Role of Plant Immune Signals and Signaling Systems in Plant Pathogenesis

Abstract

Plants possess innate immune system to resist pathogen attack. Innate immunity is the first line of defense against invading microorganisms. Pathogens possess pathogen-associated molecular patterns (PAMPs). The PAMPs are primary danger/alarm signal molecules to switch on the plant immune systems. PAMPs are evolutionarily conserved building blocks of microbial surfaces that directly bind to plant pattern recognition receptors (PRRs). Plants use the PRRs to defend themselves from microbial pathogens. The PRRs are localized at the plasma membrane and the PAMPs activate expression of the genes encoding various PRRs. When activated by the PAMP, the PRR is translocated to endocytic compartments and endocytosis of the PRR is important for activation of several downstream signaling events. The plant immune system uses several second messengers to encode information generated by the PAMPs and deliver the information downstream of PRRs to proteins which decode and interpret the signals and initiate defense gene expression. G-proteins act as molecular switches in signal transduction system. Calcium ion is an important intracellular second messenger and carries the PAMP signal downstream to initiate immune responses. Reactive oxygen species (ROS) serve as second messengers transmitting the message. ROS appears to interact with various defense signaling systems. It plays a central role in launching the defense response. Nitric oxide (NO) is a diffusible molecular messenger that plays an important role in plant immune response signal transduction. Mitogen-activated protein kinase (MAPK) cascades are major pathways downstream of PAMP/PRR signaling complex that transduce extracellular stimuli into intracellular responses in plants. The plant hormones salicylic acid (SA), jasmonates (JA), ethylene (ET), abscisic acid (ABA), auxin (AUX), cytokinin (CK), gibberellin (GA), and brassinosteroid (BR) play important role in intercellular and systemic signaling systems triggering expression of various defense-responsive genes. SA signaling is involved in triggering systemic acquired resistance (SAR). SAR is associated with priming of defense responses and the priming results in a faster and stronger induction of defense responses after pathogen attack. The priming can be inherited epigenetically and descendants of primed plants exhibit next-generation systemic acquired resistance. Thus when pathogens land on the plant surface, the PAMPs trigger highly complex defense responses against the pathogens and suppress disease development. However virulent pathogen may modify its PAMP structure during its pathogenesis to reduce its elicitor activity. Virulent pathogens may also contain inefficient PAMPs and trigger subdued defense responses favoring disease development. The reduced activity of PAMPs might facilitate the virulent pathogens to cause disease. Besides PAMP molecules, pathogens produce effectors, which play an important role in pathogenesis. Effectors specifically contribute to virulence of pathogens by targeting host plant innate immunity. The effectors secreted by various pathogens have been shown to suppress the PAMP-triggered immunity. Effectors disrupt binding of PAMP with PRR in the PAMP-PRR signaling complex. Effectors may promote ubiquitin-proteasome-mediated degradation of PRRs to impede PAMP-triggered plant immunity. Effectors have been shown to target the receptor kinase activity of the PRRs and inhibit the kinase activity to block PAMP-triggered immunity. Autophosphorylation of PRRs results in activation of PRRs and the effectors may inhibit the autophosphorylation of PRRs to suppress the PAMP-triggered immune system. Some effectors have been shown to block the action of the PRR signal amplifier BAK1. Several receptor-like cytoplasmic kinases (RLCK) including BIK1, PBS1, and PBS1-like (PBL) proteins play important role in regulation of the signaling pathways downstream of PAMP-PRR-BAK1 signaling complex and the effectors have been shown to block the action of these RLCKs. Effectors may also suppress the MAPK signaling cascade triggered by PAMPs. Effectors have been shown to suppress SA signaling system, which is involved in triggering defense responses against a broad range of plant pathogens. Pathogens may induce specific signaling systems, which may favor disease development. Pathogen hijacks ABA signaling system to suppress SA-mediated defense responses promoting disease development. JA signaling system has been reported to confer susceptibility against some pathogens and pathogens may hijack JA signaling system to cause disease. Necrotrophic pathogens use SA signaling pathway to promote disease development by suppressing JA signaling pathway. Auxin signaling system has been shown to be involved in promoting susceptibility to pathogens and inducing disease development. Pathogens hijack the host auxin metabolism leading to the accumulation of a conjugated form of the hormone, indole-3-acetic acid (IAA) – Asp, to promote disease development. Pathogens may hijack BR signaling machinery to interfere with effectual SA- and GA-controlled defenses. These studies suggest that various signals and signaling systems in plants modulate the pathogenesis inducing susceptibility and disease resistance and precise manipulation of these signaling systems will be an ideal tool to manage crop diseases.