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Brassinosteroid Signaling in Plant Immune System

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Part of the book series: Signaling and Communication in Plants ((SIGCOMM,volume 2))

Abstract

Brassinosteroids (BRs) are growth-promoting steroidal hormones in plants; they are also involved in plant innate immunity. BR signals are perceived by the plasma membrane receptors BRI1 and co-receptor BAK1. Several positive (BSK1, BSU1, PP2A, CDG1) and negative (BKI1, BIN2, MSBP1, and 14-3-3) regulators of BR signaling control the activities of BZR1 and BES1 family of transcription factors, which regulate the expression of hundreds to thousands of genes for various BR responses. BRs either positively or negatively regulate plant innate immunity. Pathogen infection results in elevation of BR signal processing. BR triggers disease resistance against some pathogens. BAK1 is a key component in BR signaling pathway. It may be involved in triggering plant disease resistance by modulating JA signaling system. BR may also induce susceptibility. BR negates disease conferred by the SA synthetic analog benzothiadiazole, suggesting negative crosstalk between BR and SA signaling pathways. BR-mediated suppression of SA defenses occurs downstream of SA biosynthesis, but upstream of NPR1 and OsWRKY45 in the SA signaling pathway. BR triggers the expression of GA repressor proteins and suppresses GA-induced defense responses. BR signaling may also negatively regulate PAMP-triggered immunity. Enhanced BR signaling resulting from either a gain-of-function mutation in BAK1, ectopic expression of BRI1, or application of BR impedes immunity triggered by the PAMP. Crosstalk between PAMP–PRR signaling and BR synthesis pathway has been reported. BRI1–BAK signaling modulates PAMP–PRR signaling pathway. Increased BR signaling triggered by BRI1 overexpression antagonized the activities of the PAMPs/MAMPs flg22, elf18, and PGN that increased BR signaling. The bHLH transcription factor HBI1 is a positive regulator of BR-triggered resistance. HBI1 has been found to be a negative regulator of PAMP-triggered immunity (PTI). HBI1 overexpression led to reduced PAMP-triggered responses. This inhibition was found to be correlated with reduced steady-state expression of immune marker genes, leading to increased susceptibility to Pseudomonas syringae in Arabidopsis thaliana. Activation of the BRI1 pathway leads to inhibition of PAMP-triggered immunity (PTI). Pathogens may exploit BRs as virulence factors and hijack the plant BR machinery to cause disease. An oomycete pathogen has been shown to co-opt the plant BR machinery as a decoy strategy to tap into the immune signaling circuitry and interfere with effectual SA- and GA-controlled defenses.

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Vidhyasekaran, P. (2015). Brassinosteroid Signaling in Plant Immune System. In: Plant Hormone Signaling Systems in Plant Innate Immunity. Signaling and Communication in Plants, vol 2. Springer, Dordrecht. https://doi.org/10.1007/978-94-017-9285-1_9

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