β-Cyclocitral is a conserved root growth regulator

Alexandra J Dickinson, Kevin Lehner, Jianing Mi, Kunpeng Jia, Medhavinee Mijar, José Dinneny, Salim Al-Babili, Philip N Benfey

Research output: Contribution to journalArticlepeer-review

105 Scopus citations

Abstract

Natural compounds capable of increasing root depth and branching are desirable tools for enhancing stress tolerance in crops. We devised a sensitized screen to identify natural metabolites capable of regulating root traits in Arabidopsis β-Cyclocitral, an endogenous root compound, was found to promote cell divisions in root meristems and stimulate lateral root branching. β-Cyclocitral rescued meristematic cell divisions in ccd1ccd4 biosynthesis mutants, and β-cyclocitral-driven root growth was found to be independent of auxin, brassinosteroid, and reactive oxygen species signaling pathways. β-Cyclocitral had a conserved effect on root growth in tomato and rice and generated significantly more compact crown root systems in rice. Moreover, β-cyclocitral treatment enhanced plant vigor in rice plants exposed to salt-contaminated soil. These results indicate that β-cyclocitral is a broadly effective root growth promoter in both monocots and eudicots and could be a valuable tool to enhance crop vigor under environmental stress.
Original languageEnglish (US)
Pages (from-to)10563-10567
Number of pages5
JournalProceedings of the National Academy of Sciences
Volume116
Issue number21
DOIs
StatePublished - May 8 2019

Bibliographical note

KAUST Repository Item: Exported on 2020-10-01
Acknowledgements: We thank Jingyuan Zhang for technical support provided for the duration of this project; Michel Havaux, Stefano D’Alessandro, Polly Hsu, and Larry Wu for helpful discussions; Dolf Weijers, Cara Winter, Colleen Drapek, and Isaiah Taylor for critical reading; and Linxing Yao (Proteomics and Metabolomics Facility, Colorado State University) for experimental assistance. This work was supported by the Arnold and Mabel Beckman Postdoctoral Fellowship (to A.J.D.); by the Howard Hughes Medical Institute and the Gordon and Betty Moore Foundation Grant GBMF3405 (to P.N.B.); and by baseline funding and Competitive Research Grant CRG4 (to S.A.-B.) from King Abdullah University of Science and Technology.

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