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// Workers AI · dad joke modeWhat did catabolite repressor say? I'm suppressing my appetite.

From Wikipedia, the free encyclopedia

Bacterial transcription factor

Catabolite repressor/activator (Cra), formerly known as fructose repressor FruR. It is a transcription factor found in enteric bacteria such as Escherichia coli and Salmonella. Its function is to control the use of carbon sources by bacteria by repressing some genes and activating others.[1]

Function

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Cra can act both as a repressor and an activator of gene expression. Its main function is to regulate genes that participate in bacterial metabolism and help bacteria adapt to the nutrients available.[1]

Role in carbon metabolism

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Cra regulates the flow of carbon in various metabolic pathways. It down-regulates some genes that participate in glycolysis and up-regulates genes involved in other metabolic pathways, such as the tricarboxylic acid cycle and gluconeogenesis.[2]

Effector binding

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Effectors are the small sugar molecules that control the activity of Cra. The protein changes shape and releases the DNA it was bound to after an effector binds to Cra, so its target genes are no longer repressed or activated.[1] Over the years, fructose-1-phosphate (F1P) and fructose-1,6-bisphosphate (FBP) were thought to act as effectors of Cra.[3] One study suggested that by responding to FBP levels in the cell, Cra works as a sensor of how fast glycolysis is running.[4] However, later research found that FBP does not directly control it and F1P is the real effector of Cra.[5]

Comparison with other systems

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Bacteria use different mechanisms for regulating carbon metabolism. In enteric bacteria, the main system uses the cAMP receptor protein (CRP) and Cra works alongside it, while in other bacteria, including most Firmicutes, a protein called CcpA is used.[6]

References

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  1. 1 2 3 Saier, M H; Ramseier, T M (June 1996). "The catabolite repressor/activator (Cra) protein of enteric bacteria". Journal of Bacteriology. 178 (12). American Society for Microbiology: 3411–3417. doi:10.1128/jb.178.12.3411-3417.1996. PMC 178107. PMID 8655535.
  2. ↑ Ramseier, T.M. (July 1996). "Cra and the control of carbon flux via metabolic pathways". Research in Microbiology. 147 (6–7): 489–493. doi:10.1016/0923-2508(96)84003-4. ISSN 0923-2508.
  3. ↑ Huang, Ying; Jia, Kai-Zhi; Zhao, Wei; Zhu, Li-Wen (November 2024). "Insights into the regulatory mechanisms and application prospects of the transcription factor Cra". Applied and Environmental Microbiology. 90 (11). American Society for Microbiology: e01228–24. doi:10.1128/aem.01228-24. PMC 11577769. PMID 39494897.
  4. ↑ Kochanowski, Karl; Volkmer, Benjamin; Gerosa, Luca; Haverkorn van Rijsewijk, Bart R.; Schmidt, Alexander; Heinemann, Matthias (January 2013). "Functioning of a metabolic flux sensor in Escherichia coli". Proceedings of the National Academy of Sciences. 110 (3): 1130–1135. doi:10.1073/pnas.1202582110. PMC 3549114. PMID 23277571.
  5. ↑ Bley Folly, Brenda; Ortega, Alvaro D.; Hubmann, Georg; Bonsing-Vedelaar, Silke; Wijma, Hein J.; van der Meulen, Pieter; Milias-Argeitis, Andreas; Heinemann, Matthias (2018). "Assessment of the interaction between the flux-signaling metabolite fructose-1,6-bisphosphate and the bacterial transcription factors CggR and Cra". Molecular Microbiology. 109 (3): 278–290. doi:10.1111/mmi.14008. ISSN 1365-2958.
  6. ↑ Görke, Boris; Stülke, Jörg (August 2008). "Carbon catabolite repression in bacteria: many ways to make the most out of nutrients". Nature Reviews Microbiology. 6 (8). Nature Publishing Group: 613–624. doi:10.1038/nrmicro1932. ISSN 1740-1534.