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WRKY23 is a component of the transcriptional network mediating auxin feedback on PIN polarity

  • Auxin is unique among plant hormones due to its directional transport that is mediated by the polarly distributed PIN auxin transporters at the plasma membrane. The canalization hypothesis proposes that the auxin feedback on its polar flow is a crucial, plant-specific mechanism mediating multiple self-organizing developmental processes. Here, we used the auxin effect on the PIN polar localization in Arabidopsis thaliana roots as a proxy for the auxin feedback on the PIN polarity during canalization. We performed microarray experiments to find regulators of this process that act downstream of auxin. We identified genes that were transcriptionally regulated by auxin in an AXR3/IAA17-and ARF7/ARF19-dependent manner. Besides the known components of the PIN polarity, such as PID and PIP5K kinases, a number of potential new regulators were detected, among which the WRKY23 transcription factor, which was characterized in more detail. Gain-and loss-of-function mutants confirmed a role for WRKY23 in mediating the auxin effect on the PINAuxin is unique among plant hormones due to its directional transport that is mediated by the polarly distributed PIN auxin transporters at the plasma membrane. The canalization hypothesis proposes that the auxin feedback on its polar flow is a crucial, plant-specific mechanism mediating multiple self-organizing developmental processes. Here, we used the auxin effect on the PIN polar localization in Arabidopsis thaliana roots as a proxy for the auxin feedback on the PIN polarity during canalization. We performed microarray experiments to find regulators of this process that act downstream of auxin. We identified genes that were transcriptionally regulated by auxin in an AXR3/IAA17-and ARF7/ARF19-dependent manner. Besides the known components of the PIN polarity, such as PID and PIP5K kinases, a number of potential new regulators were detected, among which the WRKY23 transcription factor, which was characterized in more detail. Gain-and loss-of-function mutants confirmed a role for WRKY23 in mediating the auxin effect on the PIN polarity. Accordingly, processes requiring auxin-mediated PIN polarity rearrangements, such as vascular tissue development during leaf venation, showed a higher WRKY23 expression and required the WRKY23 activity. Our results provide initial insights into the auxin transcriptional network acting upstream of PIN polarization and, potentially, canalization-mediated plant development.show moreshow less

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Author details:Tomáš Prát, Jakub Hajny ́, Wim Grunewald, Mina Vasileva, Gergely Molnár, Ricardo Tejos, Markus Schmid, Michael SauerORCiD, Jiří Friml
URN:urn:nbn:de:kobv:517-opus4-446331
DOI:https://doi.org/10.25932/publishup-44633
ISSN:1866-8372
Title of parent work (German):Postprints der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe
Publication series (Volume number):Zweitveröffentlichungen der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe (1123)
Publication type:Postprint
Language:English
Date of first publication:2021/02/16
Publication year:2018
Publishing institution:Universität Potsdam
Release date:2021/02/16
Tag:DNA-binding; apical-basal axis; arabidopsis-thaliana; canalization; efflux; gene-expression; phosphorylation; plants; root gravitropism; transport
Issue:1123
Number of pages:20
Source:Plos Genetics 14 (2018) 1, Art. e1007177 DOI: 10.1371/journal.pgen.1007177
Organizational units:Mathematisch-Naturwissenschaftliche Fakultät
Mathematisch-Naturwissenschaftliche Fakultät / Institut für Biochemie und Biologie
DDC classification:5 Naturwissenschaften und Mathematik / 57 Biowissenschaften; Biologie / 570 Biowissenschaften; Biologie
6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 610 Medizin und Gesundheit
Peer review:Referiert
Grantor:Public Library of Science (PLOS)
Publishing method:Open Access / Green Open-Access
License (German):License LogoCC-BY - Namensnennung 4.0 International
External remark:Bibliographieeintrag der Originalveröffentlichung/Quelle
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