Social cheating in a Pseudomonas aeruginosa quorum-sensing variant
Social cheating in a Pseudomonas aeruginosa quorum-sensing variant
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DOI：
10.1073/pnas.1819801116
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发表时间：
2019-04-02
影响因子：
11.1
通讯作者：
Greenberg, E. Peter
中科院分区：
文献类型：
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作者：
Chen, Ruiyi;Deziel, Eric;Greenberg, E. Peter
条件致病菌铜绿假单胞菌具有层状酰基高丝氨酸内酯（阿勒）群体感应（QS）系统，其控制多种胞外代谢物和酶的产生。LasRI系统激活基因，包括编码细胞外蛋白酶弹性蛋白酶和第二阿勒QS系统RhlRI的那些基因。铜绿假单胞菌在酪蛋白上的生长需要弹性蛋白酶的产生，并且在酪蛋白上生长的群体中出现LasR突变的社会欺骗。铜绿假单胞菌定殖于患有遗传性疾病囊性纤维化（CF）的个体的肺，并且LasR突变体可以从定殖的肺中分离;然而，与实验室产生的LasR突变体不同，这些CF分离物中的许多具有功能性RhlR-RhlI系统。我们表明，这样的突变体可以使用RhlR-RhlI系统激活弹性蛋白酶的表达和生长的酪蛋白。我们通过在酪蛋白酸盐上培养该分离株进行了社会进化实验，并且与野生型铜绿假单胞菌一样，弹性蛋白酶阴性突变体作为作弊者出现，但这些不是RhlR突变体;相反，它们是不产生非AHL假单胞菌喹诺酮信号（PQS）的突变体。此外，我们产生了一个RhlRI突变体，并表明它与亲本一起生长时具有适应性缺陷。显然，RhIR QS和PQS在功能性LasR不存在的情况下共同支持酪蛋白酸盐上的生长。我们的研究结果提供了一个合理的解释，为什么铜绿假单胞菌LasR突变体，而不是RhlR突变体，是常见的CF肺。
The opportunistic bacterial pathogen Pseudomonas aeruginosa has a layered acyl-homoserine lactone (AHL) quorum-sensing (QS) system, which controls production of a variety of extracellular metabolites and enzymes. The LasRI system activates genes including those coding for the extracellular protease elastase and for the second AHL QS system, RhlRI. Growth of P. aeruginosa on casein requires elastase production and LasR-mutant social cheats emerge in populations growing on casein. P. aeruginosa colonizes the lungs of individuals with the genetic disease cystic fibrosis (CF), and LasR mutants can be isolated from the colonized lungs; however, unlike laboratory-generated LasR mutants, many of these CF isolates have functioning RhlR-RhlI systems. We show that one such mutant can use the RhlR-RhlI system to activate expression of elastase and grow on casein. We carried out social-evolution experiments by growing this isolate on caseinate and, as with wild-type P. aeruginosa, elastase-negative mutants emerge as cheats, but these are not RhlR mutants; rather, they are mutants that do not produce the non-AHL Pseudomonas quinolone signal (PQS). Furthermore, we generated a RhlRI mutant and showed it had a fitness defect when growing together with the parent. Apparently, RhlR QS and PQS collude to support growth on caseinate in the absence of a functional LasR. Our findings provide a plausible explanation as to why P. aeruginosa LasR mutants, but not RhlR mutants, are common in CF lungs.