Abstract
Sensing of pathogen infection by plants elicits early signals that are transduced to affect defense mechanisms, such as effective blockage of pathogen entry by regulation of stomatal closure, cuticle, or callose deposition, change in water potential, and resource acquisition among many others. Pathogens, on the other hand, interfere with plant physiology and protein functioning to counteract plant defense responses. In plants, hormonal homeostasis and signaling are tightly regulated; thus, the phytohormones are qualified as a major group of signaling molecules controlling the most widely tinkered regulatory networks of defense and counter-defense strategies. Notably, the phytohormone jasmonic acid mediates plant defense responses to a wide array of pathogens. In this review, we present the synopsis on the jasmonic acid metabolism and signaling, and the regulatory roles of this hormone in plant defense against the hemibiotrophic bacterial pathogen Pseudomonas syringae. We also elaborate on how this pathogen releases virulence factors and effectors to gain control over plant jasmonic acid signaling to effectively cause disease. The findings discussed in this review may lead to ideas for the development of crop cultivars with enhanced disease resistance by genetic manipulation.
Highlights
An incidence of virulent pathogen infection in a plant, which is incapable of surmounting effective immune responses, leads to the appearance of plant disease
CORONATINE INSENSITIVE 1 (COI1) receptor and JASMONATE ZINC-FINGER EXPRESSED IN INFLORESCENCE MERISTEM (ZIM)-DOMAIN (JAZ) proteins are the integral components of the Jasmonic acid (JA) signaling [29,30]
COI1, CORONATINE INSENSITIVE 1 receptor; EIL1, ETHYLENE-INSENSITIVE 3-LIKE 1; EIN3, ETHYLENE-INSENSITIVE 3; ERF, ETHYLENE RESPONSE FACTOR; general TFs (GTFs), general transcription factors; HAC1, HISTONE ACETYLTRANSFERASE OF THE CBP FAMILY 1; HDA, HISTONE DEACETYLASE; InsP5, inositol pentakisphosphate; JA-Ile, isoleucine conjugated jasmonate; JAT1, JASMONATE TRANSPORTER 1; JAZ, JASMONATE ZINC-FINGER EXPRESSED IN INFLORESCENCE MERISTEM (ZIM)-DOMAIN PROTEIN; MED25, a subunit of the MEDIATOR transcriptional co-activator complex; MYC, MYELOCYTOMATOSIS; NINJA, NOVEL INTERACTOR OF JAZ; ORA59, OCTADECANOID-RESPONSIVE ARABIDOPSIS AP2 (APETALA2)/ERF59; PDF1.2, PLANT DEFENSIN 1.2; RNA Pol II, RNA POLYMERASE II; TPL, TOPLESS; TPR, TPL-RELATED proteins; VSP2, VEGETATIVE STORAGE PROTEIN 2
Summary
An incidence of virulent pathogen infection in a plant, which is incapable of surmounting effective immune responses, leads to the appearance of plant disease. JAs suppress plant resistance responses against biotrophic and hemibiotrophic pathogens, while salicylic acid (SA) is known to promote effective disease resistance responses to these pathogens [3,4]. This antagonism between SA and JAs has been further supported by studies in Arabidopsis thaliana where the SA-mediated signaling is noted to suppress the JA signaling, thereby protecting plants against biotrophic or hemibiotrophic pathogen infections [2,3,5,6]. The regulatory roles of JAs in plant resistance responses under biotrophic and hemibiotrophic pathogen infections appear to be very enigmatic. This review encompasses the regulatory roles of JAs in plant immunity, by mostly reviewing the latest literature on the infections of P. syringae in various plant species
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