Skip to main content
. 2021 May 29;44:102012. doi: 10.1016/j.redox.2021.102012

Fig. 1.

Fig. 1

GSH induction of virulence genes during B. pseudomallei, L. monocytogenes and P. aeruginosa infection

(a) In B. pseudomallei, exogenous GSH reduces VirA, a histidine kinase sensor present on the bacterial inner membrane. Reduction of cysteine residue 62 (C62), predicted to be present at the periplasm, results in a switch from a dimer into a monomeric form. Monomeric VirA activates T6SS5 gene expression via its cognate DNA response regulator VirG.

(b) In L. monocytogenes, exogenous GSH drives gshF expression by an unknown mechanism and increases bacterial GSH synthesis. Exogenous GSH and bacterial synthesized GSH binds allosterically to master virulence regulator PrfA. GSH binding stabilizes PrfA in an active confirmation which primes PrfA for DNA binding. Active PrfA activates the transcription of PrfA-regulated genes (PRGs).

(c) In P. aeruginosa, bacterial synthesized GSH reduces all 5 cysteine residues (cysteine residues at position 20, 38, 97, 156, and 183) on global transcription factor Vfr. Reduced Vfr activates exsA gene transcription. ExsA, in turn, regulates T3SS expression.