含蛋白的α2-宏球蛋白功能可以通过两种免疫诱导来保护Drosophila从细菌蛋白酶中
Chuping Cai1,2,3, Adrian Acker2,3, Jianqiong Huang1
1Sino-French Hoffmann Institute, Guangzhou Medical University, Guangzhou 511436, China.
概括
两种新发现的分泌,Yulü和Shenshu,保护Drosophila免受细菌外膜囊泡的影响. 这些,以及补充蛋白Tep2和Tep4,抑制细菌金属蛋白酶PrtA的活性.
科学领域:
- * 基因组学和分子生物学
- * 免疫学和传染病
- * 蛋白质组学和生物化学
背景情况:
- *在 *Drosophila* 中进行RNA测序,确定了两个免疫诱导基因,CG44404 (yulü) 和CG45045 (shenshu),最初被注释为长非编码RNA (lncRNA).
- 来自Serratia marcescens的外膜囊泡 (OMV) 通过诱导神经元亡,在虫中引起,金属蛋白酶PrtA是关键的毒性因子.
- * *Drosophila*补充系统,包括含有铁的蛋白质 (Teps),在天生的免疫力中起作用.
研究的目的:
- * 描述Drosophila*基因CG44404 (yulü) 和CG45045 (shenshu) 的功能.
- * 调查yulü和shenshu在Drosophila对细菌病原体及其成分的免疫力中的作用.
- * 为了阐明yulü/shenshu,Teps和细菌金属蛋白酶PrtA.之间的相互作用.
主要方法:
- *为*yulü*和*shenshu*基因生成和分析单个和双重无基因突变.
- *使用细菌和真菌病原体和纯化的细菌外膜囊泡 (OMVs) 进行免疫挑战测定.
- *共免疫沉试验检测蛋白相互作用,蛋白酶抑制试验评估功能活性.
主要成果:
- * *yulü* 和 *shenshu* 编码分泌的,而不是 lncRNAs,对于对来自 *Pseudomonas aeruginosa* 和 *Serratia marcescens* 的 OMV 进行保护至关重要.
- * 缺少yulü和shenshu的突变体对大多数病原体没有增加敏感性,但对OMV介导的敏感.
- * Yulü/Shenshu 与 * Drosophila * 补充蛋白 Tep2 和 Tep4 相结合,它们以一种依赖于硫和 yulü/shenshu 的方式抑制 PrtA 金属蛋白酶活性.
结论:
- * Yulü和Shenshu是涉及Drosophila先天免疫的分泌,特别是在对细菌OMVs进行保护.
- * Tep2和Tep4作为Opsonin和可能作为α2-巨型球蛋白类蛋白酶抑制剂,与yulü/shenshu一起工作.
- * yulü/shenshu-Tep2/Tep4复合体提供了一种针对 PrtA.这样的细菌毒性因子的新型防御机制.
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