AtMYB61, an R2R3-MYB transcription factor, functions as a pleiotropic regulator via a small gene network

Authors

  • Julia M. Romano,

    1. Department of Cell & Systems Biology, University of Toronto, 25 Willcocks St., Toronto, ON, Canada, M5S 3B2
    2. Centre for the Analysis of Genome Evolution and Function, University of Toronto, 25 Willcocks St., Toronto, ON, Canada, M5S 3B2
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    • These authors contributed equally to this work.

  • Christian Dubos,

    1. Department of Cell & Systems Biology, University of Toronto, 25 Willcocks St., Toronto, ON, Canada, M5S 3B2
    2. INRA, UMR1318, Institut Jean-Pierre Bourgin, RD10, F-78026, Versailles, France
    3. AgroParisTech, Institut Jean-Pierre Bourgin, RD10, F-78026, Versailles, France
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    • These authors contributed equally to this work.

  • Michael B. Prouse,

    1. Department of Cell & Systems Biology, University of Toronto, 25 Willcocks St., Toronto, ON, Canada, M5S 3B2
    2. Centre for the Analysis of Genome Evolution and Function, University of Toronto, 25 Willcocks St., Toronto, ON, Canada, M5S 3B2
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  • Olivia Wilkins,

    1. Department of Cell & Systems Biology, University of Toronto, 25 Willcocks St., Toronto, ON, Canada, M5S 3B2
    2. Centre for the Analysis of Genome Evolution and Function, University of Toronto, 25 Willcocks St., Toronto, ON, Canada, M5S 3B2
    3. Center for Genomics and Systems Biology, New York University,12 Waverly Place, New York, NY10003, USA
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  • Henry Hong,

    1. Department of Cell & Systems Biology, University of Toronto, 25 Willcocks St., Toronto, ON, Canada, M5S 3B2
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  • Mervin Poole,

    1. Campden BRI, Station Road, Chipping Campden, Gloucestershire GL55 6LD, UK
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  • Kyu-Young Kang,

    1. Department of Wood Science, University of British Columbia, 4030-2424 Main Mall, Vancouver, BC, Canada, V6T 1Z4
    2. Department of Biological and Environmental Science, Dongguk University-Seoul, 26 Pil-dong 3-ga, Jung-gu, Seoul, 100715, South Korea
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  • Eryang Li,

    1. Department of Botany, University of British Columbia, 6270 University Blvd, Vancouver, BC, Canada, V6T 1Z4
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  • Carl J. Douglas,

    1. Department of Botany, University of British Columbia, 6270 University Blvd, Vancouver, BC, Canada, V6T 1Z4
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  • Tamara L. Western,

    1. Department of Biology, McGill University, 1205 ave. Docteur Penfield, Montreal, QC, Canada, H3A 1B1
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  • Shawn D. Mansfield,

    1. Department of Wood Science, University of British Columbia, 4030-2424 Main Mall, Vancouver, BC, Canada, V6T 1Z4
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  • Malcolm M. Campbell

    1. Department of Cell & Systems Biology, University of Toronto, 25 Willcocks St., Toronto, ON, Canada, M5S 3B2
    2. Centre for the Analysis of Genome Evolution and Function, University of Toronto, 25 Willcocks St., Toronto, ON, Canada, M5S 3B2
    3. Department of Biological Sciences, University of Toronto Scarborough, 1265 Military Trail, Toronto, ON, Canada, M1C 1A4
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Author for correspondence:
Malcolm M. Campbell
Tel: +1 647 267 7714
Email: malcolm.campbell@utoronto.ca

Summary

  • Throughout their lifetimes, plants must coordinate the regulation of various facets of growth and development. Previous evidence has suggested that the Arabidopsis thaliana R2R3-MYB, AtMYB61, might function as a coordinate regulator of multiple aspects of plant resource allocation.
  • Using a combination of cell biology, transcriptome analysis and biochemistry, in conjunction with gain-of-function and loss-of-function genetics, the role of AtMYB61 in conditioning resource allocation throughout the plant life cycle was explored.
  • In keeping with its role as a regulator of resource allocation, AtMYB61 is expressed in sink tissues, notably xylem, roots and developing seeds. Loss of AtMYB61 function decreases xylem formation, induces qualitative changes in xylem cell structure and decreases lateral root formation; in contrast, gain of AtMYB61 function has the opposite effect on these traits. AtMYB61 coordinates a small network of downstream target genes, which contain a motif in their upstream regulatory regions that is bound by AtMYB61, and AtMYB61 activates transcription from this same motif. Loss-of-function analysis supports the hypothesis that AtMYB61 targets play roles in shaping subsets of AtMYB61-related phenotypes.
  • Taken together, these findings suggest that AtMYB61 links the transcriptional control of multiple aspects of plant resource allocation.

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