Acinetobacter baumannii ATCC 17978 lon suppressor

Acinetobacter baumannii is a leading cause of hospital-acquired infections, where outbreaks are driven by its ability to persist on surfaces in a desiccated state. We have shown that disruption of Lon protease enhances desiccation tolerance in this organism. In the course of culturing the lon mutant, we isolated a suppressor strain with decreased tolerance to desiccation and oxidative stress. Whole genome sequencing of the suppressor revealed an A43E substitution in the receiver domain of BfmR, the response regulator of the BfmRS two-component system. Further characterization of this mutant (lon-supp) revealed that that BfmR-dependent activation of certain transcriptional targets is enhanced in the absence of Lon.

鲍曼不动杆菌（Acinetobacter baumannii）是医院获得性感染的主要致病菌，其暴发流行源于该菌可在干燥状态下于物体表面持久存活。本研究团队已证实，Lon蛋白酶（Lon protease）的功能破坏可增强该菌的耐干燥能力。在培养lon基因突变株的过程中，我们分离得到一株耐受性降低的抑制突变株，其对干燥与氧化应激的耐受性有所下降。对该抑制株开展全基因组测序后发现，BfmRS双组分系统（BfmRS two-component system）的应答调节蛋白BfmR的接收结构域存在A43E氨基酸置换。对该lon抑制突变株（lon-supp）的进一步表征显示，在缺失Lon蛋白酶的背景下，BfmR依赖的部分转录靶标的激活过程被增强。