The metabolic enzyme fructose-1,6-bisphosphate aldolase acts as a transcriptional regulator in pathogenic Francisella

Jason Ziveri, Fabiola Tros, Ida Chiara Guerrera, Cerina Chhuon, Mathilde Audry, Marion Dupuis, Monique Barel, Sarantis Korniotis, Simon Fillatreau, Lara Gales, Edern Cahoreau and Alain Charbit ()
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Jason Ziveri: Université Paris Descartes, Sorbonne Paris Cité
Fabiola Tros: Université Paris Descartes, Sorbonne Paris Cité
Ida Chiara Guerrera: Université Paris Descartes, Sorbonne Paris Cité
Cerina Chhuon: Université Paris Descartes, Sorbonne Paris Cité
Mathilde Audry: Université Paris Descartes, Sorbonne Paris Cité
Marion Dupuis: Université Paris Descartes, Sorbonne Paris Cité
Monique Barel: Université Paris Descartes, Sorbonne Paris Cité
Sarantis Korniotis: Université Paris Descartes, Sorbonne Paris Cité
Simon Fillatreau: Université Paris Descartes, Sorbonne Paris Cité
Lara Gales: Université de Toulouse, CNRS, INRA, INSA
Edern Cahoreau: Université de Toulouse, CNRS, INRA, INSA
Alain Charbit: Université Paris Descartes, Sorbonne Paris Cité

Nature Communications, 2017, vol. 8, issue 1, 1-15

Abstract: Abstract The enzyme fructose-bisphosphate aldolase occupies a central position in glycolysis and gluconeogenesis pathways. Beyond its housekeeping role in metabolism, fructose-bisphosphate aldolase has been involved in additional functions and is considered as a potential target for drug development against pathogenic bacteria. Here, we address the role of fructose-bisphosphate aldolase in the bacterial pathogen Francisella novicida. We demonstrate that fructose-bisphosphate aldolase is important for bacterial multiplication in macrophages in the presence of gluconeogenic substrates. In addition, we unravel a direct role of this metabolic enzyme in transcription regulation of genes katG and rpoA, encoding catalase and an RNA polymerase subunit, respectively. We propose a model in which fructose-bisphosphate aldolase participates in the control of host redox homeostasis and the inflammatory immune response.

Date: 2017
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DOI: 10.1038/s41467-017-00889-7

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