Secretion of early and late substrates of the type III secretion system from Xanthomonas is controlled by HpaC and the C-terminal domain of HrcU.
Bottom Line: T3S substrate specificity is controlled by HpaC, which promotes secretion of translocon and effector proteins but prevents efficient secretion of the early substrate HrpB2.The results of mutant studies showed that cleavage of HrcU contributes to pathogenicity and secretion of late substrates but is dispensable for secretion of HrpB2, which is presumably secreted prior to HrcU cleavage.As HrcU(Y318D) did not interact with HrpB2 and HpaC, we propose that the substrate specificity switch leads to the release of HrcU(C) -bound HrpB2 and HpaC.
Affiliation: Institute of Biology, Department of Genetics, Martin-Luther University Halle-Wittenberg, D-06099 Halle (Saale), Germany.Show MeSH
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Mentions: As HrcUY318D presumably mimics a protein conformation that is permissive for the secretion of late substrates, we investigated a possible influence of the Y318D mutation on the interaction of HrcUC with HrpB2 and HpaC. For this, GST, GST–HrcU255–357 and GST–HrcU255–357/Y318D were immobilized on glutathione sepharose and incubated with HrpB2-c-Myc and HpaC-c-Myc respectively. Figure 8A shows that HrpB2-c-Myc and HpaC-c-Myc co-eluted with GST–HrcU255–357 as expected but were not detectable in the eluate of GST–HrcU255–357/Y318D, suggesting that the Y318D mutation prevents the stable binding of both HrpB2 and HpaC to HrcUC. Given the finding that HrpB2 is oversecreted by strain 85*hrcUY318DΔhpaC, it is conceivable that the interaction of HrcUC and HrpB2 is not required for efficient HrpB2 secretion after the substrate specificity switch.
Affiliation: Institute of Biology, Department of Genetics, Martin-Luther University Halle-Wittenberg, D-06099 Halle (Saale), Germany.