Regulation of Bacterial Conjugation in Microaerobiosis by Host-Encoded Functions ArcAB and SdhABCD

Abstract

The virulence plasmid of Salmonella enterica (pSLT) is an F-like conjugative plasmid. High rates of pSLT transfer occur in the mammalian gut, a microaerobic environment. In this study, we describe genetic screens for host-encoded activators and repressors of the transfer operon (tra) of pSLT. We show that the transcription factor ArcA is an activator of conjugation, especially under microaerobiosis. In turn, succinate dehydrogenase (SdhABCD) is a repressor of mating in aerobiosis. ArcA binds upstream of the main tra promoter (p traY ) and activates tra transcription, as previously described in F, R1, and R100. In the absence of ArcA, transfer of pSLT decreased 7-fold in aerobiosis and .100-fold in microaerobiosis. In aerobiosis, ArcA activates the traY promoter in an ArcB-independent manner, as described in other F-like plasmids. In microaerobiosis, however, the ArcB sensor is necessary for activation of p traY . Lack of Sdh causes a .20-fold increase in pSLT transfer in aerobiosis, but has little effect under microaerobiosis. Sdh inhibits conjugal transfer by reducing traJ transcription, probably in an indirect manner. In turn, the sdhCDAB operon is repressed by the ArcAB system under microaerobiosis. Hence, the ArcAB twocomponent system of S. enterica stimulates pSLT transfer under microaerobiosis by two concerted actions: activation of the tra operon and repression of the sdhCDAB operon.

Silencing and activating type IV secretion genes of the F-like conjugative resistance plasmid R1

“…Transcription of the tra operon, including the T4S genes, starts at the P Y promoter ( Fig. 1) and depends on the plasmid encoded TraJ protein and on the host encoded two-component response-regulator ArcA as was shown for plasmids F, R1, R100 and pSLT (Camacho & Casadesú s, 2002;Serna et al, 2010;Silverman et al, 1991;Strohmaier et al, 1998;Taki et al, 1998). It has been proposed that TraJ F acts as a de-silencing protein that clears the P Y promoter from the nucleoid associated protein H-NS and thereby enables access of RNA polymerase (Will & Frost, 2006).…”

Bacterial Stress Responses during Host Infection

“…Upon a return to aerobic conditions, the cysteine residues are oxidized by ubiquinone to deactivate ArcA. ArcB/A also regulates conjugative transfer of the Salmonella pSLT virulence plasmid under microaerobic conditions by activating the traY promoter that controls the transfer operon (Serna et al, 2010). Interestingly, while ArcA in S. Typhimurium has been shown to regulate both metabolic and flagellar genes, some genes involved in virulence are repressed by ArcA, while others appear to be activated.…”

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

“…58 However, conjugal transfer of the Salmonella virulence plasmid pSLT occurs at high frequency in the gastrointestinal tract and is dependent on ArcBA. 59 In addition, ArcA has been shown to be a significant player in the regulation of: genes that are important for complement evasion in Haemophilus influenzae; the production of cholera toxin in Vibrio cholerae via regulation of toxT; and colonization of the porcine respiratory tract in A. pleuropneumoniae.…”