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CRP and Cra have Antagonistic Roles in the Regulation of the Fructose Operon in Vibrio cholerae
Author(s) -
Beck Christina,
Perry Sayde,
Liu Jane
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.02663
Subject(s) - vibrio cholerae , repressor , catabolite repression , biology , operon , camp receptor protein , activator (genetics) , lac operon , microbiology and biotechnology , gene , transcriptional regulation , genetics , escherichia coli , promoter , gene expression , bacteria , mutant
Vibrio cholerae , the causative agent of cholera, survives in both the human small intestine, where pathogenesis occurs, and aquatic reservoirs by adapting to changes in carbon source availability. In order to metabolize fructose, one of the most prevalent sugars in freshwater environments, V. cholerae must selectively produce the necessary metabolic machinery. Here, in studying how V. cholerae regulates fructose metabolism at the genetic level, we found that Cra (catabolite repressor/activator) and CRP (cAMP receptor protein), two well‐described transcriptional regulators in Escherichia coli , have antagonistic roles in regulating the expression of fruB , a member of the fructose operon fruBKA . Using transcriptional assays, qRT‐PCR, and western blot analysis to evaluate changes in gene expression, we found Cra to be a repressor of fruB and CRP to be an activator of fruB . We also found CRP to be a repressor of Cra, suggesting that CRP and Cra interact to affect downstream fruB expression. In order to further elucidate the mechanisms by which Cra and CRP regulate fruB expression, we are currently focusing our efforts on mapping the fruB promoter region. Although more remains to be understood about the relationship between the two regulators, this work has elucidated previously unknown roles of Cra and CRP in regulating fructose metabolism at the genetic level in this facultative pathogen. Support or Funding Information National Institutes of Health, The Camille and Henry Dreyfus Foundation