Abstract
Pseudomonas syringae pv tomato strain DC3000 (Pto) delivers several effector proteins promoting virulence, including HopM1, into plant cells via type III secretion. HopM1 contributes to full virulence of Pto by inducing degradation of Arabidopsis proteins, including AtMIN7, an ADP ribosylation factor-guanine nucleotide exchange factor. Pseudomonas syringae pv phaseolicola strain NPS3121 (Pph) lacks a functional HopM1 and elicits robust defenses in Arabidopsis thaliana, including accumulation of pathogenesis related 1 (PR-1) protein and deposition of callose-containing cell wall fortifications. We have examined the effects of heterologously expressed HopM1Pto on Pph-induced defenses. HopM1 suppresses Pph-induced PR-1 expression, a widely used marker for salicylic acid (SA) signaling and systemic acquired resistance. Surprisingly, HopM1 reduces PR-1 expression without affecting SA accumulation and also suppresses the low levels of PR-1 expression apparent in SA-signaling deficient plants. Further, HopM1 enhances the growth of Pto in SA-signaling deficient plants. AtMIN7 contributes to Pph-induced PR-1 expression. However, HopM1 fails to degrade AtMIN7 during Pph infection and suppresses Pph-induced PR-1 expression and callose deposition in wild-type and atmin7 plants. We also show that the HopM1-mediated suppression of PR-1 expression is not observed in plants lacking the TGA transcription factor, TGA3. Our data indicate that HopM1 promotes bacterial virulence independent of suppressing SA-signaling and links TGA3, AtMIN7, and other HopM1 targets to pathways distinct from the canonical SA-signaling pathway contributing to PR-1 expression and callose deposition. Thus, efforts to understand this key effector must consider multiple targets and unexpected outputs of its action.
Highlights
Microbes induce active plant defense responses, the elicitors of which can be divided into two classes, microbe/pathogen associated molecular patterns (MAMPs) and pathogen encoded effector proteins [1]
Since reduced pathogenesis related 1 (PR-1) secretion might be offset by reduced stability of nonsecreted pathogenesis related (PR)-1, we cannot rule out an effect of HopM1 on secretion of PR-1 or other defense cargo
We previously showed that SID2, which often is required for defenseassociated Salicylic acid (SA) production, is required for full pv phaseolicola strain NPS3121 (Pph)-induced PR-1 protein accumulation [35,38]
Summary
Microbes induce active plant defense responses, the elicitors of which can be divided into two classes, microbe/pathogen associated molecular patterns (MAMPs) and pathogen encoded effector proteins [1]. Effectors are pathogen-encoded molecules that perturb host processes to promote pathogen virulence, but are sometimes recognized by plant-encoded resistance (R) proteins. Defense responses induced upon activation of MAMP-receptors and Rproteins are similar with the latter typically being more rapid and robust and more frequently associated with host cell death called the hypersensitive response (HR) [3]. NPR1 activates the expression of genes involved in a defenseassociated protein secretion pathway through TL1 promoter elements [9]. NPR1 activates the expression of numerous pathogenesis related (PR) genes, including PR-1, by promoting the binding of TGA-family transcription factors to as-1 promoter elements [10]. Out of 10 TGA transcription factors in Arabidopsis, 7 have been found to interact with NPR1 [11]
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