Sánchez Diego Germán, Primo Emiliano David, Damiani María Teresa, Lisa Angela Teresita
Laboratory of Phagocytosis and Intracellular Transport, School of Medicine, University of Cuyo, IHEM-CONICET, Mendoza 5500, Argentina.
Department of Molecular Biology, FCEFQN, National University of Río Cuarto, Route 36-Km 601, 5800, Argentina.
Microbiology (Reading). 2017 Sep;163(9):1343-1354. doi: 10.1099/mic.0.000502. Epub 2017 Aug 9.
Pseudomonasaeruginosa uses choline as a source of carbon and nitrogen, and also for the synthesis of glycine betaine, an osmoprotectant under stress conditions such as drought and salinity. The transcription factor GbdR is the specific regulator of choline metabolism and it belongs to the Arac/XylS family of transcriptional regulators. Despite the link between choline catabolism and bacterial pathogenicity, gbdR regulation has not been explored in detail. In the present work, we describe how gbdR transcription can be initiated from a σ54-dependent promoter. gbdR transcription can be activated by NtrC in the absence of a preferential nitrogen source, by CbrB in the absence of a preferential carbon source, and by the integration host factor favouring DNA bending. In addition, we found that BetI negatively regulates gbdR expression in the absence of choline. We identified two overlapping BetI binding sites in the gbdR promoter sequence, providing an additional example of σ54-promoter down-regulation. Based on our findings, we propose a model for gdbR regulation and its impact on choline metabolism.
铜绿假单胞菌利用胆碱作为碳源和氮源，还用于合成甘氨酸甜菜碱，后者是干旱和盐度等胁迫条件下的一种渗透保护剂。转录因子GbdR是胆碱代谢的特异性调节因子，属于Arac/XylS转录调节因子家族。尽管胆碱分解代谢与细菌致病性之间存在联系，但尚未对gbdR调节进行详细研究。在本研究中，我们描述了gbdR转录如何从一个依赖σ54的启动子起始。在没有优先氮源的情况下，gbdR转录可被NtrC激活；在没有优先碳源的情况下，可被CbrB激活；并且可被有利于DNA弯曲的整合宿主因子激活。此外，我们发现，在没有胆碱的情况下，BetI对gbdR表达起负调节作用。我们在gbdR启动子序列中鉴定出两个重叠的BetI结合位点，这为σ54启动子下调提供了另一个例子。基于我们的发现，我们提出了一个gdbR调节及其对胆碱代谢影响的模型。
