Calcium signalling in stomatal responses to pollutants

Authors

  • Martin R. McAinsh,

    Corresponding author
    1. Institute of Environmental and Natural Sciences, Department of Biological Sciences, Lancaster University, Lancaster LA1 4YQ, UK
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  • Nicky H. Evans,

    1. Institute of Environmental and Natural Sciences, Department of Biological Sciences, Lancaster University, Lancaster LA1 4YQ, UK
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  • Lucy T. Montgomery,

    1. Institute of Environmental and Natural Sciences, Department of Biological Sciences, Lancaster University, Lancaster LA1 4YQ, UK
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  • Kathryn A. North

    1. Institute of Environmental and Natural Sciences, Department of Biological Sciences, Lancaster University, Lancaster LA1 4YQ, UK
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Author for correspondence: Martin R. McAinsh Tel: +44 1524593929 Fax: +44 1524843854 Email: m.mcainsh@lancaster.ac.uk

Summary

Stomatal responses to air pollutants are complex, varying among species and with concentration, environmental conditions and age. In general, short-term exposure to sulphur dioxide (SO2) promotes stomatal opening, whereas longer-term exposure can cause partial stomatal closure. By contrast, the effects of oxides of nitrogen (NOx) are often small or insignificant. The effects of ozone, and oxidative stress, are equally complex. Short-term exposure to ozone stimulates a rapid reduction in stomatal aperture, whilst longer-term exposure causes stomatal responses to become sluggish. The response of stomata to abscisic acid (ABA) has been shown to be slower in plants exposed to a combination of SO2 and NO2 suggesting an adverse effect on guard cell ABA signal transduction. In addition, ozone causes a reduction in stomatal closure under drought conditions. There is an increasing body of evidence to suggest that air pollutants and oxidative stresses can have a marked effect on the Ca2+ homeostasis of guard cells and the intracellular machinery responsible for stomatal movements. Here we discuss the effects of air pollutants on stomatal responses and their possible effects on Ca2+ based signalling in guard cells focusing on the effects of ozone and oxidative stress.

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