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Harborough, S. R.

Publications and source records attributed to Harborough, S. R..

2 recordsLinked to original sources

Direct ETTIN-auxin interaction controls chromatin state in gynoecium development

Hormonal signalling in animals often involves direct transcription factor-hormone interactions that modulate gene expression1, 2. In contrast, plant hormone signalling is most commonly based on de-repression via the degradation of transcriptional repressors3. Recently, we uncovered a non-canonical signalling mechanism for the plant hormone auxin in organ development with strong similarity to animal hormonal pathways. In this mechanism, auxin directly affects the activity of the auxin response factor ETTIN (ETT) towards regulation of target genes without the requirement for protein degradation4, 5. Here we show that auxin binds ETT to modulate gene expression and that this ETT-auxin interaction leads to the dissociation of ETT from co-repressor proteins of the TOPLESS/TOPLESS-RELATED family followed by histone acetylation and the induction of target gene expression. Whilst canonical ARFs are classified as activators or repressors6, ETT is able to switch chromatin locally between repressive and de-repressive states in an instantly-reversible auxin-dependent manner.

plant biology↗

Selective auxin agonists induce specific AUX/IAA protein degradation to modulate plant development

Auxin phytohormones control most aspects of plant development through a complex and interconnected signaling network. In the presence of auxin, AUXIN/INDOLE-3-ACETIC ACID (AUX/IAA) transcriptional repressors are targeted for degradation by the SKP1-CULLIN1-F-BOX (SCF) ubiquitin-protein ligases containing TRANSPORT INHIBITOR RESISTANT 1/AUXIN SIGNALING F-BOX (TIR1/AFB). CULLIN1-neddylation is required for SCFTIR1/AFB functionality as exemplified by mutants deficient in the NEDD8-activating enzyme subunit AUXIN-RESISTANT 1 (AXR1). Here, we report a chemical biology screen that identifies small molecules requiring AXR1 to modulate plant development. We selected four molecules of interest, RubNeddin1 to 4 (RN1 to 4), among which RN3 and RN4 trigger selective auxin responses at transcriptional, biochemical and morphological levels. This selective activity is explained by their ability to promote the interaction between TIR1 and a specific subset of AUX/IAA proteins, stimulating the degradation of particular AUX/IAA combinations. Finally, via a genetic screen using RN4, we revealed that the chromatin remodeling ATPase BRAHMA is implicated in auxin-mediated apical hook development. These results demonstrate the power of selective auxin agonists to dissect auxin perception for plant developmental functions.

plant biology↗