通过转录抑制脂化,可以控制C. elegans的病原体耐药性
Mohamad A Nasrallah1, Nicholas D Peterson1, Elizabeth S Szumel1
1Program in Innate Immunity, Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Chan Medical School, Worcester, Massachusetts, United States of America.
PLoS pathogens
|October 31, 2023
概括
研究人员发现了一种新途径,控制脂分解,以对抗细菌感染. 失去NHR-66蛋白质会增加脂体的分解,使宿主更容易受到Pseudomonas aeruginosa的感染.
科学领域:
- 分子生物学分子生物学
- 遗传学 遗传学 是一个
- 免疫学 免疫学 免疫学
背景情况:
- 脂对细胞功能至关重要,并由特定的酶分解.
- 调节脂体代谢的机制在很大程度上是未知的.
- 了解这些机制是控制宿主-病原体相互作用的关键.
研究的目的:
- 为了识别控制脂体代谢的转录调节剂.
- 阐明脂分解在宿主对细菌感染的抵抗力中的作用.
主要方法:
- 在C. elegans中进行了RNA干扰 (RNAi) 选,以确定病原体耐药性的调节者.
- 利用并联染色体免疫沉测序 (ChIP-seq) 和RNA测序 (RNA-seq) 来分析基因调控.
- 生成nhr-66功能丧失突变体,以研究nhr-66缺乏的影响.
主要成果:
- 确定了核激素受体NHR-66作为脂代谢基因的关键转录抑制剂.
- NHR-66直接准了参与脂分解的基因.
- 丧失NHR-66会导致脂体代谢的增加,并增加对Pseudomonas aeruginosa感染的易感性.
结论:
- 定义了一种新型的转录轴,调节脂体代谢.
- 证明了转录控制脂分解对于病原体耐药性至关重要.
- NHR-66作为一个关键的守门员,对脂平衡和宿主防御起到关键作用.
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