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TIR1产生的环磷酸腺苷（cAMP）作为转录生长素信号传导中的第二信使。

TIR1-produced cAMP as a second messenger in transcriptional auxin signalling.

作者信息

Chen Huihuang, Qi Linlin, Zou Minxia, Lu Mengting, Kwiatkowski Mateusz, Pei Yuanrong, Jaworski Krzysztof, Friml Jiří

机构信息

Institute of Science and Technology Austria, Klosterneuburg, Austria.

Faculty of Synthetic Biology, Shenzhen University of Advanced Technology, Shenzhen, China.

出版信息

Nature. 2025 Apr;640(8060):1011-1016. doi: 10.1038/s41586-025-08669-w. Epub 2025 Mar 5.

DOI:10.1038/s41586-025-08669-w
PMID:40044868
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12018254/
Abstract

The phytohormone auxin (Aux) is a principal endogenous developmental signal in plants. It mediates transcriptional reprogramming by a well-established canonical signalling mechanism. TIR1/AFB auxin receptors are F-box subunits of an ubiquitin ligase complex; after auxin perception, they associate with Aux/IAA transcriptional repressors and ubiquitinate them for degradation, thus enabling the activation of auxin response factor (ARF) transcription factors. Here we revise this paradigm by showing that without TIR1 adenylate cyclase (AC) activity, auxin-induced degradation of Aux/IAAs is not sufficient to mediate the transcriptional auxin response. Abolishing the TIR1 AC activity does not affect auxin-induced degradation of Aux/IAAs but renders TIR1 non-functional in mediating transcriptional reprogramming and auxin-regulated development, including shoot, root, root hair growth and lateral root formation. Transgenic plants show that local cAMP production in the vicinity of the Aux/IAA-ARF complex by unrelated AC enzymes bypasses the need for auxin perception and is sufficient to induce ARF-mediated transcription. These discoveries revise the canonical model of auxin signalling and establish TIR1/AFB-produced cAMP as a second messenger essential for transcriptional reprograming.

摘要

植物激素生长素（Aux）是植物中一种主要的内源性发育信号。它通过一种成熟的经典信号机制介导转录重编程。TIR1/AFB生长素受体是泛素连接酶复合物的F-box亚基；在感知生长素后，它们与Aux/IAA转录抑制因子结合并使其泛素化以进行降解，从而激活生长素响应因子（ARF）转录因子。在这里，我们通过表明在没有TIR1腺苷酸环化酶（AC）活性的情况下，生长素诱导的Aux/IAAs降解不足以介导生长素转录反应，从而修正了这一范式。消除TIR1 AC活性不会影响生长素诱导的Aux/IAAs降解，但会使TIR1在介导转录重编程和生长素调节的发育（包括茎、根、根毛生长和侧根形成）中失去功能。转基因植物表明，不相关的AC酶在Aux/IAA-ARF复合物附近产生的局部cAMP绕过了对生长素感知的需求，并且足以诱导ARF介导的转录。这些发现修正了生长素信号传导的经典模型，并确立了TIR1/AFB产生的cAMP作为转录重编程所必需的第二信使。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa14/12018254/8f38abc97867/41586_2025_8669_Fig12_ESM.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa14/12018254/8f38abc97867/41586_2025_8669_Fig12_ESM.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa14/12018254/6e14882e589c/41586_2025_8669_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa14/12018254/beb237e07762/41586_2025_8669_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa14/12018254/e11b36f7c6cc/41586_2025_8669_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa14/12018254/70f2db8abd55/41586_2025_8669_Fig5_ESM.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa14/12018254/372b661d58be/41586_2025_8669_Fig6_ESM.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa14/12018254/226902e965ae/41586_2025_8669_Fig7_ESM.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa14/12018254/b934423586e3/41586_2025_8669_Fig8_ESM.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa14/12018254/889215eeabee/41586_2025_8669_Fig9_ESM.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa14/12018254/202192007482/41586_2025_8669_Fig10_ESM.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa14/12018254/51929c4828cb/41586_2025_8669_Fig11_ESM.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa14/12018254/8f38abc97867/41586_2025_8669_Fig12_ESM.jpg

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