Temperature, by Controlling Growth Rate, Regulates CRISPR-Cas Activity in Pseudomonas aeruginosa.

Temperature, by Controlling Growth Rate, Regulates CRISPR-Cas Activity in Pseudomonas aeruginosa.
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DOI:
10.1128/mbio.02184-18
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发表时间:
2018-11-13
期刊:
影响因子:
6.4
通讯作者:
Bassler BL
Bassler BL
中科院分区:
生物学1区
文献类型:
--
作者:
Høyland-Kroghsbo NM;Muñoz KA;Bassler BL

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铜绿假单胞菌是一种寄居在土壤中的细菌和植物病原体,它还会引起人类的致命感染。因此,铜绿假单胞菌在不同的环境和广泛的温度范围内茁壮成长。一些铜绿假单胞菌菌株依赖CRISPR-Cas适应性免疫系统作为噬菌体防御机制。我们的发现,低温增加CRISPR适应表明,很少发生但关键的幼稚适应事件可能主要发生在缓慢生长的条件下,例如,在细菌的土壤栖息期间和生物膜的缓慢生长期间。簇状规则间隔短回文重复(CRISPR)相关(CRISPR-Cas)系统是一种适应性防御系统,可以保护细菌和古菌免受遗传因素的入侵。在铜绿假单胞菌中,当噬菌体感染风险较高时,群体感应(QS)在高细胞密度下诱导CRISPR-Cas防御系统。在这里,我们证明了另一个线索,温度,调制铜绿假单胞菌CRISPR-Cas。与体温(即高温度)相比,CRISPR在环境温度(即低温度)下的适应能力更强。这种增加是CRISPR-Cas复合体积累的结果,再加上较低温度下铜绿假单胞菌生长速度的降低,后者为CRISPR-Cas在细胞分裂之前提供了额外的时间,使其能够巡视细胞,并成功地清除和/或获得对外来DNA的免疫力。对一个qs突变体和合成的qs化合物的分析表明,qs和温度线索是协同作用的。铜绿假单胞菌在环境中遇到的噬菌体的多样性和水平超过了人体中的水平,这可能证明了在环境温度下增加对CRISPR-CAS的依赖。
P. aeruginosa is a soil dwelling bacterium and a plant pathogen, and it also causes life-threatening infections in humans. Thus, P. aeruginosa thrives in diverse environments and over a broad range of temperatures. Some P. aeruginosa strains rely on the CRISPR-Cas adaptive immune system as a phage defense mechanism. Our discovery that low temperatures increase CRISPR adaptation suggests that the rarely occurring but crucial naive adaptation events may take place predominantly under conditions of slow growth, e.g., during the bacterium’s soil dwelling existence and during slow growth in biofilms. Clustered regularly interspaced short palindromic repeat (CRISPR)-associated (CRISPR-Cas) systems are adaptive defense systems that protect bacteria and archaea from invading genetic elements. In Pseudomonas aeruginosa, quorum sensing (QS) induces the CRISPR-Cas defense system at high cell density when the risk of bacteriophage infection is high. Here, we show that another cue, temperature, modulates P. aeruginosa CRISPR-Cas. Increased CRISPR adaptation occurs at environmental (i.e., low) temperatures compared to that at body (i.e., high) temperature. This increase is a consequence of the accumulation of CRISPR-Cas complexes, coupled with reduced P. aeruginosa growth rate at the lower temperature, the latter of which provides additional time prior to cell division for CRISPR-Cas to patrol the cell and successfully eliminate and/or acquire immunity to foreign DNA. Analyses of a QS mutant and synthetic QS compounds show that the QS and temperature cues act synergistically. The diversity and level of phage encountered by P. aeruginosa in the environment exceed that in the human body, presumably warranting increased reliance on CRISPR-Cas at environmental temperatures.