Clathrin light chains regulate hypocotyl elongation by affecting the polarization of the auxin transporter PIN3 in Arabidopsis,Journal of Integrative Plant Biology

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Clathrin light chains regulate hypocotyl elongation by affecting the polarization of the auxin transporter PIN3 in Arabidopsis
Journal of Integrative Plant Biology ( IF 9.3 ) Pub Date : 2021-09-03 , DOI: 10.1111/jipb.13171
Tianwei Hu ₁ , Shoupeng Yin ₂ , Jingbo Sun ₂ , Yuting Linghu ₁ , Jiaqi Ma ₁ , Jianwei Pan ₁ , Chao Wang _{1,

3}

Affiliation

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.

中文翻译：

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

PIN-FORMED (PIN) 依赖的定向生长素转运对植物发育至关重要。尽管由 PIN3 的极化介导的生长素再分布在调节下胚轴细胞扩张中起关键作用，但人们对 PIN3 如何重新极化到下胚轴细胞内的适当位点知之甚少。我们之前在拟南芥中产生了网格蛋白轻链clc2-1 clc3-1双突变体并发现与野生型相比，它具有拉长的下胚轴表型。在这里，我们结合活细胞成像进行了遗传、细胞生物学和药理学分析，以阐明网格蛋白轻链在下胚轴伸长中的作用的分子机制。我们的分析表明，双突变体的缺陷增强了表皮细胞中的生长素最大值，从而促进了下胚轴的伸长。在clc2-1 clc3-1突变体中，PIN3 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，PIN3 的功能丧失在很大程度上抑制了clc2-1 clc3-1的长下胚轴表型双突变体，用生长素转运抑制剂处理也是如此。基于这些数据，我们提出网格蛋白通过调节 PIN3 的丰度和极性来引导生长素通量并抑制下胚轴中的细胞伸长，从而为下胚轴伸长的调节提供新的见解。

更新日期：2021-11-10

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