Abstract：
By-products like CO₂ and organic acids, produced during Clostridium botulinum growth, appear to inhibit its development and reduce ATP production. A decrease in ATP production creates an imbalance in the ATP/GTP ratio. GTP activates CodY, which regulates BoNT expression. This toxin is released into the extracellular medium. Its light chains act as a specific endopeptidase, targeting SNARE proteins. The specific amino acids released enter the cells and are metabolized by the Stickland reaction, resulting in the synthesis of ATP. This ATP might then be used by histidine kinases to activate Spo0A, the main regulator initiating sporulation, through phosphorylation.
摘要：
副产品，如二氧化碳和有机酸，在肉毒梭菌生长过程中产生，似乎抑制了其发展并减少了ATP的产生。ATP产生的减少造成ATP/GTP比率的不平衡。GTP激活CodY,调节BoNT表达。这种毒素被释放到细胞外介质中。它的轻链作为一个特定的内肽酶，靶向陷阱蛋白。释放的特定氨基酸进入细胞并通过Stickland反应代谢，导致ATP的合成。然后，这种ATP可能被组氨酸激酶用来激活Spo0A，启动孢子形成的主调节器，通过磷酸化。
