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光调控下下胚轴不定根诱导的遗传解析。

Genetic Dissection of Light-Regulated Adventitious Root Induction in Hypocotyls.

机构信息

Department Plants and Crops, Faculty of Bioscience Engineering, Ghent University, Coupure Links 653, 9000 Ghent, Belgium.

Biotechnology Research and Development Institute, Can Tho University, Can Tho City 900000, Vietnam.

出版信息

Int J Mol Sci. 2022 May 10;23(10):5301. doi: 10.3390/ijms23105301.

DOI:10.3390/ijms23105301
PMID:35628112
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9140560/
Abstract

Photomorphogenic responses of etiolated seedlings include the inhibition of hypocotyl elongation and opening of the apical hook. In addition, dark-grown seedlings respond to light by the formation of adventitious roots (AR) on the hypocotyl. How light signaling controls adventitious rooting is less well understood. Hereto, we analyzed adventitious rooting under different light conditions in wild type and photomorphogenesis mutants in . Etiolation was not essential for AR formation but raised the competence to form AR under white and blue light. The blue light receptors CRY1 and PHOT1/PHOT2 are key elements contributing to the induction of AR formation in response to light. Furthermore, etiolation-controlled competence for AR formation depended on the COP9 signalosome, E3 ubiquitin ligase CONSTITUTIVELY PHOTOMORPHOGENIC (COP1), the COP1 interacting SUPPRESSOR OF PHYA-105 (SPA) kinase family members (SPA1,2 and 3) and Phytochrome-Interacting Factors (PIF). In contrast, ELONGATED HYPOCOTYL5 (HY5), suppressed AR formation. These findings provide a genetic framework that explains the high and low AR competence of hypocotyls that were treated with dark, and light, respectively. We propose that light-induced auxin signal dissipation generates a transient auxin maximum that explains AR induction by a dark to light switch.

摘要

黄化幼苗的光形态建成反应包括抑制下胚轴伸长和顶端弯钩打开。此外,黑暗生长的幼苗通过在下胚轴上形成不定根(AR)对光作出反应。光信号如何控制不定根形成的机制还不太清楚。为此,我们在野生型和光形态建成突变体中分析了不同光照条件下的不定根形成。黄化对不定根形成不是必需的,但提高了在白光和蓝光下形成不定根的能力。蓝光受体 CRY1 和 PHOT1/PHOT2 是响应光诱导不定根形成的关键因素。此外,黄化控制不定根形成的能力取决于 COP9 信号体、E3 泛素连接酶 CONSTITUTIVELY PHOTOMORPHOGENIC (COP1)、COP1 相互作用的 SUPPRESSOR OF PHYA-105 (SPA) 激酶家族成员(SPA1、2 和 3)和 Phytochrome-Interacting Factors (PIF)。相反,ELONGATED HYPOCOTYL5 (HY5) 抑制不定根形成。这些发现提供了一个遗传框架,解释了黑暗和光照处理的 下胚轴具有高和低不定根形成能力的原因。我们提出,光诱导的生长素信号耗散产生一个瞬时的生长素最大值,解释了黑暗到光的转变诱导不定根形成的机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1646/9140560/a8a066509647/ijms-23-05301-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1646/9140560/e26cf20d3373/ijms-23-05301-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1646/9140560/97fb38948e6d/ijms-23-05301-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1646/9140560/d59534b56055/ijms-23-05301-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1646/9140560/d3009aa730b9/ijms-23-05301-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1646/9140560/88153c25fd05/ijms-23-05301-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1646/9140560/93401583d251/ijms-23-05301-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1646/9140560/a8a066509647/ijms-23-05301-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1646/9140560/e26cf20d3373/ijms-23-05301-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1646/9140560/97fb38948e6d/ijms-23-05301-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1646/9140560/d59534b56055/ijms-23-05301-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1646/9140560/d3009aa730b9/ijms-23-05301-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1646/9140560/88153c25fd05/ijms-23-05301-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1646/9140560/93401583d251/ijms-23-05301-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1646/9140560/a8a066509647/ijms-23-05301-g007.jpg

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