scrm-D mutation causes ectopic stomata

Photo credit: The Plant Cell

The scrm-D mutation causes ectopic stomata. In the wild-type epidermis (left), stomata are separated from each other by at least one pavement cell. The scrm-Dhomozygous mutant epidermis (right) is made up entirely of stomata. Bar = 20 μm.

They All Scream for ICE1/SCRM2: Core Regulatory Units in Stomatal Development

by Hofmann N. R. (2008)

in The Plant Cell, Vol. 20: 1732, July 2008, –

http://www.plantcell.org/content/20/7/1732.full.pdf+html

The developmental program of stomata includes a series of both symmetrical and asymmetrical divisions and provides an excellent, technically accessible model for the study of patterning, cell fate specification, and regulation of cell division (reviewed in Bergmann and Sack, 2007).

Three basic-helix-loop-helix (bHLH) transcription factors, SPEECHLESS (SPCH), MUTE, and FAMA, have been shown to mediate this process at different steps. Kanaoka et al. (pages 1775– 1785) further elucidate the regulation of stomatal development by characterizing an Arabidopsis mutant, scrm-D, that forms ectopic stomata.

The homozygous scrm-D mutant has an epidermis made entirely of stomata (see figure). Because the scrm-D phenotype is identical to that caused by ectopic expression of MUTE, the authors examined the genetic interactions between scrm-D and the known regulators of stomatal development.

They found that SCRM likely acts upstream of MUTE and FAMA and that there are dose-dependent effects of SPCH on SCRM, suggesting that they might interact at the molecular level.

Read the full article: The Plant Cell

Published by

Willem Van Cotthem

Honorary Professor of Botany, University of Ghent (Belgium). Scientific Consultant for Desertification and Sustainable Development.

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