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在Staphylococcus aureus的SAE两组系统信号传输中,需要足够的皮里米丁

Dennis A DiMaggio¹, Won-Sik Yeo¹, Shaun R Brinsmade¹

¹Department of Biology, Georgetown University, Washington, DC USA.

bioRxiv : the preprint server for biology

|April 1, 2025

概括

在新的pyrimidine生物合成对于黄金葡萄球菌的毒性至关重要. 核酸代谢和膜完整性通过SAE双组分系统 (TCS) 调节毒性因子表达.

科学领域:

微生物学微生物学
分子生物学分子生物学
生物化学生物化学

背景情况:

病原体的毒性依赖于核酸代谢来实现生长,生存和免疫逃避.
黄金葡萄球菌的毒性因子由SAE双组分系统 (TCS) 调节.
由于缺少信号绑定域,SaeS传感器用于信号传感的氨酸激酶 (HK) 机制仍然不清楚.

研究的目的:

研究核酸代谢在调节SAE TCS活性中的作用.
阐明 SaeS HK 感知信号并控制病毒性基因表达的机制.

主要方法:

皮里米丁生物合成基因的遗传破坏.
测量SAE-依赖的促进者活动.
-标签电泳以评估SaeS激酶活性.
膜完整性和自由脂肪酸结合的分析.
使用细胞外脂肪酸沉的补充研究.

主要成果:

在pyrimidine受限条件下,破坏pyrimidine生物合成降低了SAE活性.
皮里米丁的限制直接影响了膜上的SaeS激酶活性.
缺陷的皮里米丁生物合成导致了膜缺陷和增加了自由脂肪酸的纳入.
通过隔离自由脂肪酸恢复膜完整性,挽救了SAE活动.

结论:

在新的pyrimidine生物合成是维持SAE TCS活动和黄金葡萄球菌的毒性至关重要的.
SaeS活动由核酸代谢和膜完整性来调节.
这项研究揭示了核酸代谢,膜平衡和病原体中毒性调节之间的新联系.

关键词:

在MRSA中,MRSA可能是MRSA.皮里米丁的新陈代谢这是SaeRSRS.黄金葡萄球菌黄金葡萄球菌免费脂肪酸是一种自由的脂肪酸.膜膜膜膜是一种代谢代谢代谢代谢皮里米丁胺是一种两个组成部分的监管系统.毒性毒性是一种毒性.毒性调节毒性的调节

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