Abstract
Rapid and complex immune responses are induced in plants upon pathogen recognition. One form of plant defense response is a programmed burst in transcription and translation of pathogenesis-related proteins, of which many rely on ER processing. Interestingly, several ER stress marker genes are up-regulated during early stages of immune responses, suggesting that enhanced ER capacity is needed for immunity. Eukaryotic cells respond to ER stress through conserved signaling networks initiated by specific ER stress sensors tethered to the ER membrane. Depending on the nature of ER stress the cell prioritizes either survival or initiates programmed cell death (PCD). At present two plant ER stress sensors, bZIP28 and IRE1, have been described. Both sensor proteins are involved in ER stress-induced signaling, but only IRE1 has been additionally linked to immunity. A second branch of immune responses relies on PCD. In mammals, ER stress sensors are involved in activation of PCD, but it is unclear if plant ER stress sensors play a role in PCD. Nevertheless, some ER resident proteins have been linked to pathogen-induced cell death in plants. In this review, we will discuss the current understanding of plant ER stress signaling and its cross-talk with immune signaling.
Highlights
In order to defend themselves against diseases, plants rely on early recognition of pathogens followed by fast responses to eliminate the attacker
Mitochondrial Outer Membrane Permeabilization (MOMP) is positively regulated by Bcl-2-Associated X/Bcl-2-Antagonist Killer (BAX/BAK), which are kept inactive by physically interacting with specific members of the B-cell lymphoma 2 (Bcl-2) family
PERK activation can induce the expression of miR-30c-2*, a microRNA that suppresses X-box Binding Protein1 (XBP1)-mediated gene expression, leading to cell death [86]. Another ER stress sensor Activating Transcription Factor 6 (ATF6), which is the functional homolog of plant Basic Leucine Zipper 28 (bZIP28), can control the expression of C/EBP Homologous Protein (CHOP) and overexpression of ATF6 enhances CHOP expression and promotes apopItnot.sJi.sM[o8l.7S]c.i.M201o5r, e16o,vpaegre,ApaTgeF6 has been demonstrated to trigger cell death in myoblast cells through expression inhibition of an anti-apoptotic protein Myeloid Cell Leukemia sequence 1 (Mcl-1) [88]
Summary
In order to defend themselves against diseases, plants rely on early recognition of pathogens followed by fast responses to eliminate the attacker. The basal layer of defense is activated by the presence of Microbe-Associated Molecular Patterns (MAMPs) in the apoplast. This layer of defense is referred to as MAMP Triggered Immunity (MTI) and protects the plant against non-specialized microorganisms. MAMPs are perceived by plasma membrane receptors, of which some dependent on maturation and ER protein folding quality control [2,3,4,5] Another ER-dependent basal defense response is the secretion of anti-microbial proteins to the apoplast [6]. In some cases specific effectors are directly or indirectly recognized by plant R proteins This recognition activates a second and more robust layer of immune response, termed Effector Triggered Immunity (ETI) [1]. We will present the current understanding of ER stress signaling in plants and highlight the cross-talk between the ER stress signaling pathways and immune responses
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