Atmospheric H 2 S exposure does not affect stomatal aperture in maize

Main conclusion Stomatal aperture in maize is not affected by exposure to a subtoxic concentration of atmospheric H 2 S. At least in maize, H 2 S, thus, is not a gaseous signal molecule that controls stomatal aperture. Abstract Sulfur is an indispensable element for the physiological functioning of plants with hydrogen sulfide (H 2 S) potentially acting as gasotransmitter in the regulation of stomatal aperture. It is often assumed that H 2 S is metabolized into cysteine to stimulate stomatal closure. To study the significance of H 2 S for the regulation of stomatal closure, maize was exposed to a subtoxic atmospheric H 2 S level in the presence or absence of a sulfate supply to the root. Similar to other plants, maize could use H 2 S as a sulfur source for growth. Whereas sulfate-deprived plants had a lower biomass than sulfate-sufficient plants, exposure to H 2 S alleviated this growth reduction. Shoot sulfate, glutathione, and cysteine levels were significantly higher in H 2 S-fumigated plants compared to non-fumigated plants. Nevertheless, this was not associated with changes in the leaf area, stomatal density, stomatal resistance, and transpiration rate of plants, meaning that H 2 S exposure did not affect the transpiration rate per stoma. Hence, it did not affect stomatal aperture, indicating that, at least in maize, H 2 S is not a gaseous signal molecule controlling this aperture.