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一种II型毒素-抗毒素系统是Pseudomonas注射器Lz4W缺乏RNase R的低温细胞死亡的原因

Pragya Mittal¹, Anurag K Sinha², Apuratha Pandiyan³

¹Centre for Cellular and Molecular Biology (CCMB), Council of Scientific and Industrial Research (CSIR), Hyderabad, India; Celtic Renewables Ltd, Edinburgh Napier University, Edinburgh, UK.

The Journal of biological chemistry

|July 26, 2024

概括

Pseudomonas syringae RNase R (rnr) 对于低温生长至关重要. 在rnr突变体中,冷敏性不是由于16SrRNA处理缺陷,而是与II型毒素-抗毒素系统的激活有关.

科学领域:

微生物学微生物学
细菌生理学细菌生理学
分子生物学分子生物学

背景情况:

RNase R (由rnr基因编码) 对于心理变质细菌Pseudomonas syringae Lz4W在低温下生长至关重要.
之前的研究将rnr删除突变的冷敏细胞死亡归因于16SrRNA处理缺陷,核糖体组装问题和低效的蛋白质合成.
最近的发现表明,RNase R保护P.syringae Lz4W免受DNA损伤和氧化应激,而不依赖于其外原核酶活性.

研究的目的:

为了调查P. syringae Lz4W rnr突变体冷感的原因.
为了确定16S rRNA处理缺陷是否有助于低温细胞死亡.
探索等离子体传递的毒素-抗毒素系统在RNase R功能和细菌寒冷适应中的作用.

主要方法:

补充了rnr删除突变的催化不活跃的RNase R (RNase R^D284A).
在野生型和突变菌株中对16SrRNA处理的分析.
在rnr突变体中对等离子体pLz4W复制数积累的评估.
通过过度表达抗毒素psA来补充rnr突变.

主要成果:

用RNaseR^D284A补充的rnr突变体表现出正常的16SrRNA处理,但保留了冷感应.
这表明16S rRNA处理缺陷不是低温细胞死亡的原因.
这种rnr突变已经积累了pLz4W本地等离子体的副本,该等离子体内含有II型毒素-抗毒素系统.
反毒素psA的过度表达挽救了rnr突变的冷敏表型.

结论:

P. syringae Lz4W rnr突变的寒冷敏感性不是由于16S rRNA处理中的缺陷造成的.
在等离子体pLz4W上II型毒素-抗毒素系统的激活有助于rnr突变的冷感应.
在RNase R,等离子体介导的毒素-抗毒素系统和细菌适应低温之间存在一种新的功能关系.

关键词:

降解RNA的降解RNA的降解在RNA解过程中.细胞死亡是细胞死亡.寒冷的敏感性寒冷的敏感性寒冷引起的DNA损伤毒素抗毒素系统

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