair or bypass of the DNA lesion, the cell returns to its resting state by a largely unknown process. We found that 2-keto-4-hydroxyglutarate aldolase (4-hydroxy-2-oxoglutarate aldolase; EC 4.1.3.16) is necessary for the recovery of respiration and that it is regulated by the SOS response. This protein was induced by DNA-damaging agents. Induction required RecA activation. When the LexA regulon was repressed, activation of RecA was not sufficient for induction, indicating the requirement for an additional protein under LexA control. Finally, a mutant in the corresponding hga gene was UV sensitive. 2-Keto-4-hydroxyglutarate aldolase also plays a role in respiratory metabolic pathways, which suggests a mechanism for respiration resumption during the termination of the SOS response.
摘要
在大肠杆菌中破坏DNA或干扰其复制的因子会通过SOS应答诱导DNA修复和诱变。这种广为人知的活性受RecA蛋白和LexA阻遏物调控。在DNA损伤修复或绕过之后，细胞通过一个很大程度上未知的过程恢复到静息状态。我们发现2-酮-4-羟基戊二酸醛缩酶（4-羟基-2-氧代戊二酸醛缩酶；EC 4.1.3.16）对于呼吸恢复是必需的，并且它受SOS应答调控。这种蛋白质由DNA损伤剂诱导产生。诱导需要RecA激活。当LexA调控子被阻遏时，RecA的激活不足以诱导，这表明需要LexA控制下的另一种蛋白质。最后，相应hga基因的一个突变体对紫外线敏感。2-酮-4-羟基戊二酸醛缩酶在呼吸代谢途径中也起作用，这提示了SOS应答终止期间呼吸恢复的一种机制。
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