来自Mycobacterium tuberculosis的YoeB类毒素RelK显示了与核糖体独立的内核分解活性
Shafinaz Rahman Sarah1, Nimisha Sinha2, Harsh A Gandhi3
1Department of Biochemistry, Sri Venkateswara College, University of Delhi, New Delhi, 110021, India; Department of Biochemistry, University of Delhi South Campus, New Delhi, 110021, India.
Biochimica et biophysica acta. Molecular cell research
|December 21, 2025
概括
来自Mycobacterium tuberculosis的RelK毒素抑制蛋白质合成,并具有DNA尼克酶活性,即使酸化. 它的活性被RelJ抗毒素中和,突出了多种类型II毒素的功能.
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 生化学
背景情况:
- 第二类毒素-抗毒素 (TA) 模块对于细菌的致病性和持久性至关重要.
- 结核菌菌有超过60个TA模块,包括RelJK磁带.
- 通过酸化调节RelK毒素的功能和调节在很大程度上仍然没有特征.
研究的目的:
- 为了阐明RelK毒素的功能活性.
- 为了研究酸化对RelK活性的影响.
- 描述RelK的核酶活性及其与RelJ抗毒素的相互作用.
主要方法:
- 无细胞转录-翻译系统.
- 在体外蛋白质合成抑制试验.
- 核糖核酶和DNA尼克酶活性测定.
- 二元阴离子调制研究.
- 分子对接模拟. 分子对接模拟.
- 位点定向的突变发生.
主要成果:
- 不酸化和酸化的RelK都抑制了体外蛋白质合成,这表明酸化增强了转化控制中的作用.
- RelK表现出与核糖体独立的RNase和剂量依赖的双链DNA尼克酶活性.
- RelK活动是由双价调节的,并且更喜欢超的DNA.
- 这种RelJ抗毒素会使RelK失活.
- 用谷氨胺取代His84取消了RelK的催化活性和细胞毒性.
结论:
- RelK是一种多功能毒素,具有翻译抑制和DNA尼克酶功能.
- 酸化增强了RelK的转化抑制.
- RelK的多样化的基质活性强调了M. tb II型毒素的功能性可塑性.
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