1. Plant Biology Laboratory,
2. Howard Hughes Medical Institute, and,
3. Laboratory of Neuronal Structure and Function, The Salk Institute for Biological Studies, La Jolla, California 92037, USA

Correspondence to: Joanne Chory^1,2 Correspondence and requests for materials should be addressed to J.C. (Email: chory@salk.edu).

Abstract

The size of an organism is genetically determined, yet how a plant or animal achieves its final size is largely unknown. The shoot of higher plants has a simple conserved body plan based on three major tissue systems: the epidermal (L1), sub-epidermal (L2) and inner ground and vascular (L3) tissues. Which tissue system drives or restricts growth has been a subject of debate for over a century^{1, 2, 3, 4}. Here, we use dwarf, brassinosteroid biosynthesis and brassinosteroid response mutants in conjunction with tissue-specific expression of these components as tools to examine the role of the epidermis in shoot growth. We show that expression of the brassinosteroid receptor or a brassinosteroid biosynthetic enzyme in the epidermis, but not in the vasculature, of null mutants is sufficient to rescue their dwarf phenotypes. Brassinosteroid signalling from the epidermis is not sufficient to establish normal vascular organization. Moreover, shoot growth is restricted when brassinosteroids are depleted from the epidermis and brassinosteroids act locally within a leaf. We conclude that the epidermis both promotes and restricts shoot growth by providing a non-autonomous signal to the ground tissues.

1. Plant Biology Laboratory,
2. Howard Hughes Medical Institute, and,
3. Laboratory of Neuronal Structure and Function, The Salk Institute for Biological Studies, La Jolla, California 92037, USA

Correspondence to: Joanne Chory^1,2 Correspondence and requests for materials should be addressed to J.C. (Email: chory@salk.edu).

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