Microtubule-Associated Protein CLASP Sustains Cell Proliferation through a Brassinosteroid Signaling Negative Feedback Loop
Abstract
The capacity for sustained cell division within the plant meristem is a critical determinant of organ structure and performance. This capacity is diminished in mutants lacking the microtubule-associated protein CLASP and when brassinosteroid signaling is increased. Here, we discovered that CLASP is both targeted by and promotes activity of the brassinosteroid pathway in Arabidopsis root apical meristems. We show that enhanced brassinosteroid signaling reduces CLASP transcript and protein levels, dramatically shifts microtubule organization, and reduces the number of cells in the meristem. In turn, CLASP, which tethers sorting nexin 1 vesicles to microtubules, sustains brassinosteroid signaling by fostering retrieval of endocytosed BRI1 receptors to the plasma membrane. clasp-1 null mutants have dampened brassinosteroid (BR)-mediated transcriptional activity and responses. Global transcript profiling confirmed the collapse of cell-cycle activity in clasp-1 and identified CLASP-mediated hormone crosstalk. Together, these findings reveal an unprecedented form of negative feedback supporting meristem homeostasis.
Additional Information
© 2018 Elsevier Ltd. Received 22 February 2018, Revised 19 April 2018, Accepted 20 June 2018, Available online 23 August 2018. We thank Joanne Chory for the BRI1pro:BRI1-GFP line, Tonglin Mao for the bri1-5 mutant lines, and Viktor Kirik for the 35Spro:YFP-CLASP line; Salar Fazeli and Junsu Kwon for technical assistance; Trevor Hart for statistical advice; and Zhiyong Wang, Yanhai Yin, Mathias Schuetz, Katherine Celler, and Michael Savage for helpful discussions. Microscopy was conducted in the UBC Bioimaging Facility with the expert assistance of Kevin Hodgson. This work was supported by NSERC Discovery Grants 2014-06080 (to G.O.W.) and 2015-478114 (to M.F.B.), the Canada Research Chairs Program (to G.O.W.), and the Canada Foundation for Innovation (to G.O.W.). Author Contributions: Conceptualization, G.O.W., Y.R., and L.S.H.; Methodology, Y.R., G.O.W., C.A., S.J., L.S.H., D.K., and M.F.B.; Formal Analysis, Y.R., L.S.H., and D.K.; Investigation, Y.R., L.S.H., S.J., and D.K.; Writing – Original Draft, Y.R., G.O.W., L.S.H., and D.K.; Writing – Review and Editing, G.O.W., L.S.H., C.A., D.K., and M.F.B.; Visualization, Y.R., L.S.H., D.K., and G.O.W.; Supervision, G.O.W. and M.F.B.; Funding Acquisition, G.O.W. and M.F.B. The authors declare no competing interests.Attached Files
Supplemental Material - 1-s2.0-S096098221830839X-mmc1.pdf
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Additional details
- Eprint ID
- 89977
- Resolver ID
- CaltechAUTHORS:20180926-145742339
- 2014-06080
- Natural Sciences and Engineering Research Council of Canada (NSERC)
- 2015-478114
- Natural Sciences and Engineering Research Council of Canada (NSERC)
- Canada Research Chairs Program
- Canada Foundation for Innovation
- Created
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2018-09-26Created from EPrint's datestamp field
- Updated
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2021-11-16Created from EPrint's last_modified field