HpaB-Dependent Secretion of Type III Effectors in the Plant Pathogens Ralstonia solanacearum and Xanthomonas campestris pv. vesicatoria

Abstract

Plant pathogenic bacteria exerts their pathogenicity through the injection of large repertoires of type III effectors (T3Es) into plant cells, a mechanism controlled in part by type III chaperones (T3Cs). In Ralstonia solanacearum, the causal agent of bacterial wilt, little is known about the control of type III secretion at the post-translational level. Here, we provide evidence that the HpaB and HpaD proteins do act as bona fide R. solanacearum class IB chaperones that associate with several T3Es. Both proteins can dimerize but do not interact with each other. After screening 38 T3Es for direct interactions, we highlighted specific and common interacting partners, thus revealing the first picture of the R. solanacearum T3C-T3E network. We demonstrated that the function of HpaB is conserved in two phytopathogenic bacteria, R. solanacearum and Xanthomonas campestris pv. vesicatoria (Xcv). HpaB from Xcv is able to functionally complement a R. solanacearum hpaB mutant for hypersensitive response elicitation on tobacco plants. Likewise, Xcv is able to translocate a heterologous T3E from R. solanacearum in an HpaB-dependent manner. This study underlines the central role of the HpaB class IB chaperone family and its potential contribution to the bacterial plasticity to acquire and deliver new virulence factors.

Identification of RipAZ1 as an avirulence determinant of Ralstonia solanacearum in Solanum americanum

“…The number of surviving plants was counted on a daily basis. Plants with complete wilting were considered dead (Lonjon et al, 2017). The percentage of survival was plotted using the Kaplan–Meier survival analysis with log‐rank (Mantel–Cox) test.…”

Host–Pathogen Interactions between Xanthomonas fragariae and Its Host Fragaria × ananassa Investigated with a Dual RNA-Seq Analysis

“…This transcription factor is an expression activator of the T3SS encoding genes and T3E genes [59]. Two additional T3SS regulation factors, hpa1 and hpaB (hypersensitive response and pathogenicity associated), reported to influence virulence with the host [58,60], were found to be more expressed at 12 dpi. While comparing with the change of expression of these genes between bacteria growing on microbiological medium and in planta, expression of all of them was significantly higher in strawberry plants 15 days after inoculation, which confirms that the T3SS is important in the early stage of infection [61].…”

HrpB7 from Xanthomonas campestris pv. vesicatoria is an essential component of the type III secretion system and shares features of HrpO/FliJ/YscO family members

“…Notably, an interaction with T3S chaperones was also described for FliJ, Spa13, and InvI, suggesting that HrpO/FliJ/YscO family members are involved in a network of interactions with T3SS components and chaperones (Evans et al, ; Evans & Hughes, ). In Xcv , the T3S chaperone HpaB is essential for the efficient secretion and translocation of multiple effector proteins and was previously identified as interaction partner of T3SS components including the ATPase, the C ring, and the cytoplasmic domains of components of the export apparatus (Büttner et al, ; Büttner et al, ; Hartmann & Büttner, ; Lonjon et al, ; Lorenz & Büttner, ; Lorenz et al, ; Prochaska et al, ). The presence of multiple binding sites for HpaB in the T3SS suggests that HrpB7 does not play an exclusive role in the recruitment of chaperone complexes but might rather be of general importance for T3S.…”

“…Hrc and Hrp proteins are essential for T3S as structural components, whereas the accessory Hpa (Hrp associated) proteins are often involved in the control of T3S. One example is the T3S chaperone HpaB, which binds to type III effectors and presumably targets them to the T3S ATPase (Büttner et al, 2004;Büttner et al, 2006;Lonjon et al, 2017;Lorenz & Büttner, 2009;Prochaska et al, 2018;Scheibner et al, 2018). HpaB contributes to the translocation of most effector proteins and is, therefore, essential for pathogenicity.…”