Fnr mediates carbohydrate-dependent regulation of catabolic and enterotoxin genes in <em>Bacillus cereus</em> F4430/73 - INRAE - Institut national de recherche pour l’agriculture, l’alimentation et l’environnement Access content directly
Journal Articles Research in Microbiology Year : 2010

Fnr mediates carbohydrate-dependent regulation of catabolic and enterotoxin genes in Bacillus cereus F4430/73

Abstract

We had previously demonstrated that Fnr is required for fermentative growth and oxic production of hemolysin BL (Hbl) and non-hemolytic enterotoxin (Nhe) in the food-borne pathogen Bacillus cereus F4430/73. In the present work, the regulatory impact of Fnr on microaerobic growth and enterotoxin production in response to carbohydrates was examined using glucose, fructose, sucrose or a glucose–fructose mixture as carbon and energy sources. Growth parameters, byproduct spectra and transcription levels of catabolic and enterotoxin genes were analyzed in a strain lacking Fnr in comparison to the parental F4430/73 strain. The results showed that B. cereus prefers glucose to other carbohydrates for microaerobic growth, and that lacking of Fnr less strongly affected the respiro-fermentative catabolism of glucose than fructose and, to a lesser extent than sucrose. In addition, lacking of Fnr strongly decreased expression of hbl and nhe genes, leading to the absence of Hbl and low production of Nhe independently of the carbohydrate used as carbon source. We conclude that Fnr is an important element for carbon source regulation in B. cereus F4430/73 and that the regulation of enterotoxin gene expression in response to carbohydrates may represent one aspect of overall catabolite control mediated by Fnr

Dates and versions

hal-02668377 , version 1 (31-05-2020)

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Kahina Messaoudi, Thierry Clavel, Philippe Schmitt, Catherine Duport. Fnr mediates carbohydrate-dependent regulation of catabolic and enterotoxin genes in Bacillus cereus F4430/73. Research in Microbiology, 2010, 161 (1), pp.30-39. ⟨10.1016/j.resmic.2009.11.003⟩. ⟨hal-02668377⟩
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