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首页> 外文期刊>Infection and immunity >Staphylococcus aureus Aconitase Inactivation Unexpectedly Inhibits Post-Exponential-Phase Growth and Enhances Stationary-Phase Survival
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Staphylococcus aureus Aconitase Inactivation Unexpectedly Inhibits Post-Exponential-Phase Growth and Enhances Stationary-Phase Survival

机译：金黄色葡萄球菌乌头酸酶失活意外地抑制了指数期后的生长并提高了固定期的存活率

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Staphylococcus aureus preferentially catabolizes glucose, generating pyruvate, which is subsequently oxidized to acetate under aerobic growth conditions. Catabolite repression of the tricarboxylic acid (TCA) cycle results in the accumulation of acetate. TCA cycle derepression coincides with exit from the exponential growth phase, the onset of acetate catabolism, and the maximal expression of secreted virulence factors. These data suggest that carbon and energy for post-exponential-phase growth and virulence factor production are derived from the catabolism of acetate mediated by the TCA cycle. To test this hypothesis, the aconitase gene was genetically inactivated in a human isolate of S. aureus, and the effects on physiology, morphology, virulence factor production, virulence for mice, and stationary-phase survival were examined. TCA cycle inactivation prevented the post-exponential growth phase catabolism of acetate, resulting in premature entry into the stationary phase. This phenotype was accompanied by a significant reduction in the production of several virulence factors and alteration in host-pathogen interaction. Unexpectedly, aconitase inactivation enhanced stationary-phase survival relative to the wild-type strain. Aconitase is an iron-sulfur cluster-containing enzyme that is highly susceptible to oxidative inactivation. We speculate that reversible loss of the iron-sulfur cluster in wild-type organisms is a survival strategy used to circumvent oxidative stress induced during host-pathogen interactions. Taken together, these data demonstrate the importance of the TCA cycle in the life cycle of this medically important pathogen.
机译：金黄色葡萄球菌优先代谢葡萄糖，生成丙酮酸，然后在有氧生长条件下将其氧化为乙酸盐。三羧酸（TCA）循环的分解代谢阻遏导致乙酸盐的积累。 TCA周期抑制与退出指数生长期，乙酸酯分解代谢的开始以及分泌的毒力因子的最大表达相吻合。这些数据表明，用于指数后阶段​​生长和产生毒力因子的碳和能量来自于由TCA循环介导的乙酸酯分解代谢。为了检验这一假设，乌头酸酶基因在人类分离的 S中被基因灭活。观察了金黄色葡萄球菌的含量及其对生理，形态，毒力因子产生，小鼠的毒力和固定期存活率的影响。 TCA循环失活阻止了乙酸的指数后生长期分解代谢，导致过早进入固定相。该表型伴随着几种毒力因子的产生和宿主-病原体相互作用的改变而显着减少。出乎意料的是，乌头酸酶失活相对于野生型菌株提高了固定相的存活率。乌头酸酶是一种含铁-硫簇的酶，对氧化失活高度敏感。我们推测，野生型生物中铁-硫簇的可逆损失是一种用于规避宿主-病原体相互作用期间诱导的氧化应激的生存策略。综上所述，这些数据证明了TCA循环在这种医学上重要的病原体生命周期中的重要性。

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