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一个介导细胞间通讯温度控制的调控模块促进了树木芽休眠的解除。

A regulatory module mediating temperature control of cell-cell communication facilitates tree bud dormancy release.

作者信息

Pandey Shashank K, Maurya Jay Prakash, Aryal Bibek, Drynda Kamil, Nair Aswin, Miskolczi Pal, Singh Rajesh Kumar, Wang Xiaobin, Ma Yujiao, de Souza Moraes Tatiana, Bayer Emmanuelle M, Farcot Etienne, Bassel George W, Band Leah R, Bhalerao Rishikesh P

机构信息

Umeå Plant Science Centre, Department of Forest Genetics and Plant Physiology, Swedish University of Agricultural Sciences, SE-901 87, Umeå, Sweden.

Plant Development and Molecular Biology Lab, Department of Botany, Institute of Science, Banaras Hindu University, Varanasi, 221005, Uttar Pradesh, India.

出版信息

EMBO J. 2024 Dec;43(23):5793-5812. doi: 10.1038/s44318-024-00256-5. Epub 2024 Oct 3.

DOI:10.1038/s44318-024-00256-5
PMID:39363036
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11612439/
Abstract

The control of cell-cell communication via plasmodesmata (PD) plays a key role in plant development. In tree buds, low-temperature conditions (LT) induce a switch in plasmodesmata from a closed to an open state, which restores cell-to-cell communication in the shoot apex and releases dormancy. Using genetic and cell-biological approaches, we have identified a previously uncharacterized transcription factor, Low-temperature-Induced MADS-box 1 (LIM1), as an LT-induced, direct upstream activator of the gibberellic acid (GA) pathway. The LIM1-GA module mediates low temperature-induced plasmodesmata opening, by negatively regulating callose accumulation to promote dormancy release. LIM1 also activates expression of FT1 (FLOWERING LOCUS T), another LT-induced factor, with LIM1-FT1 forming a coherent feedforward loop converging on low-temperature regulation of gibberellin signaling in dormancy release. Mathematical modeling and experimental validation suggest that negative feedback regulation of LIM1 by gibberellin could play a crucial role in maintaining the robust temporal regulation of bud responses to low temperature. These results reveal genetic factors linking temperature control of cell-cell communication with regulation of seasonally-aligned growth crucial for adaptation of trees.

摘要

通过胞间连丝(PD)进行的细胞间通讯控制在植物发育中起着关键作用。在树木芽中,低温条件(LT)会诱导胞间连丝从关闭状态转变为开放状态,从而恢复茎尖的细胞间通讯并解除休眠。利用遗传学和细胞生物学方法,我们鉴定出一种先前未被表征的转录因子,即低温诱导MADS盒1(LIM1),它是低温诱导的赤霉素(GA)途径的直接上游激活因子。LIM1-GA模块通过负调控胼胝质积累来促进休眠解除,从而介导低温诱导的胞间连丝开放。LIM1还激活FT1(开花位点T)的表达,FT1是另一种低温诱导因子,LIM1-FT1形成一个相干前馈环,汇聚于休眠解除过程中赤霉素信号的低温调控。数学建模和实验验证表明,赤霉素对LIM1的负反馈调节可能在维持芽对低温反应的稳健时间调控中起关键作用。这些结果揭示了将细胞间通讯的温度控制与对树木适应至关重要的季节性生长调节联系起来的遗传因素。

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