奥地利科学技术研究所Jirí Friml课题组的一项最新研究提出了TIR1产生cAMP作为生长素转录信号传导的第二信使。2025年3月5日出版的《自然》杂志发表了这项成果。

在这里，该课题组修改了这一范式，表明没有TIR1腺苷酸环化酶（AC）活性，生长素诱导的Aux/IAAs降解不足以介导生长素的转录反应。去除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控的发育（包括茎、根、根毛生长和侧根形成）中不起作用。转基因植物表明，在Aux/ IAA-ARF复合物附近，由不相关的AC酶产生的局部cAMP绕过生长素感知的需要，足以诱导ARF介导的转录。这些发现修订了生长素信号传导的标准模型，并确立了TIR1/ AFB产生的cAMP是转录重编程的第二信使。

研究人员表示，植物激素生长素（Aux）是植物主要的内源性发育信号。它通过一个完善的典型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；在生长素感知后，它们与Aux/IAA转录抑制因子结合，并使其泛素化降解，从而激活生长素反应因子（ARF）转录因子。

附：英文原文

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

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

Issue&Volume: 2025-03-05

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 factors1,2,3. Here we revise this paradigm by showing that without TIR1 adenylate cyclase (AC) activity4, 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.

DOI: 10.1038/s41586-025-08669-w

Source: https://www.nature.com/articles/s41586-025-08669-w