Many plant pathogens induce water-soaked lesions in infected tissues. In the case of Pseudomonas syringae (Pst), water-soaking effectors stimulate abscisic acid (ABA) production and signaling, resulting in stomatal closure. This reduces transpiration, increases water accumulation, and induces an apoplastic microenvironment favorable for bacterial growth. Stomata are sensitive to environmental conditions, including light. Here, we show that a period of darkness is required for water-soaking, and that a constant light regime abrogates stomatal closure by Pst. We find that constant light induces resistance to Pst, and that this effect requires salicylic acid (SA). Constant light did not alter effector-induced accumulation of ABA, but induced greater SA production, promoting stomatal opening despite the presence of ABA. Furthermore, application of a SA analog was sufficient to prevent pathogen-induced stomatal closure and water-soaking. Our results suggest potential approaches for interfering with a common virulence strategy, as well as providing a physiological mechanism by which SA functions in defense against pathogens.

Upon establishment of an infection, many plant pathogens induce an aqueous microenvironment in the extracellular space of their host, resulting in water-soaked lesions. In the case of Pseudomonas syringae (Pst), this is accomplished through the activity of water-soaking effectors that stimulate abscisic acid (ABA) production and signaling, which results in stomatal closure. This reduces transpiration and induces a microenvironment favorable for bacterial growth. Stomata are also highly sensitive to environmental conditions, including light and circadian rhythm. Here, we show that a period of darkness is required for water-soaking, and that a constant light regime abrogates the water-soaking activity of Pst effectors. Additionally, we show that constant light induces resistance against Pst and that this effect requires salicylic acid (SA). An increase in SA production upon infection under constant light did not affect effector-induced ABA signaling, but rather abrogated ABA's ability to induce stomatal closure. Indeed, under normal diurnal light regimes, application of a SA analog is sufficient to prevent the ability of the pathogen to induce stomatal closure and a water-rich niche in the apoplast. Our results provide a novel approach to interfering with a common virulence strategy, as well as providing a physiological mechanism by which SA functions in defense against certain pathogens.