Department of Plant Molecular Biology, University of Lausanne, CH-1015, Lausanne, Switzerland.
Institute of Plant and Microbial Biology, University of Zurich, Zurich-Basel Plant Science Center, CH-8008, Zurich, Switzerland.
Nat Commun. 2023 Jan 26;14(1):423. doi: 10.1038/s41467-023-36200-0.
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). How excess CLE45-BAM3 signaling interferes with protophloem development and whether it does so directly or indirectly remains unclear. 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. Our data thus reveal antagonism between CLE45-BAM3-PBL signaling and PIP5K that converges on auxin efflux regulation through dynamic control of PAX polarity. 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.
生长素通过质膜整合 PIN 形成（PIN）载体的外排对于植物组织组织和紧密调节至关重要。例如，分子变阻器在拟南芥根发育原韧皮部筛分子中，对 PIN 介导的生长素运输进行关键控制。变阻器蛋白 BRX 和与 BRX 相关的蛋白激酶（PAX）与质膜的关联通过与磷酸肌醇-4-磷酸-5-激酶（PIP5K）的相互作用得到加强。遗传证据表明，BRX 通过其受体 BARELY ANY MERISTEM 3（BAM3）减弱 CLAVATA3/EMBRYO SURROUNDING REGION-RELATED 45（CLE45）肽的自分泌信号。多余的 CLE45-BAM3 信号如何干扰原韧皮部的发育，以及它是直接还是间接干扰，目前尚不清楚。在这里，我们表明变阻器的极性独立于 PIN 的极性，但与 PIP5K 相互依赖。无催化活性的 PIP5K 赋予变阻器极性而不加强其定位，揭示了可能的 PIP5K 支架功能。此外，PIP5K 和 PAX 合作控制局部 PIN 丰度。我们还发现，CLE45-BAM3 信号通过 RLCK-VII/PBS1-LIKE（PBL）细胞质激酶分支，以破坏变阻器的定位。因此，我们的数据揭示了 CLE45-BAM3-PBL 信号与 PIP5K 之间的拮抗作用，该作用通过对 PAX 极性的动态控制，汇聚于生长素外排的调节。由于第二位点 bam3 突变抑制了 pip5k 突变体的根和芽表型，因此 CLE 肽信号可能在各种发育背景下调节依赖磷酸肌醇的过程。
