AUTHOR=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 

TITLE=Integrated Proteomic and Transcriptomic Analyses Reveal the Roles of Brucella Homolog of BAX Inhibitor 1 in Cell Division and Membrane Homeostasis of Brucella suis S2

JOURNAL=Frontiers in Microbiology

VOLUME=12

YEAR=2021

URL=https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2021.632095

DOI=10.3389/fmicb.2021.632095

ISSN=1664-302X

ABSTRACT=<p>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. <italic>Brucella</italic>, 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 <italic>Brucella</italic> homolog of BI-1, BrBI, in <italic>Brucella suis</italic> S2, we constructed the <italic>brbI</italic> deletion mutant strain and its complemented strain. <italic>brbI</italic> deletion altered the membrane properties of <italic>Brucella suis</italic> S2 and decreased its resistance to acidic pH, H<sub>2</sub>O<sub>2</sub>, polymyxin B, and lincomycin. Additionally, deleting <italic>brbI</italic> led to defective growth, cell division, and viability in <italic>Brucella suis</italic> S2. We then revealed the effect of <italic>brbI</italic> deletion on the physiological characteristics of <italic>Brucella suis</italic> S2 via integrated transcriptomic and proteomic analyses. The integrated analysis showed that <italic>brbI</italic> 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 <italic>brbI</italic> mutant strain, and the extensively affected membrane proteins and transporter-associated proteins were consistent with the phenotype of the membrane properties’ alterations of the <italic>brbI</italic> mutant strain. In conclusion, our results revealed that BrBI is a bacterial cytoprotective protein involved in membrane homeostasis, cell division, and stress resistance in <italic>Brucella suis</italic> S2.</p>