通过甲基受体识别细菌配体的动态进化
Nicole M Paterson1,2, Hussein Al-Zubieri1, Joseph Ragona3
1Institute of Ecology and Evolution, University of Oregon, Eugene, Oregon, USA.
Genome biology and evolution
|September 30, 2023
概括
甲基受体 (FPR) 对于检测病原体至关重要. 在FPRs的基因进化影响动物如何识别微生物,特定的变化调整对细菌连接体的反应.
科学领域:
- 免疫学 免疫学 免疫学
- 进化生物学 进化生物学
- 基因组学就是基因组学.
背景情况:
- 细胞表面受体,如甲基受体 (FPRs),对于对病原体的先天免疫防御至关重要.
- FPRs识别微生物分子,启动炎症反应和白细胞迁移到感染部位.
- 免疫受体基因进化推动了多样化,但差异的功能影响在很大程度上是未知的.
研究的目的:
- 研究灵长类动物和食肉动物中FPRs的基因损失,多样化和连接体识别模式.
- 确定FPR分歧对与细菌连接体相互作用的功能后果.
- 了解自然选择如何在对各种微生物分子的反应中塑造FPR激活.
主要方法:
- 比较基因组学分析FPR基因损失和灵长类动物和食肉动物的多样化.
- 氨基酸变异分析以确定FPR1和FPR2.2中正选择下的区域.
- 带结合试验用于测量灵长类FPRs与细菌蛋白质 (金黄色葡萄球菌肠毒素B和FLIPr类) 之间的相互作用.
主要成果:
- 在人类免疫系统中必不可少的FPR1已经在新世界灵长类动物中消失.
- 灵长类动物和食肉动物FPR1和FPR2中的氨基酸变异表明在联结域上存在正选择.
- 灵长类FPRs中快速进化的部位显著改变了对细菌蛋白质的识别,包括激动剂和抑制剂.
结论:
- 包括遗失和多样化在内的FPR基因进化影响物种间的先天免疫识别.
- 在FPR细胞外域上的积极选择微调了对微生物配体的反应.
- 即使是FPR的微小序列变化也可以调节与细菌分子的相互作用,突出显示进化的适应性.
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