KAI2 promotes Arabidopsis root hair elongation at low external phosphate by controlling local accumulation of AUX1 and PIN2.

KAI2 promotes Arabidopsis root hair elongation at low external phosphate by controlling local accumulation of AUX1 and PIN2.
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KAI2 通过控制 AUX1 和 PIN2 的局部积累,在低外部磷酸盐条件下促进拟南芥根毛伸长。

DOI:
10.1016/j.cub.2021.10.044
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发表时间:
2022
期刊:
CB
影响因子:
--
通讯作者:
Villaécija-Aguilar JA
Villaécija-Aguilar JA
中科院分区:
--
文献类型:
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作者:
Villaécija-Aguilar JA

文献摘要

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根毛(RH)生长以增加吸收根表面积是植物限制土壤中磷酸盐有效性的关键适应措施。尽管这一性状很重要,特别是对于幼苗的存活,但人们对磷酸盐饥饿感应和相对湿度生长调节之间的分子事件知之甚少。 KARRIKIN INSENSITIVE2 (KAI2) 是一种未知植物激素(“KAI2-配体”[KL])的 α/β-水解酶受体,是 RH 延伸所必需的。1KAI2 与 F-box 蛋白 MORE AXILLIARY BRANCHING2 (MAX2) 相互作用,以靶向 MAX2 1 (SMAX1) 家族抑制因子的调节蛋白进行降解。2在这里,我们证明 Pi 饥饿通过 KAI2 和 MAX2 的转录激活增加拟南芥根中的 KL 信号传导。在这些条件下,这两个基因都是 RH 延伸所必需的,而 smax1 smxl2 突变体即使在高 Pi 可用性下也具有组成型长 RH。 Kai2突变体中RH伸长减弱的原因是从根尖向茎部生长素的运输减少,导致RH区的生长素信号减少,这是由于Pi饥饿时无法增加生长素输入蛋白AUX1)和生长素输出蛋白PIN-FORMED2(PIN2)的局部积累所致。与通过乙烯信号传导介导的 AUX1 和 PIN2 积累一致,31-氨基环丙烷-1-羧基化合酶 7 (ACS7) 的表达在低 Pi 下以 aKAI2 依赖性方式增加,并且用乙烯前体处理可恢复 acs7 的 RH 伸长,但不能恢复 aux1 和 pin2 的 RH 伸长。因此,磷酸盐饥饿会增强 KAI2 信号传导,从而触发 RH 延伸所需的乙烯-AUX1/PIN2-生长素级联。
Root hair (RH) growth to increase the absorptive root surface area is a key adaptation of plants to limiting phosphate availability in soils. Despite the importance of this trait, especially for seedling survival, little is known about the molecular events connecting phosphate starvation sensing and RH growth regulation. KARRIKIN INSENSITIVE2 (KAI2), an α/β-hydrolase receptor of a yet-unknown plant hormone ("KAI2-ligand" [KL]), is required for RH elongation.1KAI2 interacts with the F-box protein MORE AXILLIARY BRANCHING2 (MAX2) to target regulatory proteins of the SUPPRESSOR of MAX2 1 (SMAX1) family for degradation.2Here, we demonstrate that Pistarvation increases KL signaling inArabidopsisroots through transcriptional activation ofKAI2andMAX2. Both genes are required for RH elongation under these conditions, whilesmax1 smxl2mutants have constitutively long RHs, even at high Piavailability. Attenuated RH elongation inkai2mutants is explained by reduced shootward auxin transport from the root tip resulting in reduced auxin signaling in the RH zone, caused by an inability to increase localized accumulation of the auxin importer AUXIN TRANSPORTER PROTEIN1 (AUX1) and the auxin exporter PIN-FORMED2 (PIN2) upon Pistarvation. Consistent with AUX1 and PIN2 accumulation being mediated via ethylene signaling,3expression of1-AMINOCYCLOPROPANE-1-CARBOXYLATE SYNTHASE 7(ACS7) is increased at low Piin aKAI2-dependent manner, and treatment with an ethylene precursor restores RH elongation ofacs7, but not ofaux1andpin2. Thus, KAI2 signaling is increased by phosphate starvation to trigger an ethylene- AUX1/PIN2-auxin cascade required for RH elongation.