Abscisic acid (ABA) is a stress hormone that accumulates under different abiotic and biotic stresses. A typical effect of ABA on leaves is to reduce transpirational water loss by closing stomata and parallelly defend against microbes by restricting their entry through stomatal pores. ABA can also promote the accumulation of polyamines, sphingolipids, and even proline. Stomatal closure by compounds other than ABA also helps plant defense against both abiotic and biotic stress factors. Further, ABA can interact with other hormones, such as methyl jasmonate (MJ) and salicylic acid (SA). Such cross-talk can be an additional factor in plant adaptations against environmental stresses and microbial pathogens. The present review highlights the recent progress in understanding ABA’s multifaceted role under stress conditions, particularly stomatal closure. We point out the importance of reactive oxygen species (ROS), reactive carbonyl species (RCS), nitric oxide (NO), and Ca2+ in guard cells as key signaling components during the ABA-mediated short-term plant defense reactions. The rise in ROS, RCS, NO, and intracellular Ca2+ triggered by ABA can promote additional events involved in long-term adaptive measures, including gene expression, accumulation of compatible solutes to protect the cell, hypersensitive response (HR), and programmed cell death (PCD). Several pathogens can counteract and try to reopen stomata. Similarly, pathogens attempt to trigger PCD of host tissue to their benefit. Yet, ABA-induced effects independent of stomatal closure can delay the pathogen spread and infection within leaves. Stomatal closure and other ABA influences can be among the early steps of defense and a crucial component of plants’ innate immunity response. Stomatal guard cells are quite sensitive to environmental stress and are considered good model systems for signal transduction studies. Further research on the ABA-induced stomatal closure mechanism can help us design strategies for plant/crop adaptations to stress.

Stomatal guard cells are specialized epidermal cells regulating gas exchange. The ability to open or close in response to external and internal cues makes stomata a dynamic and fascinating system. Stomatal closure upon infection ensures restriction of pathogen entry into the plant and forms an essential component of innate immunity. The opening or closure of stomata is dependent on the turgidity or flaccidity of guard cells, respectively, facilitated by several signaling components, including reactive oxygen species, nitric oxide (NO) and Ca 2+ . Among these, NO is the most extensively studied gasotransmitter. Its pivotal role in stomatal closure by modulating various downstream components as well as regulation of crucial proteins by post-translational modifications makes NO an essential factor. Two more gasotransmitters, carbon monoxide and hydrogen sulfide, also trigger stomatal closure. Other gaseous molecules, like ethylene, methane, sulfur dioxide, ozone, and CO2, can modulate stomatal closure, but they are not considered strictly as gasotransmitters due to specific criteria. We review the signaling events in guard cells triggered by these gasotransmitters leading to stomatal closure. We point out the dual role of NO to promote stomatal closure and stomatal opening. Both NO and H2S help in reinforcing the innate immunity against pathogen attack. Although there is extensive information on the mechanism of NO action on stomata, the enzymatic source of NO or CO is still ambiguous. Similarly, research is warranted to establish the relative importance of and interactions among the three main gasotransmitters. Further studies on gasotransmitters would answer the ambiguity about their functions and confirm if they can act independently.

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