Distinct functions of TIR1 and AFB1 receptors in auxin signalling.

Chen H, Li L, Zou M, Qi L, Friml J. 2023. Distinct functions of TIR1 and AFB1 receptors in auxin signalling. Molecular Plant. 16(7), 1117–1119.

Download
OA 2023_MolecularPlant_Chen.pdf 1.00 MB

Journal Article | Published | English

Scopus indexed
Department
Abstract
Auxin is the major plant hormone regulating growth and development (Friml, 2022). Forward genetic approaches in the model plant Arabidopsis thaliana have identified major components of auxin signalling and established the canonical mechanism mediating transcriptional and thus developmental reprogramming. In this textbook view, TRANSPORT INHIBITOR RESPONSE 1 (TIR1)/AUXIN-SIGNALING F-BOX (AFBs) are auxin receptors, which act as F-box subunits determining the substrate specificity of the Skp1-Cullin1-F box protein (SCF) type E3 ubiquitin ligase complex. Auxin acts as a “molecular glue” increasing the affinity between TIR1/AFBs and the Aux/IAA repressors. Subsequently, Aux/IAAs are ubiquitinated and degraded, thus releasing auxin transcription factors from their repression making them free to mediate transcription of auxin response genes (Yu et al., 2022). Nonetheless, accumulating evidence suggests existence of rapid, non-transcriptional responses downstream of TIR1/AFBs such as auxin-induced cytosolic calcium (Ca2+) transients, plasma membrane depolarization and apoplast alkalinisation, all converging on the process of root growth inhibition and root gravitropism (Li et al., 2022). Particularly, these rapid responses are mostly contributed by predominantly cytosolic AFB1, while the long-term growth responses are mediated by mainly nuclear TIR1 and AFB2-AFB5 (Li et al., 2021; Prigge et al., 2020; Serre et al., 2021). How AFB1 conducts auxin-triggered rapid responses and how it is different from TIR1 and AFB2-AFB5 remains elusive. Here, we compare the roles of TIR1 and AFB1 in transcriptional and rapid responses by modulating their subcellular localization in Arabidopsis and by testing their ability to mediate transcriptional responses when part of the minimal auxin circuit reconstituted in yeast.
Publishing Year
Date Published
2023-07-01
Journal Title
Molecular Plant
Acknowledgement
We thank all the authors for sharing the published materials. This research was supported by the Lab Support Facility and the Imaging and Optics Facility of ISTA. We thank Lukáš Fiedler (ISTA) for critical reading of the manuscript. This project was funded by the European Research Council Advanced Grant (ETAP-742985).
Volume
16
Issue
7
Page
1117-1119
ISSN
eISSN
IST-REx-ID

Cite this

Chen H, Li L, Zou M, Qi L, Friml J. Distinct functions of TIR1 and AFB1 receptors in auxin signalling. Molecular Plant. 2023;16(7):1117-1119. doi:10.1016/j.molp.2023.06.007
Chen, H., Li, L., Zou, M., Qi, L., & Friml, J. (2023). Distinct functions of TIR1 and AFB1 receptors in auxin signalling. Molecular Plant. Elsevier . https://doi.org/10.1016/j.molp.2023.06.007
Chen, Huihuang, Lanxin Li, Minxia Zou, Linlin Qi, and Jiří Friml. “Distinct Functions of TIR1 and AFB1 Receptors in Auxin Signalling.” Molecular Plant. Elsevier , 2023. https://doi.org/10.1016/j.molp.2023.06.007.
H. Chen, L. Li, M. Zou, L. Qi, and J. Friml, “Distinct functions of TIR1 and AFB1 receptors in auxin signalling.,” Molecular Plant, vol. 16, no. 7. Elsevier , pp. 1117–1119, 2023.
Chen H, Li L, Zou M, Qi L, Friml J. 2023. Distinct functions of TIR1 and AFB1 receptors in auxin signalling. Molecular Plant. 16(7), 1117–1119.
Chen, Huihuang, et al. “Distinct Functions of TIR1 and AFB1 Receptors in Auxin Signalling.” Molecular Plant, vol. 16, no. 7, Elsevier , 2023, pp. 1117–19, doi:10.1016/j.molp.2023.06.007.
All files available under the following license(s):
Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0):
Main File(s)
Access Level
OA Open Access
Date Uploaded
2024-01-29
MD5 Checksum
6012b7e4a2f680ee6c1f84001e2b945f


Export

Marked Publications

Open Data ISTA Research Explorer

Web of Science

View record in Web of Science®

Sources

PMID: 37393433
PubMed | Europe PMC

Search this title in

Google Scholar