Calmodulin‐like protein CML24 interacts with CAMTA2 and WRKY46 to regulate ALMT1‐dependent Al resistance in Arabidopsis thaliana

Summary ALUMINUM‐ACTIVATED MALATE TRANSPORTER1 (ALMT1)‐mediated malate exudation from roots is critical for aluminium (Al) resistance in Arabidopsis. Its upstream molecular signalling regulation is not yet well understood. The role of CALMODULIN‐LIKE24 (CML24) in Al‐inhibited root growth and downstr...

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Published in:The New phytologist Vol. 233; no. 6; pp. 2471 - 2487
Main Authors: Zhu, Xue, Wang, Peng, Bai, Zhimin, Herde, Marco, Ma, Yanqi, Li, Na, Liu, Shuo, Huang, Chao‐Feng, Cui, Rongxiu, Ma, Hongyu, Zhang, Meng, Wang, Hui, Wei, Tiandi, Quan, Taiyong, Zhang, Wei, Liu, Chunguang, Zhang, Tao, Yang, Zhong‐Bao
Format: Journal Article
Language:English
Published: England Wiley Subscription Services, Inc 01-03-2022
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Summary:Summary ALUMINUM‐ACTIVATED MALATE TRANSPORTER1 (ALMT1)‐mediated malate exudation from roots is critical for aluminium (Al) resistance in Arabidopsis. Its upstream molecular signalling regulation is not yet well understood. The role of CALMODULIN‐LIKE24 (CML24) in Al‐inhibited root growth and downstream molecular regulation of ALMT1‐meditaed Al resistance was investigated. CML24 confers Al resistance demonstrated by an increased root‐growth inhibition of the cml24 loss‐of‐function mutant under Al stress. This occurs mainly through the regulation of the ALMT1‐mediated malate exudation from roots. The mutation and overexpression of CML24 leads to an elevated and reduced Al accumulation in the cell wall of roots, respectively. Al stress induced both transcript and protein abundance of CML24 in root tips, especially in the transition zone. CML24 interacts with CALMODULIN BINDING TRANSCRIPTION ACTIVATOR2 (CAMTA2) and promotes its transcriptional activity in the regulation of ALMT1 expression. This results in an enhanced malate exudation from roots and less root‐growth inhibition under Al stress. Both CML24 and CAMTA2 interacted with WRKY46 suppressing the transcriptional repression of ALMT1 by WRKY46. The study provides novel insights into understanding of the upstream molecular signalling of the ALMT1‐depdendent Al resistance. See also the Commentary on this article by Huang & Ma, 233: 2327–2329.
Bibliography:These authors contributed equally to this work.
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Huang & Ma
2327–2329.
See also the Commentary on this article by
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ISSN:0028-646X
1469-8137
DOI:10.1111/nph.17812