Direct ETTIN-auxin interaction controls chromatin states in gynoecium development
Abstract
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 repressors3-5. Recently, we uncovered a non-canonical signalling mechanism for the plant hormone auxin whereby auxin directly affects the activity of the atypical auxin response factor (ARF), ETTIN towards target genes without the requirement for protein degradation6,7. Here we show that ETTIN directly binds auxin, leading to dissociation from co-repressor proteins of the TOPLESS/TOPLESS-RELATED family followed by histone acetylation and induction of gene expression. This mechanism is reminiscent of animal hormone signalling as it affects the activity towards regulation of target genes and provides the first example of a DNA-bound hormone receptor in plants. Whilst auxin affects canonical ARFs indirectly by facilitating degradation of Aux/IAA repressors, direct ETTIN-auxin interactions allow switching between repressive and de-repressive chromatin states in an instantly-reversible manner.
Data availability
All data generated or analysed during this study are included in the manuscript and supporting files. Source data files have been provided for Figures 1, 2, 3, 4 and 5
Article and author information
Author details
Funding
Biotechnology and Biological Sciences Research Council (BB/S002901/1)
- Lars Østergaard
Biotechnology and Biological Sciences Research Council (BB/L010623/1)
- Stefan Kepinski
Biotechnology and Biological Sciences Research Council (BB/M011216/1)
- André Kuhn
Biotechnology and Biological Sciences Research Council (BB/J004553/1)
- Lars Østergaard
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Copyright
© 2020, Kuhn et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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