Abstract
Plants need to finely balance resources allocated to growth and immunity to achieve optimal fitness. A tradeoff between pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and brassinosteroid (BR)-mediated growth was recently reported, but more information about the underlying mechanisms is needed. Here, we identify the basic helix-loop-helix (bHLH) transcription factor homolog of brassinosteroid enhanced expression2 interacting with IBH1 (HBI1) as a negative regulator of PTI signaling in Arabidopsis (Arabidopsis thaliana). HBI1 expression is down-regulated in response to different PAMPs. HBI1 overexpression leads to reduced PAMP-triggered responses. This inhibition correlates with reduced steady-state expression of immune marker genes, leading to increased susceptibility to the bacterium Pseudomonas syringae. Overexpression of the HBI1-related bHLHs brassinosteroid enhanced expression2 (BEE2) and cryptochrome-interacting bHLH (CIB1) partially inhibits immunity, indicating that BEE2 and CIB1 may act redundantly with HBI1. In contrast to its expression pattern upon PAMP treatment, HBI1 expression is enhanced by BR treatment. Also, HBI1-overexpressing plants are hyperresponsive to BR and more resistant to the BR biosynthetic inhibitor brassinazole. HBI1 is nucleus localized, and a mutation in a conserved leucine residue within the first helix of the protein interaction domain impairs its function in BR signaling. Interestingly, HBI1 interacts with several inhibitory atypical bHLHs, which likely keep HBI1 under negative control. Hence, HBI1 is a positive regulator of BR-triggered responses, and the negative effect of PTI is likely due to the antagonism between BR and PTI signaling. This study identifies a novel component involved in the complex tradeoff between innate immunity and BR-regulated growth.
Highlights
Plants need to finely balance resources allocated to growth and immunity to achieve optimal fitness
BOTRYTIS-INDUCED KINASE1 (BIK1) associates with CHITIN ELICITOR RECEPTOR KINASE1 (CERK1) and is required for chitininduced responses (Zhang et al, 2010), indicating that BIK1 may be the first convergent component shared by the FLS2, ELONGATION FACTOR TU RECEPTOR (EFR), and CERK1 pathways, which lead to largely overlapping transcriptional changes (Wan et al, 2008)
We initially focused on At2g18300, which encodes the putative basic helix-loophelix (bHLH) transcription factor
Summary
Plants need to finely balance resources allocated to growth and immunity to achieve optimal fitness. Similar to the role of BIK1 in the FLS2/EFR pathways (Lu et al, 2010; Zhang, et al, 2010), BR binding leads to the phosphorylation-mediated activation and release of the receptor-like cytoplasmic kinases BRASSINOSTEROID SIGNALING KINASES (BSKs) and CONSTITUTIVE DIFFERENTIAL GROWTH1 (CDG1) from the BRI1-BAK1 complex (Clouse, 2011; Kim et al, 2011). BIN2 acts as a central negative regulator of BR signaling by phosphorylating the basic helix-loop-helix (bHLH) transcription factors BRASSINAZOLE-RESISTANT1 (BZR1) and BZR2/ BRI1-ETHYL METHANESULFONATE-SUPPRESSOR1 (BES1) that are master switches of BR-mediated responses (Clouse, 2011; Kim et al, 2011). While it is currently clear that activation of the BR pathway has an inhibitory effect on PTI signaling, the actual mechanisms underlying or regulating this antagonism are still unclear (Vert and Chory, 2011; Choudhary et al, 2012; Wang et al, 2012)
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