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WAV E3 ubiquitin ligases mediate degradation of IAA32/34 in the TMK1-mediated auxin signaling pathway during apical hook development.

WAV E3 ubiquitin ligases mediate degradation of IAA32/34 in the TMK1-mediated auxin signaling pathway during apical hook development.

Authors :
Wang JL
Wang M
Zhang L
Li YX
Li JJ
Li YY
Pu ZX
Li DY
Liu XN
Guo W
Di DW
Li XF
Guo GQ
Wu L
Source :
Proceedings of the National Academy of Sciences of the United States of America [Proc Natl Acad Sci U S A] 2024 Apr 23; Vol. 121 (17), pp. e2314353121. Date of Electronic Publication: 2024 Apr 18.
Publication Year :
2024

Abstract

Auxin regulates plant growth and development through downstream signaling pathways, including the best-known SCF <superscript>TIR1/AFB</superscript> -Aux/IAA-ARF pathway and several other less characterized "noncanonical" pathways. Recently, one SCF <superscript>TIR1/AFB</superscript> -independent noncanonical pathway, mediated by Transmembrane Kinase 1 (TMK1), was discovered through the analyses of its functions in Arabidopsis apical hook development. Asymmetric accumulation of auxin on the concave side of the apical hook triggers DAR1-catalyzed release of the C-terminal of TMK1, which migrates into the nucleus, where it phosphorylates and stabilizes IAA32/34 to inhibit cell elongation, which is essential for full apical hook formation. However, the molecular factors mediating IAA32/34 degradation have not been identified. Here, we show that proteins in the CYTOKININ INDUCED ROOT WAVING 1 (CKRW1)/WAVY GROWTH 3 (WAV3) subfamily act as E3 ubiquitin ligases to target IAA32/34 for ubiquitination and degradation, which is inhibited by TMK1c-mediated phosphorylation. This antagonistic interaction between TMK1c and CKRW1/WAV3 subfamily E3 ubiquitin ligases regulates IAA32/34 levels to control differential cell elongation along opposite sides of the apical hook.<br />Competing Interests: Competing interests statement:The authors declare no competing interest.

Details

Language :
English
ISSN :
1091-6490
Volume :
121
Issue :
17
Database :
MEDLINE
Journal :
Proceedings of the National Academy of Sciences of the United States of America
Publication Type :
Academic Journal
Accession number :
38635634
Full Text :
https://doi.org/10.1073/pnas.2314353121