Diverse AvrPtoB Homologs from SeveralPseudomonas syringaePathovars Elicit Pto-Dependent Resistance and Have Similar Virulence Activities

Abstract

AvrPtoB is a type III effector protein from Pseudomonas syringae pv. tomato that physically interacts with the tomato Pto kinase and, depending on the host genotype, either elicits or suppresses programmed cell death associated with plant immunity. We reported previously that avrPtoB-related sequences are present in diverse gram-negative phytopathogenic bacteria. Here we describe characterization of avrPtoB homologs from P. syringae pv. tomato T1, PT23, and JL1065, P. syringae pv. syringae B728a, and P. syringae pv. maculicola ES4326. The avrPtoB homolog from P. syringae pv. maculicola, hopPmaL, was identified previously. The four new genes identified in this study are designated avrPtoB T1 , avrPtoB PT23 , avrPtoB JL1065 , and avrPtoB B728a . The AvrPtoB homologs exhibit 52 to 66% amino acid identity with AvrPtoB. Transcripts of each of the avrPtoB homologs were detected in the Pseudomonas strains from which they were isolated. Proteins encoded by the homologs were detected in all strains except P. syringae pv. tomato T1, suggesting that T1 suppresses accumulation of AvrPtoB T1 . All of the homologs interacted with the Pto kinase in a yeast two-hybrid system and elicited a Pto-dependent defense response when they were delivered into leaf cells by DC3000⌬avrPto⌬avrPtoB, a P. syringae pv. tomato strain with a deletion of both avrPto and avrPtoB. Like AvrPtoB, all of the homologs enhanced the ability of DC3000⌬avrPto⌬avrPtoB to form lesions on leaves of two susceptible tomato lines. With the exception of HopPmaL which lacks the C-terminal domain, all AvrPtoB homologs suppressed programmed cell death elicited by the AvrPto-Pto interaction in an Agrobacterium-mediated transient assay. Thus, despite their divergent sequences, AvrPtoB homologs from diverse P. syringae pathovars have conserved avirulence and virulence activities similar to AvrPtoB activity.

RD19, anArabidopsisCysteine Protease Required for RRS1-R–Mediated Resistance, Is Relocalized to the Nucleus by theRalstonia solanacearumPopP2 Effector

“…However, the possibility that other unknown host factors mediate interaction between the three proteins cannot be ruled out. Some bacterial type III effectors do indeed target multiple host components (Belkhadir et al, 2004;Chisholm et al, 2006;Grant et al, 2006;Lin et al, 2006), and some additional PopP2-interacting candidate proteins from Arabidopsis currently under investigation were recently identified (M. Bernoux, C. Tasset, Y. Marco, and L. Deslandes, unpublished data). Contribution of these additional PopP2-interacting host factors to the full perception of PopP2 by RRS1-R could then explain the partial loss of resistance of the rd19 mutant in response to Ralstonia infection.…”

Natural Variation in the Pto Disease Resistance Gene Within Species of Wild Tomato (Lycopersicon). II. Population Genetics of Pto

“…AvrPto can suppress the cell death response to nonhost pathogens (Kang et al 2004) and suppresses cell-wall-based defense in Arabidopsis (Hauck et al 2003). Likewise, AvrPtoB, which encodes an E3 ubiquitin ligase, is capable of suppressing programmed cell death in Nicotiana benthamiana (Abramovitch et al 2003;Jamir et al 2004;Lin et al 2006). AvrPtoB is a homolog of a gene encoding another well-characterized virulence factor, VirPphA, and when AvrPtoB is expressed in a disabled strain of P.s.…”

Tomato GOLDEN2-LIKE Transcription Factors Reveal Molecular Gradients That Function during Fruit Development and Ripening

“…The full-length sequences of GLK1 and GLK2 cDNA were cloned into pBI121 (Clontech) and pBTEX (Lin et al, 2006) vectors digested with SmaI/SacI and SmaI/SalI, respectively, under the control of the cauliflower mosaic virus 35S promoter. The fidelity of the construct was confirmed by DNA sequencing and transgenic 'Ailsa Craig' (U/U) and 'M82' (u/u) tomato plants were generated by Agrobacterium tumefaciens-mediated (strain LBA4404) transformation using previously described methods (Fillatti et al, 1987).…”