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删除菌株分裂因子导致单细胞的异型性崩

E Hesper Rego^1,1, Rebecca E Audette^1,1, Eric J Rubin^1,1

¹Department of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA.

|June 2, 2017

概括

结核菌通过使用LamA蛋白产生细胞变异性,增强抗生素耐药性. 删除Lama会减少这种异质性,使细菌群体更容易受到抗生素的影响.

科学领域:

微生物学
细胞生物学
细菌致病性

背景情况:

微生物群中的个体细胞行为可以显著影响整体群体动态和治疗结果.
结核病的治疗需要长时间的抗生素疗程,因为尽管大多数结核菌细胞迅速死亡,但仍存在生存的亚群.
菌根菌在细胞分裂过程中表现出高频变异,产生具有不同特性的子细胞,但潜在的机制尚不清楚.

研究的目的:

研究菌菌产生细胞异质性的机制.
确定新基因在控制这种变异中的作用.
了解细胞异质性如何促进Mycobacterium结核病的抗生素生存.

主要方法:

使用光报道系统来追踪细胞.
采用光激活细胞分类 (FACS) 基的转子子屏幕来识别相关基因.
产生基因删除突变,特别针对lamA,用于表型分析.

主要成果:

确定了以前未知功能的lamA基因,作为真菌异质性的关键调节者.
通过减少不对称的极性生长,证明了lamA的删除显著降低了种群异质性.
表明Lama是菌根分裂体的保存成分,可以抑制新极的生长.
在lamA删除突变中观察到抗生素具有更均和更快速的杀死动力.

结论:

菌根细菌通过涉及Lama蛋白的机制积极创造细胞异质性.
LamA控制细胞生长模式,有助于增加人群异质性和抗生素压力下的生存率.
向Lama或其途径可能是改善结核病治疗疗效的新方法.

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