Plasmid fitness costs are caused by specific genetic conflicts
Plasmid fitness costs are caused by specific genetic conflicts
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质粒适应度成本是由特定的遗传冲突引起的
DOI：
10.1101/2021.04.10.439128
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发表时间：
2021
期刊：
影响因子：
--
通讯作者：
Hall J
中科院分区：
文献类型：
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作者：
Hall J
质粒酶在细菌基因组进化中起着重要作用，它通过在谱系之间转移基因而发挥作用。与质粒获得相关的适应性成本预计将成为基因交换的障碍，但质粒适应性成本的原因知之甚少。单个补偿突变通常足以完全改善质粒适应性成本，这表明这种成本是由特定的遗传冲突引起的，而不是质粒的一般特性，如它们的大小，代谢负荷或表达水平。在这里，我们显示-使用实验进化，反向遗传学和转录组学的组合-健身成本的两个不同的大质粒inPseudomonasfluorescensare引起的诱导适应不良表达的染色体tailocin毒素操纵子。与毒素操纵子无关且位于染色体或质粒上的单个基因的突变改善了与质粒获得相关的破坏。我们确定了这些补偿位点之一，染色体基因PFLU 4242，作为两种质粒的健身成本的关键调解人，与其他补偿位点要么减少该基因的表达或减轻其有害影响，通过上调一个假定的质粒携带的ParAB操纵子。染色体移动的遗传元件Tn 6291，它使用质粒进行传输，保持上调，即使在补偿菌株，表明移动的遗传元件通过独立于一般生理中断的途径进行通信。由特定遗传冲突引起的质粒适应性成本不太可能成为水平基因转移的长期障碍，因为它们倾向于通过单一补偿突变进行改善，这解释了为什么质粒在细菌基因组中如此常见。
Plasmids play an important role in bacterial genome evolution by transferring genes between lineages. Fitness costs associated with plasmid acquisition are expected to be a barrier to gene exchange, but the causes of plasmid fitness costs are poorly understood. Single compensatory mutations are often sufficient to completely ameliorate plasmid fitness costs, suggesting that such costs are caused by specific genetic conflicts rather than generic properties of plasmids, such as their size, metabolic burden, or expression level. Here we show — using a combination of experimental evolution, reverse genetics, and transcriptomics — that fitness costs of two divergent large plasmids inPseudomonas fluorescensare caused by inducing maladaptive expression of a chromosomal tailocin toxin operon. Mutations in single genes unrelated to the toxin operon, and located on either the chromosome or the plasmid, ameliorated the disruption associated with plasmid acquisition. We identify one of these compensatory loci, the chromosomal genePFLU4242, as the key mediator of the fitness costs of both plasmids, with the other compensatory loci either reducing expression of this gene or mitigating its deleterious effects by upregulating a putative plasmid-borne ParAB operon. The chromosomal mobile genetic element Tn6291, which uses plasmids for transmission, remained upregulated even in compensated strains, suggesting that mobile genetic elements communicate through pathways independent of general physiological disruption. Plasmid fitness costs caused by specific genetic conflicts are unlikely to act as a long-term barrier to horizontal gene transfer due to their propensity for amelioration by single compensatory mutations, explaining why plasmids are so common in bacterial genomes.