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Natural competence in V ibrio cholerae is controlled by a nucleoside scavenging response that requires CytR ‐dependent anti‐activation
Author(s) -
Antonova Elena S.,
Bernardy Eryn E.,
Hammer Brian K.
Publication year - 2012
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/mmi.12054
Subject(s) - biology , vibrio cholerae , cytidine , repressor , camp receptor protein , mutant , gene , biochemistry , nucleoside , microbiology and biotechnology , gene expression , bacteria , genetics , promoter , enzyme
Summary Competence for genetic transformation in V ibrio cholerae is triggered by chitin‐induced transcription factor TfoX and quorum sensing ( QS ) regulator HapR . Transformation requires expression of ComEA , described as a DNA receptor in other competent bacteria. A screen for mutants that poorly expressed a comEA –luciferase fusion identified cytR , encoding the nucleoside scavenging cyt idine r epressor, previously shown in V . cholerae to be a biofilm repressor and positively regulated by TfoX , but not linked to transformation . A Δ cytR mutant was non‐transformable and defective in expression of comEA and additional TfoX ‐induced genes, including pilA (transformation pseudopilus) and chiA‐1 (chitinase). In E scherichia coli , ‘anti‐activation’ of nucleoside metabolism genes, via protein–protein interactions between critical residues in CytR and CRP ( c AMP r eceptor p rotein), is disrupted by exogenous cytidine. Amino acid substitutions of the corresponding V . cholerae CytR residues impaired expression of comEA , pilA and chiA‐1 , and halted DNA uptake; while exogenous cytidine hampered comEA expression levels and prevented transformation. Our results support a speculative model that when V . cholerae reaches high density on chitin, CytR – CRP interactions ‘anti‐activate’ multiple genes, including a possible factor that negatively controls DNA uptake. Thus, a nucleoside scavenging mechanism couples nutrient stress and cell–cell signalling to natural transformation in V . cholerae as described in other bacterial pathogens.