Clathrin light chains regulate hypocotyl elongation by affecting the polarization of the auxin transporter PIN3 in Arabidopsis

Clathrin light chains regulate hypocotyl elongation by affecting the polarization of the auxin transporter PIN3 in Arabidopsis
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网格蛋白轻链通过影响拟南芥中生长素转运蛋白 PIN3 的极化来调节下胚轴伸长

DOI:
10.1111/jipb.13171
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发表时间:
2021-11-01
影响因子:
11.4
通讯作者:
Wang, Chao
Wang, Chao
中科院分区:
生物学1区
文献类型:
--
作者:
Hu, Tianwei;Yin, Shoupeng;Wang, Chao

文献摘要

被引文献

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生长素的定向运输是植物生长发育的关键。尽管由PIN 3极化介导的生长素重新分配在调节下胚轴细胞扩张中发挥关键作用,但PIN 3如何重新极化至下胚轴细胞内的适当位点仍知之甚少。我们先前在拟南芥中产生了网格蛋白轻链clc 2 -1 clc 3 -1双突变体,并发现其与野生型相比具有延长的下胚轴表型。在这里,我们进行了遗传,细胞生物学和药理学分析结合活细胞成像,以阐明下胚轴伸长的网格蛋白轻链的作用的分子机制。我们的分析表明,双突变体的缺陷增强表皮细胞中的生长素极大,从而促进下胚轴伸长。在clc 2 -1和clc 3 -1突变体中,PIN 3重新定位到下胚轴内胚层细胞的侧面,以将生长素重定向到表皮细胞层。此外,PIN 3功能的丧失在很大程度上抑制了clc 2 -1 clc 3 -1双突变体的长下胚轴表型,用生长素转运抑制剂处理也是如此。基于这些数据,我们提出,网格蛋白调节PIN 3的丰度和极性,直接生长素通量和抑制细胞伸长下胚轴,下胚轴伸长的调节提供了新的见解。
PIN-FORMED (PIN)-dependent directional auxin transport is crucial for plant development. Although the redistribution of auxin mediated by the polarization of PIN3 plays key roles in modulating hypocotyl cell expansion, how PIN3 becomes repolarized to the proper sites within hypocotyl cells is poorly understood. We previously generated the clathrin light chain clc2-1 clc3-1 double mutant in Arabidopsis thaliana and found that it has an elongated hypocotyl phenotype compared to the wild type. Here, we performed genetic, cell biology, and pharmacological analyses combined with live-cell imaging to elucidate the molecular mechanism underlying the role of clathrin light chains in hypocotyl elongation. Our analyses indicated that the defects of the double mutant enhanced auxin maxima in epidermal cells, thus, promoting hypocotyl elongation. PIN3 relocated to the lateral sides of hypocotyl endodermal cells in clc2-1 clc3-1 mutants to redirect auxin toward the epidermal cell layers. Moreover, the loss of function of PIN3 largely suppressed the long hypocotyl phenotype of the clc2-1 clc3-1 double mutant, as did treatment with auxin transport inhibitors. Based on these data, we propose that clathrin modulates PIN3 abundance and polarity to direct auxin flux and inhibit cell elongation in the hypocotyl, providing novel insights into the regulation of hypocotyl elongation.