Zhang Guangdong, Zhong Fangli, Chen Lei, Qin Peipei, Li Junmei, Zhi Feijie, Tian Lulu, Zhou Dong, Lin Pengfei, Chen Huatao, Tang Keqiong, Liu Wei, Jin Yaping, Wang Aihua
College of Veterinary Medicine, Northwest A&F University, Yangling, China.
Key Laboratory of Animal Biotechnology, Ministry of Agriculture, Northwest A&F University, Yangling, China.
Front Microbiol. 2021 Jan 28;12:632095. doi: 10.3389/fmicb.2021.632095. eCollection 2021.
BAX inhibitor 1 (BI-1) is an evolutionarily conserved transmembrane protein first identified in a screening process for human proteins that suppress BAX-induced apoptosis in yeast cells. Eukaryotic BI-1 is a cytoprotective protein that suppresses cell death induced by multiple stimuli in eukaryotes. , the causative agent of brucellosis that threatens public health and animal husbandry, contains a conserved gene that encodes BI-1-like protein. To explore the role of the homolog of BI-1, BrBI, in S2, we constructed the deletion mutant strain and its complemented strain. deletion altered the membrane properties of S2 and decreased its resistance to acidic pH, HO, polymyxin B, and lincomycin. Additionally, deleting led to defective growth, cell division, and viability in S2. We then revealed the effect of deletion on the physiological characteristics of S2 via integrated transcriptomic and proteomic analyses. The integrated analysis showed that deletion significantly affected the expression of multiple genes at the mRNA and/or protein levels. Specifically, the affected divisome proteins, FtsB, FtsI, FtsL, and FtsQ, may be the molecular basis of the impaired cell division of the mutant strain, and the extensively affected membrane proteins and transporter-associated proteins were consistent with the phenotype of the membrane properties' alterations of the mutant strain. In conclusion, our results revealed that BrBI is a bacterial cytoprotective protein involved in membrane homeostasis, cell division, and stress resistance in S2.
BAX抑制剂1（BI-1）是一种在进化上保守的跨膜蛋白，最初是在筛选抑制酵母细胞中BAX诱导凋亡的人类蛋白质的过程中鉴定出来的。真核生物的BI-1是一种细胞保护蛋白，可抑制真核生物中多种刺激诱导的细胞死亡。布鲁氏菌病是威胁公共卫生和畜牧业的病原体，它含有一个编码BI-1样蛋白的保守基因。为了探究布鲁氏菌中BI-1的同源物BrBI在布鲁氏菌S2中的作用，我们构建了BrBI缺失突变株及其互补菌株。BrBI缺失改变了布鲁氏菌S2的膜特性，并降低了其对酸性pH、过氧化氢、多粘菌素B和林可霉素的抗性。此外，缺失BrBI导致布鲁氏菌S2生长、细胞分裂和活力出现缺陷。然后，我们通过整合转录组学和蛋白质组学分析揭示了BrBI缺失对布鲁氏菌S2生理特性的影响。整合分析表明，BrBI缺失在mRNA和/或蛋白质水平上显著影响了多个基因的表达。具体而言，受影响的分裂体蛋白FtsB、FtsI、FtsL和FtsQ可能是突变株细胞分裂受损的分子基础，而广泛受影响的膜蛋白和转运蛋白相关蛋白与突变株膜特性改变的表型一致。总之，我们的结果表明BrBI是一种细菌细胞保护蛋白，参与布鲁氏菌S2的膜稳态、细胞分裂和应激抗性。
