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首页> 外文期刊>PLoS Genetics >The conserved transcriptional regulator CdnL is required for metabolic homeostasis and morphogenesis in Caulobacter
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The conserved transcriptional regulator CdnL is required for metabolic homeostasis and morphogenesis in Caulobacter

机译：保守的转录调节剂CDN1是代谢稳态和形态发生在<斜体>梗裂杆菌中的形态发生

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Bacterial growth and division require regulated synthesis of the macromolecules used to expand and replicate components of the cell. Transcription of housekeeping genes required for metabolic homeostasis and cell proliferation is guided by the sigma factor σ ~(70). The conserved CarD-like transcriptional regulator, CdnL, associates with promoter regions where σ ~(70) localizes and stabilizes the open promoter complex. However, the contributions of CdnL to metabolic homeostasis and bacterial physiology are not well understood. Here, we show that Caulobacter crescentus cells lacking CdnL have severe morphological and growth defects. Specifically, ΔcdnL cells grow slowly in both rich and defined media, and are wider, more curved, and have shorter stalks than WT cells. These defects arise from transcriptional downregulation of most major classes of biosynthetic genes, leading to significant decreases in the levels of critical metabolites, including pyruvate, α-ketoglutarate, ATP, NAD ~(+), UDP-N-acetyl-glucosamine, lipid II, and purine and pyrimidine precursors. Notably, we find that ΔcdnL cells are glutamate auxotrophs, and Δ cdnL is synthetic lethal with other genetic perturbations that limit glutamate synthesis and lipid II production. Our findings implicate CdnL as a direct and indirect regulator of genes required for metabolic homeostasis that impacts morphogenesis through availability of lipid II and other metabolites.
机译：细菌生长和划分需要调节用于扩增和复制细胞组分的大分子的合成。代谢稳态和细胞增殖所需的内政基因的转录被Sigma因子σ〜（70）引导。保守的卡样转录调节剂CDN1，与σ〜（70）定位的启动子区域的缔解促进和稳定开放启动子复合物。然而，CDN1对代谢稳态和细菌生理学的贡献尚不清楚。在这里，我们表明缺乏CDNL的肺病患者细胞具有严重的形态和生长缺陷。具体地，ΔCdn1细胞在富含和定义的介质中缓慢生长，并且更宽，更弯曲，并且具有比WT细胞更短的茎。这些缺陷来自大多数主要类生物合成基因的转录下调，导致临界代谢物水平显着降低，包括丙酮酸，α-酮戊酸，ATP，NAD〜（+），UDP-N-乙酰甘黄胺，脂质II和嘌呤和嘧啶前体。值得注意的是，我们发现ΔCDNL细胞是谷氨酸营养丰制性，并且δCDN1是合成的致死，其与其他遗传扰动限制谷氨酸合成和脂质II产生。我们的研究结果将CDNL含义作为代谢稳态所需的基因的直接和间接调节剂，其通过脂质II和其他代谢物的可用性影响形态发生。

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