Functional RelBE-Family Toxin-Antitoxin Pairs Affect Biofilm Maturation and Intestine Colonization in Vibrio cholerae.
Toxin-antitoxin (TA) systems are small genetic elements that typically encode a stable toxin and its labile antitoxin. These cognate pairs are abundant in prokaryotes and have been shown to regulate various cellular functions. Vibrio cholerae, a human pathogen that is the causative agent of cholera, harbors at least thirteen TA loci. While functional HigBA, ParDE have been shown to stabilize plasmids and Phd/Doc to mediate cell death in V. cholerae, the function of seven RelBE-family TA systems is not understood. In this study we investigated the function of the RelBE TA systems in V. cholerae physiology and found that six of the seven relBE loci encoded functional toxins in E. coli. Deletion analyses of each relBE locus indicate that RelBE systems are involved in biofilm formation and reactive oxygen species (ROS) resistance. Interestingly, all seven relBE loci are induced under the standard virulence induction conditions and two of the relBE mutants displayed a colonization defect, which was not due to an effect on virulence gene expression. Although further studies are needed to characterize the mechanism of action, our study reveals that RelBE systems are important for V. cholerae physiology.
Department of Microbiology, Nanjing Agricultural University, Nanjing, China; State Key Laboratory for Infectious Disease Prevention and Control, National Institute for Communicable Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing, China; Department of Microbiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, United States of America.
Yuning
Y
Wang
Department of Microbiology, Nanjing Agricultural University, Nanjing, China.
Hui
H
Wang
Department of Microbiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, United States of America.
Amanda J
AJ
Hay
Department of Microbiology, Nanjing Agricultural University, Nanjing, China.
Zengtao
Z
Zhong
Department of Microbiology, Nanjing Agricultural University, Nanjing, China; Department of Microbiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, United States of America.
Jun
J
Zhu
State Key Laboratory for Infectious Disease Prevention and Control, National Institute for Communicable Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing, China; Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Hangzhou, China.
Biao
B
Kan
D000818:Animals; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism*; D018441:Biofilms / Q000254:growth & development*; D002771:Cholera / Q000235:genetics / Q000378:metabolism; D005786:Gene Expression Regulation / Q000502:physiology*; D006801:Humans; D007422:Intestines / Q000382:microbiology*; D051379:Mice; D050296:Microbial Viability; D009154:Mutation; D014734:Vibrio cholerae / Q000502:physiology*; D037521:Virulence Factors / Q000096:biosynthesis* / Q000235:genetics
D001426:Bacterial Proteins; D037521:Virulence Factors