Atmospheric H₂S exposure does not affect stomatal aperture in maize

Stomatal aperture in maize is not affected by exposure to a subtoxic concentration of atmospheric H₂S. At least in maize, H₂S, thus, is not a gaseous signal molecule that controls stomatal aperture. Sulfur is an indispensable element for the physiological functioning of plants with hydrogen sulfide (H₂S) potentially acting as gasotransmitter in the regulation of stomatal aperture. It is often assumed that H₂S is metabolized into cysteine to stimulate stomatal closure. To study the significance of H₂S for the regulation of stomatal closure, maize was exposed to a subtoxic atmospheric H₂S level in the presence or absence of a sulfate supply to the root. Similar to other plants, maize could use H₂S as a sulfur source for growth. Whereas sulfate-deprived plants had a lower biomass than sulfate-sufficient plants, exposure to H₂S alleviated this growth reduction. Shoot sulfate, glutathione, and cysteine levels were significantly higher in H₂S-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 H₂S exposure did not affect the transpiration rate per stoma. Hence, it did not affect stomatal aperture, indicating that, at least in maize, H₂S is not a gaseous signal molecule controlling this aperture.