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• W4283008445 startingPage "e1010581" @default.
• W4283008445 abstract "Vibrio cholerae is the etiologic agent of the severe human diarrheal disease cholera. To colonize mammalian hosts, this pathogen must defend against host-derived toxic compounds, such as nitric oxide (NO) and NO-derived reactive nitrogen species (RNS). RNS can covalently add an NO group to a reactive cysteine thiol on target proteins, a process called protein S-nitrosylation, which may affect bacterial stress responses. To better understand how V . cholerae regulates nitrosative stress responses, we profiled V . cholerae protein S-nitrosylation during RNS exposure. We identified an S-nitrosylation of cysteine 235 of AphB, a LysR-family transcription regulator that activates the expression of tcpP , which activates downstream virulence genes. Previous studies show that AphB C235 is sensitive to O 2 and reactive oxygen species (ROS). Under microaerobic conditions, AphB formed dimer and directly repressed transcription of hmpA , encoding a flavohemoglobin that is important for NO resistance of V . cholerae . We found that tight regulation of hmpA by AphB under low nitrosative stress was important for V . cholerae optimal growth. In the presence of NO, S-nitrosylation of AphB abolished AphB activity, therefore relieved hmpA expression. Indeed, non-modifiable aphB C235S mutants were sensitive to RNS in vitro and drastically reduced colonization of the RNS-rich mouse small intestine. Finally, AphB S-nitrosylation also decreased virulence gene expression via debilitation of tcpP activation, and this regulation was also important for V . cholerae RNS resistance in vitro and in the gut. These results suggest that the modulation of the activity of virulence gene activator AphB via NO-dependent protein S-nitrosylation is critical for V . cholerae RNS resistance and colonization." @default.
• W4283008445 created "2022-06-18" @default.
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• W4283008445 date "2022-06-17" @default.
• W4283008445 modified "2023-10-18" @default.
• W4283008445 title "S-Nitrosylation of the virulence regulator AphB promotes Vibrio cholerae pathogenesis" @default.
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• W4283008445 doi "https://doi.org/10.1371/journal.ppat.1010581" @default.
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