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光敏色素 B 通过稳定 IAA14 和抑制 ARF7 和 ARF19 来抑制黑暗诱导的下胚轴不定根形成。

Phytochrome B inhibits darkness-induced hypocotyl adventitious root formation by stabilizing IAA14 and suppressing ARF7 and ARF19.

机构信息

National Key Laboratory of Plant Molecular Genetics, Chinese Academy of Sciences Center for Excellence in Molecular Plant Sciences, Institute of Plant Physiology and Ecology, Chinese Academy of Sciences, Shanghai, 200032, China.

University of Chinese Academy of Sciences, Beijing, 100049, China.

出版信息

Plant J. 2021 Mar;105(6):1689-1702. doi: 10.1111/tpj.15142. Epub 2021 Jan 28.

Abstract

Adventitious roots (ARs) are an important root type for plants and display a high phenotypic plasticity in response to different environmental stimuli. Previous studies found that dark-light transition can trigger AR formation from the hypocotyl of etiolated Arabidopsis thaliana, which was used as a model for the identification of regulators of AR biogenesis. However, the central regulatory machinery for darkness-induced hypocotyl AR (HAR) remains elusive. Here, we report that photoreceptors suppress HAR biogenesis through regulating the molecular module essential for lateral roots. We found that hypocotyls embedded in soil or in continuous darkness are able to develop HARs, wherein photoreceptors act as negative regulators. Distinct from wound-induced ARs that require WOX11 and WOX12, darkness-induced HARs are fully dependent on ARF7, ARF19, WOX5/7, and LBD16. Further studies established that PHYB interacts with IAA14, ARF7, and ARF9. The interactions stabilize IAA14 and inhibit the transcriptional activities of ARF7 and ARF19 and thus suppress biogenesis of darkness-induced HARs. This finding not only revealed the central machinery controlling HAR biogenesis but also illustrated that AR formation could be initiated by multiple pathways.

摘要

不定根(ARs)是植物的一种重要根类型,对不同的环境刺激表现出很高的表型可塑性。先前的研究发现,暗-光转换可以触发拟南芥黄化幼苗下胚轴的不定根形成,这被用作鉴定不定根发生调节因子的模型。然而,黑暗诱导的下胚轴不定根(HAR)形成的中心调节机制仍不清楚。在这里,我们报告说光受体通过调节侧根发生所必需的分子模块来抑制 HAR 的生物发生。我们发现,埋在土壤中的或处于连续黑暗中的下胚轴能够发育出 HAR,其中光受体作为负调节因子发挥作用。与需要 WOX11 和 WOX12 的创伤诱导的 AR 不同,黑暗诱导的 HAR 完全依赖于 ARF7、ARF19、WOX5/7 和 LBD16。进一步的研究确定 PHYB 与 IAA14、ARF7 和 ARF9 相互作用。这些相互作用稳定了 IAA14,并抑制了 ARF7 和 ARF19 的转录活性,从而抑制了黑暗诱导的 HAR 的生物发生。这一发现不仅揭示了控制 HAR 生物发生的中心机制,还表明 AR 的形成可以通过多种途径启动。

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