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光触发 PILS 依赖性核生长素信号转导减少,从而引发生长转变。

Light triggers PILS-dependent reduction in nuclear auxin signalling for growth transition.

机构信息

Department of Applied Genetics and Cell Biology, University of Natural Resources and Life Sciences (BOKU), Muthgasse 18, 1190 Vienna, Austria.

Department of Plant Systems Biology, VIB and Department of Plant Biotechnology and Bioinformatics, Ghent University, Technologiepark 927, 9052 Gent, Belgium.

出版信息

Nat Plants. 2017 Jul 17;3:17105. doi: 10.1038/nplants.2017.105.

DOI:10.1038/nplants.2017.105
PMID:28714973
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5524181/
Abstract

The phytohormone auxin induces or represses growth depending on its concentration and the underlying tissue type. However, it remains unknown how auxin signalling is modulated to allow tissues transiting between repression and promotion of growth. Here, we used apical hook development as a model for growth transitions in plants. A PIN-FORMED (PIN)-dependent intercellular auxin transport module defines an auxin maximum that is causal for growth repression during the formation of the apical hook. Our data illustrate that growth transition for apical hook opening is largely independent of this PIN module, but requires the PIN-LIKES (PILS) putative auxin carriers at the endoplasmic reticulum. PILS proteins reduce nuclear auxin signalling in the apical hook, leading to the de-repression of growth and the onset of hook opening. We also show that the phytochrome (phy) B-reliant light-signalling pathway directly regulates PILS gene activity, thereby enabling light perception to repress nuclear auxin signalling and to control growth. We propose a novel mechanism, in which PILS proteins allow external signals to alter tissue sensitivity to auxin, defining differential growth rates.

摘要

植物激素生长素根据其浓度和潜在的组织类型,诱导或抑制生长。然而,生长素信号如何被调节以允许组织在抑制和促进生长之间转换仍不清楚。在这里,我们使用顶端弯钩发育作为植物生长转变的模型。一个由 PIN 形成(PIN)依赖的细胞间生长素运输模块定义了一个生长素最大值,该最大值在顶端弯钩形成过程中对生长抑制是因果关系的。我们的数据表明,顶端弯钩张开的生长转变在很大程度上独立于这个 PIN 模块,但需要内质网上的 PIN 样(PILS)假定的生长素载体。PILS 蛋白降低顶端弯钩中的核生长素信号,导致生长去抑制和弯钩张开的开始。我们还表明,依赖于光敏色素(phy)B 的光信号通路直接调节 PILS 基因活性,从而使光感知能够抑制核生长素信号并控制生长。我们提出了一个新的机制,其中 PILS 蛋白允许外部信号改变组织对生长素的敏感性,定义不同的生长速率。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47be/5524181/3301bb3d29e9/emss-73085-f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47be/5524181/0cf16c5ed026/emss-73085-f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47be/5524181/0475f6fe8f7a/emss-73085-f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47be/5524181/c65aaf674b5b/emss-73085-f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47be/5524181/1950824def8b/emss-73085-f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47be/5524181/00b192d5c2b2/emss-73085-f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47be/5524181/3301bb3d29e9/emss-73085-f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47be/5524181/0cf16c5ed026/emss-73085-f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47be/5524181/0475f6fe8f7a/emss-73085-f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47be/5524181/c65aaf674b5b/emss-73085-f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47be/5524181/1950824def8b/emss-73085-f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47be/5524181/00b192d5c2b2/emss-73085-f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47be/5524181/3301bb3d29e9/emss-73085-f006.jpg

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