Abstract

BackgroundThe transcription factor AtMYBR1 (MYB44) is a member of the MYB family of transcription factors and is expressed throughout the plant life cycle and especially in senescing and wounded leaves. It has previously been shown to be involved in responses to abiotic stress and is regulated by phosphorylation.ResultsWhen MYBR1 was over-expressed under the control of the constitutive 35S promoter in Arabidopsis thaliana (OxMYBR1), leaf senescence was delayed. In contrast loss-of-function mybr1 plants showed more rapid chlorophyll loss and senescence. The MYBR1 promoter strongly drove β-GLUCURONIDASE reporter gene expression in tissues immediately after wounding and many wounding/pathogenesis genes were downregulated in OxMYBR1. OxMYBR1 plants were more susceptible to injury under water stress than wildtype, which was correlated with suppression of many ABA inducible stress genes in OxMYBR1. Conversely, mybr1 plants were more tolerant of water stress and exhibited reduced rates of water loss from leaves. MYBR1 physically interacted with ABA receptor PYR1-LIKE8 (PYL8) suggesting a direct involvement of MYBR1 in early ABA signaling. MYBR1 appears to exhibit partially redundant functions with AtMYBR2 (MYB77) and double mybr1 X mybr2 mutants exhibited stronger senescence and stress related phenotypes than single mybr1 and mybr2 mutants.ConclusionsMYBR1 is a negative regulator of ABA, stress, wounding responses and blocks senescence. It appears to have a homeostatic function to maintain growth processes in the event of physical damage or stress.

Highlights

  • The transcription factor AtMYBR1 (MYB44) is a member of the MYB family of transcription factors and is expressed throughout the plant life cycle and especially in senescing and wounded leaves

  • We show that MYBR1 down regulates many abscisic acid (ABA) responsive genes including those involved in abiotic stresses and negatively regulates drought responses and senescence

  • AtMYBR1 represses genes induced by a hyperactive ABA analog We showed in a previous study that AtMYBR1 was induced weakly by (+)-ABA and more strongly by 24 h treatment with a hyperactive ABA analog PBI425 ((+)-8′ acetylene ABA) indicating MYBR1 is likely a component of the ABA signaling pathway [14]

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Summary

Introduction

The transcription factor AtMYBR1 (MYB44) is a member of the MYB family of transcription factors and is expressed throughout the plant life cycle and especially in senescing and wounded leaves. A family of 14 novel START domain proteins, named as PYR/PYL/RCARs (PYRABACTIN RESISTANCE/PYR1 LIKE/REGULATORY COMPONENT OF ABA RECEPTOR) has been identified as intracellular ABA receptors that interact with and inhibit several protein phosphatase 2Cs (PP2Cs) including ABA INSENSITIVE1 and 2 (ABI1, ABI2), HOMOLOGY TO ABI1 (HAB1), and PP2CA [2,3,4] Such phosphatases are negative regulators of ABA signaling. A recent model for ABA signaling, based on several independent crystallographic studies for example [5], proposes that in the presence of ABA, receptors of the PYR/PYL/RCAR family bind to PP2Cs which in turn release inhibition on a subfamily of SNF1-RELATED PROTEIN KINASE2 (SnRK2) kinases These kinases phosphorylate and subsequently activate transcription factors including ABA RESPONSIVE ELEMENTS-BINDING FACTOR (ABF)/ ABA RESPONSIVE ELEMENTS-BINDING PROTEIN (AREB)-type bZIP TFs. ABFs in turn bind to ABAresponsive promoter elements (ABRE) to activate ABAresponsive gene expression

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