SifA SUMOylation通过调节 lysosomal 功能来控制沙门氏菌 Typhimurium 细胞内生存
Hridya Chandrasekhar1, Gayatree Mohapatra2, Kirti Kajal1
1Regional Centre for Biotechnology, Faridabad, India.
PLoS pathogens
|September 29, 2023
概括
沙门氏菌Typhimurium利用宿主SUMOylation机制来调节效应因子SifA,影响细菌的生存. 损坏的SifA SUMOylation 危害了沙门氏菌 Typhimurium 的生命.
科学领域:
- 微生物学 微生物学
- 细胞生物学 细胞生物学
- 病原体与宿主之间的相互作用
背景情况:
- 沙门氏菌 Typhimurium 感染涉及使用宿主后翻译修饰 (PTM) 机制的病原体效应体.
- 沙门氏菌 Typhimurium 存在于真空体 (SCV) 中,并形成细丝 (SIF) 以获取营养和保持稳定.
- 效应因子SifA和宿主因子如PLEKHM1/2和Rab GTPases对于SCV完整性和SIF形成至关重要.
研究的目的:
- 调查SUMOylation的作用,一个PTM,在调节沙门氏菌Typhimurium效应剂SifA.A.的功能.
- 为了阐明SifA SUMOylation对沙门氏菌Typhimurium细胞内生存和毒性的影响.
主要方法:
- 产生和分析缺少SifA SUMOylation (SifAK11R) 的沙门氏菌Typhimurium突变体.
- 在实验室中评估细菌细胞内增殖,SIF形成和 lysosomal 酸化.
- 进行小鼠竞争指数实验,以评估体内毒性.
主要成果:
- SifA SUMOylation在氨酸11是萨尔门氏菌 Typhimurium细胞内增殖的必要条件.
- SifAK11R突变体表现出缺陷的SIF形成和增强的溶酶体酸化.
- 在体内研究显示,SifAK11R突变体的毒性和细菌负载减少,模仿SifA淘汰赛.
结论:
- SifA的SUMOylation是Salmonella Typhimurium的一个新机制,用于调节其细胞内生存.
- SifA SUMOylation 的失调通过影响 Rab9-MPR lysosomal 酸化途径,损害了细菌的增殖.
- 这突出了关键的病原体-宿主交叉声涉及PTMs的细菌病原性.
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