Reactive Carbonyl Species Mediate ABA Signaling in Guard Cells

Abstract

Drought is responsible for a massive reduction in crop yields. In response to drought, plants synthesize the hormone ABA, which induces stomatal closure, thus reducing water loss. In guard cells, ABA triggers production of reactive oxygen species (ROS), which is mediated by NAD(P)H oxidases. The production of ROS is a key factor for ABA-induced stomatal closure, but it remains to be clarified how the production of ROS is transduced into downstream signaling components in guard cells. We investigated roles of reactive carbonyl species (RCS) in ABA-induced stomatal closure using transgenic tobacco (Nicotiana tabacum) overexpressing Arabidopsis 2-alkenal reductase (AER-OE), which scavenges RCS. ABA and hydrogen peroxide (H₂O₂) induced accumulation of RCS including acrolein and 4-hydroxy-(E)-2-nonenal in wild-type tobacco but not in AER-OE. Stomatal closure and RCS accumulation in response to ABA and H₂O₂ were inhibited in AER-OE unlike in the wild type, while ABA-induced H₂O₂ production in guard cells was observed in AER-OE as well as in the wild type. Moreover, ABA inhibited inward-rectifying K⁺ channels in wild-type guard cells but not in AER-OE guard cells. These results suggest that RCS is involved in ABA-induced stomatal closure and functions downstream of H₂O₂ production in the ABA signaling pathway in guard cells.

Keywords: ABA; Reactive carbonyl species; Reactive oxygen species; Stomatal closure.