Stomatal pores are formed by guard cell pairs in the epidermis of leaves. Stomata regulate the diffusion of CO2 into leaves for photosynthetic carbon fixation and control transpirational water loss of plants. A network of signal transduction mechanisms in guard cells sense and transduce CO2, water status, light and other environmental stimuli to regulate stomatal apertures for optimization of CO2 influx, water loss and plant growth under diverse conditions. Elevated CO2 concentrations in leaves cause stomatal closure, whereas reduced CO2 concentrations result in stomatal opening. Photosynthesis and respiration cause CO2 concentration changes in leaves. Moreover, atmospheric [CO2] is predicted to double within the present century and these ambient CO2 increases reduce stomatal apertures of different plant species by up to 40 %. However, relatively little is known about the molecular signal transduction mechanisms in guard cells that mediate CO2-induced stomatal movements. A study suggests that cytosolic calcium ([Ca2+]cyt) elevations contribute to CO2-induced stomatal movements. New findings in the P.I.'s laboratory show that changes in [CO2] modulate cytosolic [Ca2+]cyt elevations in Arabidopsis guard cells. The guard cell CO2 response provides an opportune system to analyze hypotheses that cytosolic Ca2+ patterns contribute to signal transduction in plants. The long term goal of this research is to achieve an understanding of the molecular mechanisms that mediate CO2 signal transduction in guard cells. The research will investigate the hypothesis that CO2 modulation of the [Ca2+]cyt elevation pattern in guard cells contributes to CO2-induced signal transduction during stomatal closing and/or opening. To test this hypothesis, studies with the following specific aims will be pursued: Characterize CO2 responses of wildtype guard cells. Examine the effects on CO2 signal transduction of known mutants that affect Ca2+ and/or abscisic acid signaling at distinct points within the guard cell signaling network, to characterize genetic mechanisms that affect CO2 signaling and to determine which components are specific to defined signaling pathways. Gain insight into how [Ca2+]cyt is transduced and specifically define the roles of selected guard cell-expressed CDPKs in stomatal responses. Characterize new CO2 signaling mutants. The P.I. will further pursue outreach efforts through public forums and through research and career training and preparation of undergraduate and high school students. Understanding the molecular mechanisms by which CO2 modulates stomatal apertures is fundamental to understanding the regulation of gas exchange between plants and the atmosphere, will help to predict effects of atmospheric CO2 elevation on stomata and may also contribute to future engineering of crop plants and plant carbon sinks in the face of changing environmental conditions.
