One-carbon metabolism (OCM) pathways are responsible for several functions, producing a number of one-carbon unit intermediates (formyl, methylene, methenyl, methyl) that are required for the synthesis of various amino acids and other biomolecules such as purines, thymidylate, redox regulators, and, in most microbes, folate. As humans must acquire folate from the diet, folate production is a target for antimicrobials such as sulfonamides. OCM impacts the regulation of microbial virulence such that in a number of instances, limiting the availability of para-aminobenzoic acid (pABA), an essential OCM precursor, causes a reduction in pathogenicity. Porphyromonas gingivalis, however, displays increased pathogenicity in response to lower pABA levels, and exogenous pABA exerts a calming influence on heterotypic communities of P. gingivalis with pABA-producing partner species. Differential responses to pABA may reflect both the physiology of the organisms and their host microenvironment. OCM plays an integral role in regulating the global rate of protein translation, where the alarmones ZMP and ZTP sense insufficient stores of intracellular folate and coordinate adaptive responses to compensate and restore folate to sufficient levels. The emerging interconnections between OCM, protein synthesis, and context-dependent pathogenicity provide novel insights into the dynamic host–microbe interface.

中文翻译：

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一碳代谢与微生物致病性

一碳代谢 (OCM) 途径负责多种功能，产生许多合成各种氨基酸和其他生物分子（如嘌呤、胸苷酸）所需的一碳单元中间体（甲酰基、亚甲基、次甲基、甲基） 、氧化还原调节剂，以及大多数微生物中的叶酸。由于人类必须从饮食中获取叶酸，因此叶酸的产生是磺酰胺等抗菌药物的目标。OCM 影响微生物毒力的调节，因此在许多情况下，限制对氨基苯甲酸 (pABA)（一种重要的 OCM 前体）的可用性会导致致病性降低。然而，牙龈卟啉单胞菌对较低的 pABA 水平表现出更高的致病性，并且外源 pABA 对牙龈卟啉单胞菌与产生 pABA 的伙伴物种的异型群落产生镇定作用。对 pABA 的不同反应可能反映了生物体的生理学及其宿主微环境。OCM 在调节蛋白质翻译的整体速率中发挥着不可或缺的作用，其中警报素 ZMP 和 ZTP 感知细胞内叶酸储存不足并协调适应性反应以补偿叶酸并将叶酸恢复到足够的水平。OCM、蛋白质合成和背景依赖性致病性之间新兴的相互联系为动态宿主-微生物界面提供了新的见解。