The Borrelia burgdorferi adenylyl cyclase, CyaB, is important for virulence factor production and mammalian infection

作者：Vanessa M. Ante, Lauren C. Farris, Elizabeth P. Saputra, Allie J. Hall, Nathaniel S. O’Bier, Adela S. Oliva Chávez, Richard T. Marconi, Meghan Lybecker, Jenny A. Hyde · 发表于：bioRxiv (Cold Spring Harbor Laboratory) · 年份：2021 · DOI：10.1101/2021.03.04.433918 · 研究领域：Vector-borne infectious diseases、Insect symbiosis and bacterial influences、Viral Infections and Vectors

Abstract Borrelia burgdorferi, the causative agent of Lyme disease, traverses through vastly distinct environments between the tick vector and the multiple phases of the mammalian infection that requires genetic adaptation for the progression of pathogenesis. Borrelial gene expression is highly responsive to changes in specific environmental signals that initiate the RpoS regulon for mammalian adaptation, but the mechanism(s) for direct detection of environmental cues has yet to be identified. Secondary messenger cyclic adenosine monophosphate (cAMP) produced by adenylate cyclase is responsive to environmental signals, such as carbon source and pH, in many bacterial pathogens to promote virulence by altering gene regulation. B. burgdorferi encodes a single non-toxin class IV adenylate cyclase ( bb0723, cyaB ). This study investigates cyaB expression along with its influence on borrelial virulence regulation and mammalian infectivity. Expression of cyaB was specifically induced with co-incubation of mammalian host cells that was not observed with cultivated tick cells suggesting that cyaB expression is influenced by cellular factor(s) unique to mammalian cell lines. The 3’ end of cyaB also encodes a small RNA, SR0623, in the same orientation that overlaps with bb0722 . The differential processing of cyaB and SR0623 transcripts may alter the ability to influence function in the form of virulence determinant regulation and infectivity. Two independent cyaB deletion B31 strains w...