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Nature Communications:磷酸肌醇枢纽关联CLE肽信号和极性生长素外流调控

已有 1776 次阅读 2023-2-6 22:23 |个人分类:每日摘要|系统分类:论文交流

A phosphoinositide hub connects CLE peptide signaling and polar auxin efflux regulation

第一作者Qian Wang

第一单位洛桑大学

通讯作者Christian S. Hardtke


 ABSTRACT 

背景回顾:Auxin efflux through plasma-membrane-integral PIN-FORMED (PIN) carriers is essential for plant tissue organization and tightly regulated. For instance, a molecular rheostat critically controls PIN-mediated auxin transport in developing protophloem sieve elements of Arabidopsis roots. Plasma-membrane-association of the rheostat proteins, BREVIS RADIX (BRX) and PROTEIN KINASE ASSOCIATED WITH BRX (PAX), is reinforced by interaction with PHOSPHATIDYLINOSITOL-4-PHOSPHATE-5-KINASE (PIP5K). Genetic evidence suggests that BRX dampens autocrine signaling of CLAVATA3/EMBRYO SURROUNDING REGION-RELATED 45 (CLE45) peptide via its receptor BARELY ANY MERISTEM 3 (BAM3). 


提出问题How excess CLE45-BAM3 signaling interferes with protophloem development and whether it does so directly or indirectly remains unclear. 


结果Here we show that rheostat polarity is independent of PIN polarity, but interdependent with PIP5K. Catalytically inactive PIP5K confers rheostat polarity without reinforcing its localization, revealing a possible PIP5K scaffolding function. Moreover, PIP5K and PAX cooperatively control local PIN abundance. We further find that CLE45-BAM3 signaling branches via RLCK-VII/PBS1-LIKE (PBL) cytoplasmic kinases to destabilize rheostat localization. 


结论Our data thus reveal antagonism between CLE45-BAM3-PBL signaling and PIP5K that converges on auxin efflux regulation through dynamic control of PAX polarity. 


推测Because second-site bam3 mutation suppresses root as well as shoot phenotypes of pip5k mutants, CLE peptide signaling likely modulates phosphoinositide-dependent processes in various developmental contexts.


image.png


 摘 要 

由PIN蛋白介导的生长素外流对于植物组织的系统性是十分重要的,并且受到紧密调控。比如,在拟南芥根的原韧皮部筛分子的发育过程中,一个分子变阻器严苛地控制PIN介导的生长素运输。变阻器蛋白BRX和PAX通过与PIP5K的互作,增强了与质膜的关联性。遗传学证据表明,BRX通过其受体BAM3抑制小肽CLV3/CLE45的自分泌信号。但是,过量的CLE45-BAM3信号途径如何干扰原生韧皮部的发育,及其是直接还是间接影响的,这人仍不清楚。本文中,作者发现变阻器极性不依赖于PIN蛋白的极性,但是与PIP5K相互依赖。催化活性丧失的PIP5K能够赋予变阻器极性,但是并不增强其定位,说明PIP5K可能起到一个“支架”的作用。此外,PIP5K和P协同控制局域的PIN丰度。作者进一步发现CLE45-BAM3信号转导分支通过RLCK-VII/PBS1-LIKE细胞质激酶,降低变阻器定位的稳定性。因此,本文的研究结果揭示了CLE45-BAM3-PBL信号转导与PIP5K之间的拮抗作用,二者会通过对PAX极性的动态调控收敛于生长素外流的控制。由于bam3突变抑制了pip5k突变体的根和茎表型,说明CLE肽信号转导很有可能在不同的发育环境中调节磷酸肌醇依赖性过程。




** Christian S. Hardtke **


个人简介:

1997年,慕尼黑大学,博士;

1998年,多伦多大学,博士后;

1998-2000年,耶鲁大学,博士后。


研究方向:植物的生长和发育。


doi: https://doi.org/10.1038/s41467-023-36200-0


Journal: Nature Communications

Published date: January 26, 2023


Cite:
Qian Wang, A. Cecilia Aliaga Fandino, Moritz Graeff, Thomas A. DeFalco, Cyril Zipfel, Christian S. Hardtke. A phosphoinositide hub connects CLE peptide signaling and polar auxin efflux regulation. Nature Communications, 2023, 14: 423. DOI: https://doi.org/10.1038/s41467-023-36200-0




https://blog.sciencenet.cn/blog-3158122-1375131.html

上一篇:Current Biology:pH依赖性CLE多肽感知作用于拟南芥根中的韧皮部分化
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