Plant stomata: a checkpoint of host immunity and pathogen virulence

Abstract

Stomata are microscopic pores formed by pairs of guard cells in the epidermis of terrestrial plants; they are essential for gas exchange with the environment and controlling water loss. Accordingly, plants regulate stomatal aperture in response to environmental conditions, such as relative humidity, CO(2) concentration, and light intensity. Stomatal openings are also a major route of pathogen entry into the plant and plants have evolved mechanisms to regulate stomatal aperture as an immune response against bacterial invasion. In this review, we highlight studies that begin to elucidate signaling events involved in bacterium-triggered stomatal closure and discuss how pathogens may have exploited environmental conditions or, in some cases, have evolved virulence factors to actively counter stomatal closure to facilitate invasion.

Figure 1

A model showing some of the signaling components involved in MAMP/bacterium-triggered stomatal closure. Pst DC3000 is illustrated as an example. In guard cells, MAMPs (e.g., flagellin) are perceived by their cognate PRRs (pattern recognition receptors), such as the flagellin receptor FLS2. Perception of MAMPs triggers stomatal closure, which requires phytohormones SA and ABA, as well as some SA and ABA signaling components. MAMP signaling prevents stomatal opening by inhibiting inwardly rectifying K⁺ channels (K⁺_in) through some ABA signaling components (GPA1 and likely others). COR inhibits MAMP-triggered stomatal closure; this process requires COI1 (a receptor of COR) and RIN4. RIN4 binds and activates the proton pump (H⁺-ATPase), causing membrane hyperpolarization, activation of K⁺ influx (K⁺_in), and stomatal opening. Dashed lines indicate uncertain connections.