Modulation of Asymmetric Division Diversity through Cytokinin and SPEECHLESS Regulatory Interactions in the Arabidopsis Stomatal Lineage
Abstract
Coordinated growth of organs requires communication among cells within and between tissues. In plants, leaf growth is largely dictated by the epidermis; here, asymmetric and self-renewing divisions of the stomatal lineage create two essential cell types—pavement cells and guard cells—in proportions reflecting inputs from local, systemic, and environmental cues. The transcription factor SPEECHLESS (SPCH) is the prime regulator of divisions, but whether and how it is influenced by external cues to provide flexible development is enigmatic. Here, we show that the phytohormone cytokinin (CK) can act as an endogenous signal to affect the extent and types of stomatal lineage divisions and forms a regulatory circuit with SPCH. Local domains of low CK signaling are created by SPCH-dependent cell-type-specific activity of two repressive type-A ARABIDOPSIS RESPONSE REGULATORs (ARRs), ARR16 and ARR17, and two secreted peptides, CLE9 and CLE10, which, together with SPCH, can customize epidermal cell-type composition.
Additional Information
© 2018 Elsevier Inc. Received 25 May 2017, Revised 6 June 2018, Accepted 8 August 2018, Available online 6 September 2018. We thank Professor T. Kakimoto for reagents and the members of the Bergmann lab for discussions and comments on the manuscript. Funding was provided by EMBO Postdoctoral fellowship ALTF 707-2012 to A.V., NSF IOS-1546837 to Z.L.N., and NIHRO1GM086632 to D.C.B. P.T.T. was supported by NIH R01GM104244 and Howard Hughes Medical Institute (HHMI)/Gordon and Betty Moore Foundation GBMF3406 (awarded to E. Meyerowitz). D.C.B. is an HHMI investigator. Author Contributions: A.V. designed and performed all experiments (except as noted below), analyzed results, performed statistical analysis, and wrote the manuscript. C.L.S. and Z.L.N. created cle9 and cle10 mutants. P.T.T. created and provided reporter lines and clones to enable manipulation of CK levels. D.C.B. analyzed results and wrote the manuscript. The authors declare no competing interests.Attached Files
Accepted Version - nihms-990626.pdf
Supplemental Material - 1-s2.0-S1534580718306725-mmc1.pdf
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Additional details
- PMCID
- PMC6177308
- Eprint ID
- 89414
- Resolver ID
- CaltechAUTHORS:20180906-125123454
- ALTF 707-2012
- European Molecular Biology Organization (EMBO)
- IOS-1546837
- NSF
- R01GM086632
- NIH
- R01GM104244
- NIH
- Howard Hughes Medical Institute (HHMI)
- GBMF3406
- Gordon and Betty Moore Foundation
- Created
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2018-09-07Created from EPrint's datestamp field
- Updated
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2022-02-17Created from EPrint's last_modified field