文献类型：期刊文献

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

作者：Hu, Tianwei[1];Yin, Shoupeng[2];Sun, Jingbo[2];Linghu, Yuting[1];Ma, Jiaqi[1];Pan, Jianwei[1];Wang, Chao[1,3]

机构：[1]Lanzhou Univ, Sch Life Sci, Minist Educ, Key Lab Cell Act & Stress Adaptat, Lanzhou 730000, Peoples R China;[2]Zhejiang Normal Univ, Coll Chem & Life Sci, Jinhua 321004, Zhejiang, Peoples R China;[3]Shaoxing Univ, Coll Life Sci, Shaoxing 312000, Peoples R China

年份：2021

卷号：63

期号：11

起止页码：1922

外文期刊名：JOURNAL OF INTEGRATIVE PLANT BIOLOGY

收录：SCI-EXPANDED(收录号：WOS:000715999300008)、、Scopus(收录号：2-s2.0-85118645359)、WOS

基金：We thank ABRC for providing the T-DNA insertion lines used in this study. We thank Prof. Sebastian Y. Bednarek for the clc2-2 clc3-2 double mutant. We are grateful to Dr. Yahu Gao, Liping Guan, Liang Peng, and Dr. Yang Zhao (Core Facility for Life Science Research, Lanzhou University) for their technical assistance. This work was supported by the National Natural Science Foundation of China (Nos. 31801193, 31820103008, 91754104, and 31670283) and by the Fundamental Research Funds for the Central Universities (Nos. lzujbky-2018-28 and lzujbky-2020-it13).

语种：英文

外文关键词：Arabidopsis; auxin; clathrin light chains; hypocotyl elongation; PIN3

外文摘要：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.