TheArabidopsisTranscription Factor MYB77 Modulates Auxin Signal Transduction

Abstract

Auxin is a key plant hormone that regulates plant development, apical dominance, and growth-related tropisms, such as phototropism and gravitropism. In this study, we report a new Arabidopsis thaliana transcription factor, MYB77, that is involved in auxin response. In MYB77 knockout plants, we found that auxin-responsive gene expression was greatly attenuated. Lateral root density in the MYB77 knockout was lower than the wild type at low concentrations of indole-3-acetic acid (IAA) and also under low nutrient conditions. MYB77 interacts with auxin response factors (ARFs) in vitro through the C terminus (domains III and IV) of ARFs and the activation domain of MYB77. A synergistic genetic interaction was demonstrated between MYB77 and ARF7 that resulted in a strong reduction in lateral root numbers. Experiments with protoplasts confirmed that the coexpression of MYB77 and an ARF C terminus enhance reporter gene expression. R2R3 MYB transcription factors have not been previously implicated in regulating the expression of auxin-inducible genes. Also it was previously unknown that ARFs interact with proteins other than those in the Aux/IAA family via conserved domains. The interaction between MYB77 and ARFs defines a new type of combinatorial transcriptional control in plants. This newly defined transcription factor interaction is part of the plant cells' repertoire for modulating response to auxin, thereby controlling lateral root growth and development under changing environmental conditions.

MYB transcription factor genes as regulators for plant responses: an overview

“…Role of MYBs in root development and differentiation has been reported by various workers (Feng et al 2004;Shin et al 2007;Mu et al 2009). AtMYB59 regulated root development through the control of cell cycle progression at the root tips (Mu et al 2009) and the expression of auxin-inducible genes was modulated by AtMYB77 regulating lateral root formation (Shin et al 2007).…”

“…AtMYB59 regulated root development through the control of cell cycle progression at the root tips (Mu et al 2009) and the expression of auxin-inducible genes was modulated by AtMYB77 regulating lateral root formation (Shin et al 2007). Feng et al (2004) found that AtMYB68 is expressed specifically in root pericycle cells and was involved in some steps in root development.…”

Quadruple 9-mer-Based Protein Binding Microarray Analysis Confirms AACnG as the Consensus Nucleotide Sequence Sufficient for the Specific Binding of AtMYB44

“…However, AtMYB44 and AtMYB77 have quite different biological roles. AtMYB77 is involved in auxin responses to control lateral root growth and development under changing environmental conditions (Shin et al, 2007). Double-knockout mutations of AtMYB44 and At-MYB77 (myb44myb77) did not change the auxin-responsive phenotypes of myb77.…”

“…Instead, this transcription factor may function either by working cooperatively with other transcription factors or through stimulus-induced structural modification. Indeed, the C-terminus activation domain of At-MYB77 interacts with auxin response factors (ARFs) in vitro, resulting in a strong reduction in lateral root numbers (Shin et al, 2007). Similarly, it appears that the functional specificity of AtMYB44 results from its interaction with other protein(s), not from the specificity of the binding sequence on the promoter regions of target genes.…”

Auxin-Binding Protein 1 is a negative regulator of the SCFTIR1/AFB pathway

“…An attractive hypothesis is that the ABP1 pathway would confer auxin conditionality to the interaction between TIR1/AFBs and AUX/IAAs. Such conditionality might result from a change in subcellular or nuclei protein localization of AUX/IAA and/or TIR1/AFB proteins 22,33 , from the presence or absence of another protein or peptide interacting or competing with one of the component of the transcriptional regulatory module [34][35][36][37] or from post-translational modification affecting the relative affinity between TIR1/AFBs 38 and AUX/ IAAs 28,39 . A future challenge will be to elucidate the molecular basis of the action of ABP1 on the SCF TIR1/AFB pathway and to identify ABP1 downstream signalling elements filling the gap between ABP1 and the nuclear-localized SCF TIR1/AFB pathway.…”