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The AFB1 auxin receptor controls the cytoplasmic auxin response pathway in Arabidopsis thaliana

摘要The phytohormone auxin triggers root growth inhibition within seconds via a non-transcriptional pathway.Among members of the TIR1/AFB auxin receptor family,AFB1 has a primary role in this rapid response.However,the unique features that confer this specific function have not been identified.Here we show that the N-terminal region of AFB1,including the F-box domain and residues that contribute to auxin binding,is essential and sufficient for its specific role in the rapid response.Substitu-tion of the N-terminal region of AFB1 with that of TIR1 disrupts its distinct cytoplasm-enriched localiza-tion and activity in rapid root growth inhibition by auxin.Importantly,the N-terminal region of AFB1 is indispensable for auxin-triggered calcium influx,which is a prerequisite for rapid root growth inhibition.Furthermore,AFB1 negatively regulates lateral root formation and transcription of auxin-induced genes,suggesting that it plays an inhibitory role in canonical auxin signaling.These results suggest that AFB1 may buffer the transcriptional auxin response,whereas it regulates rapid changes in cell growth that contribute to root gravitropism.

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作者 Shiv Mani Dubey [1] Soeun Han [2] Nathan Stutzman [3] Michael J.Prigge [3] Eva Medvecká [1] Matthieu Pierre Platre [4] Wolfgang Busch [4] Matyá? Fendrych [1] Mark Estelle [3] 学术成果认领
作者单位 Department of Experimental Plant Biology,Faculty of Sciences,Charles University,Prague,Czech Republic [1] Section of Cell and Developmental Biology,University of California San Diego,La Jolla,CA,USA;Department of Biology,Chungbuk National University,Cheongju,Korea [2] Section of Cell and Developmental Biology,University of California San Diego,La Jolla,CA,USA [3] Plant Molecular and Cellular Biology Laboratory and Integrative Biology Laboratory,Salk Institute for Biological Studies,La Jolla,CA,USA [4]
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DOI 10.1016/j.molp.2023.06.008
发布时间 2023-12-20(万方平台首次上网日期,不代表论文的发表时间)
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分子植物(英文版)

分子植物(英文版)

2023年16卷7期

1120-1130页

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