Abstract

In plants, activation of growth and activation of immunity are opposing processes that define a trade-off. In the past few years, the growth-promoting hormones brassinosteroids (BR) have emerged as negative regulators of pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI), promoting growth at the expense of defense. The crosstalk between BR and PTI signaling was described as negative and unidirectional, since activation of PTI does not affect several analyzed steps in the BR signaling pathway. In this work, we describe that activation of PTI by the bacterial PAMP flg22 results in the reduced expression of BR biosynthetic genes. This effect does not require BR perception or signaling, and occurs within 15 min of flg22 treatment. Since the described PTI-induced repression of gene expression may result in a reduction in BR biosynthesis, the crosstalk between PTI and BR could actually be negative and bidirectional, a possibility that should be taken into account when considering the interaction between these two pathways.

Highlights

  • Plants need to integrate multiple environmental signals to finely regulate their growth and development in an adaptive manner

  • As part of these transcriptional changes, we observed that flg22 treatment consistently results in down-regulation of the BR marker gene CPD, which encodes a protein involved in BR biosynthesis (Szekeres et al, 1996; Table 1)

  • Activation of PAMP-triggered immunity (PTI) signaling was achieved by exogenous flg22 treatment, within a time scale of min to very few hours, and any potential longer-term effect of this pathway could have gone unnoticed

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Summary

Introduction

Plants need to integrate multiple environmental signals to finely regulate their growth and development in an adaptive manner. In the absence of pathogen challenge, growth is prioritized over defense; upon detection of a pathogen, defense responses are initiated, at the expense of growth. This trade-off between growth and defense is regulated at multiple levels, and its control has been shown to depend on the action of several plant hormones, including jasmonates, gibberellins, brassinosteroids (BR), and salicylic acid (Navarro et al, 2008; Albrecht et al, 2012; Belkhadir et al, 2012; Yang et al, 2012; Lozano-Durán et al, 2013; Chandran et al, 2014; Fan et al, 2014; Malinovsky et al, 2014). The growth-promoting hormones BR can inhibit PTI: activation

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