Functional RelBE-Family Toxin-Antitoxin Pairs Affect Biofilm Maturation and Intestine Colonization in Vibrio cholerae.

Functional RelBE-Family Toxin-Antitoxin Pairs Affect Biofilm Maturation and Intestine Colonization in Vibrio cholerae.
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功能性 RelBE-家族毒素-抗毒素对影响霍乱弧菌生物膜成熟和肠道定植。

DOI:
10.1371/journal.pone.0135696
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发表时间:
2015
期刊:
影响因子:
3.7
通讯作者:
Kan B
Kan B
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Wang Y;Wang H;Hay AJ;Zhong Z;Zhu J;Kan B

文献摘要

相似文献

毒素-抗毒素(TA)系统是一种小的遗传元件,通常编码稳定的毒素及其不稳定的抗毒素。这些同源对在原核生物中大量存在,并已被证明调节各种细胞功能。霍乱弧菌是一种人类病原体,是霍乱的病原体,至少含有13个TA基因座。虽然HigBA、Parde在霍乱弧菌中起稳定作用,而Phd/Doc在介导细胞死亡中起作用,但7个RelBE家族TA系统的功能尚不清楚。在本研究中,我们研究了RelBE TA系统在霍乱弧菌生理中的功能,发现7个relBE基因座中有6个编码了霍乱弧菌中的功能性毒素。对每个relBE基因座的缺失分析表明,RelBE系统参与了生物膜的形成和抗活性氧(ROS)。有趣的是,所有7个relBE基因座都是在标准毒力诱导条件下诱导的,其中两个relBE突变体表现出定植缺陷,这不是由于对毒力基因表达的影响。虽然还需要进一步的研究来确定作用机制,但我们的研究表明,RelBE系统对霍乱弧菌的生理学很重要。
Toxin–antitoxin (TA) systems are small genetic elements that typically encode a stable toxin and its labile antitoxin. These cognate pairs are abundant in prokaryotes and have been shown to regulate various cellular functions. Vibrio cholerae, a human pathogen that is the causative agent of cholera, harbors at least thirteen TA loci. While functional HigBA, ParDE have been shown to stabilize plasmids and Phd/Doc to mediate cell death in V. cholerae, the function of seven RelBE-family TA systems is not understood. In this study we investigated the function of the RelBE TA systems in V. cholerae physiology and found that six of the seven relBE loci encoded functional toxins in E. coli. Deletion analyses of each relBE locus indicate that RelBE systems are involved in biofilm formation and reactive oxygen species (ROS) resistance. Interestingly, all seven relBE loci are induced under the standard virulence induction conditions and two of the relBE mutants displayed a colonization defect, which was not due to an effect on virulence gene expression. Although further studies are needed to characterize the mechanism of action, our study reveals that RelBE systems are important for V. cholerae physiology.