Direct roles of SPEECHLESS in the specification of stomatal self-renewing cells
A complex network makes simple pores
Stomata, the pores found on the surface of plant leaves, form at intervals from stem cells. Development of stomata is controlled by the SPEECHLESS transcription factor. Lau et al. surveyed the genes that SPEECHLESS itself controls. Targets include genes involved in hormone signaling, control of cell proliferation, and the specification of asymmetric cell fates. Despite the apparent simplicity of a single pore, the genetic network that generates that pore is anything but simple.
Science, this issue p. 1605
Abstract
Lineage-specific stem cells are critical for the production and maintenance of specific cell types and tissues in multicellular organisms. In Arabidopsis, the initiation and proliferation of stomatal lineage cells is controlled by the basic helix-loop-helix transcription factor SPEECHLESS (SPCH). SPCH-driven asymmetric and self-renewing divisions allow flexibility in stomatal production and overall organ growth. How SPCH directs stomatal lineage cell behaviors, however, is unclear. Here, we improved the chromatin immunoprecipitation (ChIP) assay and profiled the genome-wide targets of Arabidopsis SPCH in vivo. We found that SPCH controls key regulators of cell fate and asymmetric cell divisions and modulates responsiveness to peptide and phytohormone-mediated intercellular communication. Our results delineate the molecular pathways that regulate an essential adult stem cell lineage in plants.
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Supplementary Material
Summary
Materials and Methods
Figs. S1 to S15
Tables S1 to S8
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Science
Volume 345 | Issue 6204
26 September 2014
26 September 2014
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Copyright © 2014, American Association for the Advancement of Science.
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Received: 3 June 2014
Accepted: 25 August 2014
Published in print: 26 September 2014
Acknowledgments
We thank Z.-Y. Wang (Carnegie) for the antibody to YFP and the bin2-1 allele; Y. Yin (Iowa State University) for the BES1pro:bes1-D-GFP construct; J. Chory (SALK) for the bes1 RNAi line; and members of our laboratory for critical comments. Funding for this work was provided by National Institutes of Health (NIH) 1R01GM086632. O.S.L. was a Croucher Fellow, K.A.D. was supported by Cellular and Molecular Biology Training Program NIH5T32GM007276 and by a National Science Foundation graduate research fellowship, and J.A. was supported by the DAAD. D.C.B. is a Gordon and Betty Moore Foundation Investigator of the Howard Hughes Medical Institute. The ChIP-seq and RNA-seq data in this study can be found in National Center for Biotechnology Information’s Gene Expression Omnibus repository (www.ncbi.nlm.nih.gov/geo) as GSE57954. The supplementary materials contain additional data.
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