GRAMINIFOLIA promotes growth and polarity of Antirrhinum leaves

Development. 2004 Aug;131(15):3661-70. doi: 10.1242/dev.01221. Epub 2004 Jun 30.

Abstract

The leaves of higher plants develop distinct cell types along their adaxial-abaxial (dorsal-ventral) axes. Interaction between leaf primordium cells with adaxial and abaxial identities is necessary for lateral growth of the developing leaf blade. We show that the growth and asymmetry of leaves in Antirrhinum majus involves the related YABBY transcription factors GRAMINIFOLIA (GRAM) and PROLONGATA (PROL). GRAM is expressed in abaxial margins of organ primordia where it promotes lateral growth and abaxial cell fate. GRAM, however, is not needed for abaxial fate in the absence of adaxial cell specification, suggesting that it promotes abaxial fate by excluding adaxial identity. Although GRAM expression is abaxially restricted, it functions redundantly with its abaxially expressed paralogue, PROL, and with the ubiquitously expressed PHANTASTICA gene to promote adaxial identity via intercellular signalling. This non cell-autonomous behaviour is consistent with the ability of GRAM in only the abaxial most cell layer to direct normal development of more adaxial cells. The contrasting roles of GRAM in promoting and inhibiting adaxial identity might serve to reinforce and maintain the distinction between adaxial and abaxial domains in the growing leaf primordium.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antirrhinum / genetics
  • Antirrhinum / growth & development*
  • Flowers / cytology
  • Flowers / growth & development
  • Gene Expression Regulation, Plant*
  • Genes, Plant
  • In Situ Hybridization
  • Morphogenesis*
  • Phylogeny
  • Plant Leaves / cytology
  • Plant Leaves / growth & development*
  • Plant Proteins / classification
  • Plant Proteins / genetics
  • Plant Proteins / metabolism*
  • Plants, Genetically Modified
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*

Substances

  • Plant Proteins
  • Transcription Factors