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BIL1 介导的 MP 磷酸化整合了次生生长中的 PXY 和细胞分裂素信号传导。

BIL1-mediated MP phosphorylation integrates PXY and cytokinin signalling in secondary growth.

机构信息

Department of Life Sciences, Pohang University of Science and Technology, Pohang, Korea.

Centre for Organismal Studies (COS), Heidelberg University, Heidelberg, Germany.

出版信息

Nat Plants. 2018 Aug;4(8):605-614. doi: 10.1038/s41477-018-0180-3. Epub 2018 Jul 9.

DOI:10.1038/s41477-018-0180-3
PMID:29988154
Abstract

Vascular cambium proliferation in plants is crucial for the generation of vascular tissues and for mechanical strength. Phytohormones and mobile peptides are key regulators of vascular cambial activity during secondary growth; however, the signalling cross-talk underlying their coordinated action is largely unknown. Here, we reveal that BIN2-LIKE 1 (BIL1), a glycogen synthase kinase 3, integrates the PHLOEM INTERCALATED WITH XYLEM/tracheary element differentiation inhibitory factor (TDIF) RECEPTOR (PXY/TDR) module into MONOPTEROS/AUXIN RESPONSE FACTOR 5 (MP/ARF5) transcription factor action during secondary growth. BIL1-mediated phosphorylation of MP/ARF5 enhances its negative effect on vascular cambial activity, which upregulates the negative regulators of cytokinin signalling ARABIDOPSIS RESPONSE REGULATOR 7 (ARR7) and ARR15. PXY/TDR inhibits BIL1 activity, which attenuates the effect of MP/ARF5 on ARR7 and ARR15 expression, thus increasing vascular cambial activity. Together, these results suggest that BIL1 is a key mediator that links peptide signalling with auxin-cytokinin signalling for the maintenance of cambial activity.

摘要

植物中的维管形成层增殖对于维管组织的产生和机械强度至关重要。植物激素和移动肽是次生生长过程中维管形成层活性的关键调节剂;然而,它们协调作用的信号交叉对话在很大程度上是未知的。在这里,我们揭示了糖原合酶激酶 3 BIN2-LIKE 1(BIL1)将 PHLOEM INTERCALATED WITH XYLEM/tracheary element differentiation inhibitory factor(PXY/TDIF 受体)模块整合到 MONOPTEROS/AUXIN RESPONSE FACTOR 5(MP/ARF5)转录因子的作用中,以调节次生生长。BIL1 介导的 MP/ARF5 磷酸化增强了其对维管形成层活性的负调控作用,从而上调细胞分裂素信号转导的负调控因子 ARABIDOPSIS RESPONSE REGULATOR 7(ARR7)和 ARR15。PXY/TDR 抑制 BIL1 的活性,从而减弱了 MP/ARF5 对 ARR7 和 ARR15 表达的影响,从而增加了维管形成层的活性。总之,这些结果表明 BIL1 是一个关键的中介物,将肽信号与生长素-细胞分裂素信号联系起来,以维持形成层的活性。

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