Fluidity is an inherent property of biological membranes and its maintenance (homeoviscous adaptation) is important for optimal functioning of membrane‐associated processes. The fluidity of bacterial cytoplasmic membrane increases with temperature or an increase in the proportion of unsaturated fatty acids and vice versa. We found that strains deficient in the synthesis of guanine nucleotide analogs (p)ppGpp and lacking FadR, a transcription factor involved in fatty acid metabolism exhibited a growth defect that was rescued by an increase in growth temperature or unsaturated fatty acid content. The strain lacking (p)ppGpp was sensitive to genetic or chemical perturbations that decrease the proportion of unsaturated fatty acids over saturated fatty acids. Microscopy showed that the growth defect was associated with cell filamentation and lysis and rescued by combined expression of cell division genes ftsQ, ftsA, and ftsZ from plasmid or the gain‐of‐function ftsA* allele but not over‐expression of ftsN. The results implicate (p)ppGpp in positive regulation of cell division during membrane fluidity loss through enhancement of FtsZ proto‐ring stability. To our knowledge, this is the first report of a (p)ppGpp‐mediated regulation needed for adaptation to membrane fluidity loss in bacteria.

中文翻译：

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（p）当大肠杆菌膜流动性降低时，ppGpp 可缓冲细胞分裂


流动性是生物膜的固有特性，其维持（稳态粘性适应）对于膜相关过程的最佳功能非常重要。细菌细胞质膜的流动性随温度或不饱和脂肪酸比例的增加而增加，反之亦然。我们发现，缺乏鸟嘌呤核苷酸类似物合成 （p）ppGpp 且缺乏 FadR（一种参与脂肪酸代谢的转录因子）的菌株表现出生长缺陷，可通过生长温度或不饱和脂肪酸含量的增加来挽救。缺乏 （p） ppGpp 的菌株对遗传或化学扰动敏感，这些扰动会降低不饱和脂肪酸相对于饱和脂肪酸的比例。显微镜显示，生长缺陷与细胞丝化和裂解有关，并通过质粒或功能获得性 ftsA* 等位基因的细胞分裂基因 ftsQ 、 ftsA 和 ftsZ 的联合表达来挽救，但不是 ftsN 的过表达。结果表明 （p） ppGpp 通过增强 FtsZ 原环稳定性在膜流动性损失过程中对细胞分裂进行正调节。据我们所知，这是首次报道了适应细菌膜流动性损失所需的 （p） ppGpp 介导的调节。