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蛋白质稳定剂调节抗生素耐药细菌中的基因剂量演变

Chinmaya Jena¹, Saillesh Chinnaraj¹, Soham Deolankar¹

¹Department of Biology, Indian Institute of Science Education and Research, Pune, India.

|March 12, 2025

概括

细菌抗生素耐药性通过基因表达变化而演变. 我们发现基因重复,特别是folA基因,增强二叶酸减少酶 (DHFR) 水平,有助于E. coli的三甲素耐药性.

科学领域:

微生物学微生物学
进化生物学进化生物学
遗传学遗传学是一个

背景情况:

细菌的抗生素耐药性通常是由基因表达的变化驱动的.
之前的研究表明,在大肠杆菌中mgrB位点的突变导致在三甲胺暴露下二叶酸还原酶 (DHFR) 过度表达.
folA基因对DHFR进行编码.

研究的目的:

研究细菌适应trimethoprim时DHFR水平如何进一步增强.
探索基因重复和复制数进化的作用在抗生素耐药性.
了解细菌进化中的抗生素压力,基因剂量和蛋白质稳定之间的相互作用.

主要方法:

研究了埃舍里希亚大肠杆菌中包括folA基因的自发基因组段重复.
在三甲胺压力下的野生类型和单独淘汰菌株的复制频率的比较.
进行了长期进化实验,观察A重复和点突变的动态.
研究了蛋白质分解对DHFR突变和基因拷贝数演变的影响.

主要成果:

观察到含有folA的基因组段的自发重复,显著增加了DHFR水平.
复制频率在单击淘汰菌株中升高,影响了早期的三甲适应.
在抗生素的压力下,folA重复最初被逆转,但与抵抗转移点突变相结合时变得稳定.
一些种群即使有耐药的DHFR突变,也保持了folA重复,以弥补稀少的丰度.
耐药DHFR突变体的蛋白质分解加剧了表达需求,有利于基因拷贝数的进化.

结论:

基因剂量进化,特别是folA重复,受到抗生素产生的表达需求的影响.
蛋白质稳定,通过耐药DHFR突变体的蛋白质分解,在确定抗生素耐药细菌的拷贝数演变方面发挥着新的作用.
这项研究提出了一个新的机制,将蛋白质稳定性与细菌适应中的基因拷贝数变化联系起来.

关键词:

美国大肠杆菌 (E. coli).抗微生物耐药性抗微生物耐药性双叶酸减少酶是什么基因复制是基因的复制.遗传学遗传学遗传学是一个基因组学就是基因组学.传染病是一种传染性疾病.微生物学的微生物.蛋白质稳定症是一种蛋白质稳定症.三甲胺是什么?三甲胺是什么?

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