Guard cell metabolism and CO2 sensing

Abstract

In this review we concentrate on guard cell metabolism and CO2 sensing. Although a matter of some controversy, it is generally accepted that the Calvin cycle plays a minor role in stomatal movements. Recent data emphasise the importance of guard cell starch degradation and of carbon import from the guard cell apoplast in promoting and maintaining stomatal opening. Chloroplast maltose and glucose transporters appear to be crucial to the export of carbon from both guard and mesophyll cells. The way guard cells sense CO2 remains an unresolved question. However, a better understanding of the cellular events downstream from CO2 sensing is emerging. We now recognise that there are common as well as unique steps in abscisic acid (ABA) and CO2 signalling pathways. For example, while ABA and CO2 both trigger increases in cytoplasmic free calcium, unlike ABA, CO2 does not promote a cytoplasmic pH change. Future advances in this area are likely to result from the increased use of techniques and resources, such as, reverse genetics, novel mutants, confocal imaging, and microarray analyses of the guard cell transcriptome.