Novel Roles of SoxR, a Transcriptional Regulator from X anthomonas campestris, in Sensing Redox-Cycling Drugs and Regulating a Protective Gene That Have Overall Implications for Bacterial Stress Physiology and Virulence on a Host Plant

Abstract

In Xanthomonas campestris pv. campestris, SoxR likely functions as a sensor of redox-cycling drugs and as a transcriptional regulator. Oxidized SoxR binds directly to its target site and activates the expression of xcc0300, a gene that has protective roles against the toxicity of redox-cycling compounds. In addition, SoxR acts as a noninducible repressor of its own expression. X. campestris pv. campestris requires SoxR both for protection against redox-cycling drugs and for full virulence on a host plant. The X. campestris model of the gene regulation and physiological roles of SoxR represents a novel variant of existing bacterial SoxR models.

Transcriptional regulation of bacterial virulence gene expression by molecular oxygen and nitric oxide

“…102 The SoxRS and SoxR systems have been associated with fluoroquinolone resistance in Salmonella serovars, the ability of P. aeruginosa to survive in macrophages, cause systemic infections following burn wounds and cause pulmonary infections, and virulence of Vibrio vulnificus and Xanthomonas campestris. [103][104][105][106][107] SoxR is a homodimeric, MerR family protein. 107 Each monomer has a cluster of four cysteine residues (Cys-X 2 -Cys-X-Cys-X 5 -Cys) that binds a solvent-exposed [2Fe-2S] 1C center in an asymmetric electrostatic environment.…”

Copper chloride induces antioxidant gene expression but reduces ability to mediate H2O2 toxicity in Xanthomonas campestris

“…H 2 O 2 can further activate genes in the OxyR regulon via oxidation of OxyR. Furthermore, Xcc contains five putative open reading frames homologous to SOD, none of which are regulated by SoxR, the superoxide anion/redox cycling drug sensor and transcriptional regulator (Mahavihakanont et al, 2012).…”

“…We hypothesized that if superoxide radicals, H 2 O 2 , and ROOH are generated by CuCl 2 treatment, high levels of oxidant-scavenging enzymes SOD (a superoxide scavenger), catalase (an H 2 O 2 scavenger), and alkyl hydroperoxide reductase (an ROOH scavenger) should lower the magnitude of induction of sufB (an IscR-regulated gene), ahpC (an OxyR-regulated gene) and ohr (an OhrRregulated gene), respectively, in CuCl 2 -treated cells. Similar rationales have been used to differentiate the major ROS responsible for activation of transcriptional regulators (Gu & Imlay, 2011;Mahavihakanont et al, 2012). Hence, copper induction experiments were repeated in Xcc wild-type strain harbouring pSodBI (Saenkham et al, 2007), pKatG (Jittawuttipoka et al, 2009) and pAhpCF (Charoenlap et al, 2005).…”

“…However, sodium hypochlorite-mediated inactivation of OhrR has been reported (Chi et al, 2011). Although X. campestris possesses SoxR, it appears that this transcriptional regulator senses redox-active drugs rather than superoxide anions (Mahavihakanont et al, 2012).…”

“…Ohr (organic hydroperoxide reductase), whose expression is controlled by OhrR, is upregulated in cells challenged with ROOH and sodium hypochlorite (Chi et al, 2011;Panmanee et al, 2006). Some of these genes, including katA, katG, oxyR and soxR, are required for full virulence of this phytopathogen (Charoenlap et al, 2011;Jittawuttipoka et al, 2009;Mahavihakanont et al, 2012). OxyR and OhrR are thiolbased redox sensors and transcriptional regulators; peroxide activation of OxyR and deactivation of OhrR occur via the oxidation of a thiol group of the sensing cysteine residue and subsequent disulfide bond formation.…”