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直接 ETTIN-生长素相互作用控制雌蕊发育中的染色质状态。

Direct ETTIN-auxin interaction controls chromatin states in gynoecium development.

机构信息

Department of Crop Genetics, John Innes Centre, Norwich Research Park, Norwich, United Kingdom.

Centre for Plant Sciences, Faculty of Biological Sciences, University of Leeds, Leeds, United Kingdom.

出版信息

Elife. 2020 Apr 8;9:e51787. doi: 10.7554/eLife.51787.

DOI:10.7554/eLife.51787
PMID:32267233
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7164952/
Abstract

Hormonal signalling in animals often involves direct transcription factor-hormone interactions that modulate gene expression. In contrast, plant hormone signalling is most commonly based on de-repression via the degradation of transcriptional repressors. 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 degradation. 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.

摘要

动物中的激素信号通常涉及直接的转录因子-激素相互作用,从而调节基因表达。相比之下,植物激素信号主要是通过转录抑制子的降解来实现去抑制。最近,我们发现了一种植物激素生长素的非典型信号机制,生长素可以直接影响非典型生长素反应因子(ARF)ETTIN 对靶基因的活性,而不需要蛋白质降解。在这里,我们表明 ETTIN 直接结合生长素,导致与 TOPLESS/TOPLESS-RELATED 家族的共抑制蛋白解离,随后发生组蛋白乙酰化和基因表达诱导。这种机制类似于动物激素信号,因为它影响活性以调节靶基因,并为植物中的 DNA 结合激素受体提供了第一个例子。虽然生长素通过促进Aux/IAA 抑制物的降解间接影响典型的 ARF,但 ETTIN-生长素的直接相互作用允许以瞬间可逆的方式在抑制性和去抑制性染色质状态之间切换。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/780b/7164952/7a657f3831b2/elife-51787-fig5.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/780b/7164952/7a657f3831b2/elife-51787-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/780b/7164952/4c7cc5d60d78/elife-51787-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/780b/7164952/4ca3d12cf725/elife-51787-fig1-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/780b/7164952/34444830a0dd/elife-51787-fig1-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/780b/7164952/8ef7d6a65d7b/elife-51787-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/780b/7164952/b1108becde91/elife-51787-fig2-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/780b/7164952/cd24ae34573c/elife-51787-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/780b/7164952/d69f49d991c7/elife-51787-fig3-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/780b/7164952/0de270ec401d/elife-51787-fig3-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/780b/7164952/c10b7aff309a/elife-51787-fig3-figsupp3.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/780b/7164952/7a657f3831b2/elife-51787-fig5.jpg

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