Flagellin receptor FLAGELLIN-SENSING2 in mediating stomatal response to Pseudomonas syringae


A prominent role of the flagellin receptor FLAGELLIN-SENSING2 in mediating stomatal response to Pseudomonas syringae pv tomato DC3000 in Arabidopsis.

by Zeng W., He S.Y. (2010)

Weiqing Zeng, Sheng Yang He

in Plant Physiol. 153:1188–1198. – doi: 10.1104/pp.110.157016 –

PubMed Abstract | CrossRef Full Text | Google Scholar –


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The FLAGELLIN-SENSING2 (FLS2) receptor kinase recognizes bacterial flagellin and initiates a battery of downstream defense responses to reduce bacterial invasion through stomata in the epidermis and bacterial multiplication in the apoplast of infected plants.

Recent studies have shown that during Pseudomonas syringae pv tomato (Pst) DC3000 infection of Arabidopsis (Arabidopsis thaliana), FLS2-mediated immunity is actively suppressed by effector proteins (such as AvrPto and AvrPtoB) secreted through the bacterial type III secretion system (T3SS).

We provide evidence here that T3SS effector-based suppression does not appear to be sufficient to overcome FLS2-based immunity during Pst DC3000 infection, but that the phytotoxin coronatine (COR) produced by Pst DC3000 also plays a critical role. COR-deficient mutants of Pst DC3000 are severely reduced in virulence when inoculated onto the leaf surface of wild-type Columbia-0 plants, but this defect was rescued almost fully in fls2 mutant plants.

Although bacteria are thought to carry multiple microbe-associated molecular patterns, stomata of fls2 plants are completely unresponsive to COR-deficient mutant Pst DC3000 bacteria. The responses of fls2 plants were similar to those of the Arabidopsis Gprotein alpha subunit13 mutant, which is defective in abscisic acid-regulated stomatal closure, but were distinct from those of the Arabidopsis nonexpressor of PR genes1 mutant, which is defective in salicylic acid-dependent stomatal closure and apoplast defense.

Epistasis analyses show that salicylic acid signaling acts upstream of abscisic acid signaling in bacterium-triggered stomatal closure. Taken together, these results suggest a particularly important role of FLS2-mediated resistance to COR-deficient mutant Pst DC3000 bacteria, and nonredundant roles of COR and T3SS effector proteins in the suppression of FLS2-mediated resistance in the Arabidopsis-Pst DC3000 interaction.


Stomatal and/or apoplastic defenses against Pseudomonas syringae

Photo credit: Google

Infection of tomato fruit, tomato leaves and Arabidopsis with P. syringae pv. tomato (photos by Tom Zitter and R. Thilmony)


A genetic screen reveals Arabidopsis stomatal and/or apoplastic defenses against Pseudomonas syringae pv. tomato DC3000

by Zeng W., Brutus A., Kremer J. M., Withers J. C., Gao X., Jones A. D., He S. Y. (2011)

Department of Energy Plant Research Laboratory, Howard Hughes Medical Institute, Department of Plant Biology, Michigan State University, East Lansing, Michigan, USA

in PLoS Pathogens. 2011;7:e1002291.- doi:10.1371/journal.ppat.1002291. – 

[PMC free article] [PubMed] – 


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Bacterial infection of plants often begins with colonization of the plant surface, followed by entry into the plant through wounds and natural openings (such as stomata), multiplication in the intercellular space (apoplast) of the infected tissues, and dissemination of bacteria to other plants.

Historically, most studies assess bacterial infection based on final outcomes of disease and/or pathogen growth using whole infected tissues; few studies have genetically distinguished the contribution of different host cell types in response to an infection.

The phytotoxin coronatine (COR) is produced by several pathovars of Pseudomonas syringae. COR-deficient mutants of P. s. tomato (Pst) DC3000 are severely compromised in virulence, especially when inoculated onto the plant surface.

We report here a genetic screen to identify Arabidopsis mutants that could rescue the virulence of COR-deficient mutant bacteria. Among the susceptible to coronatine-deficient Pst DC3000 (scord) mutants were two that were defective in stomatal closure response, two that were defective in apoplast defense, and four that were defective in both stomatal and apoplast defense.

Isolation of these three classes of mutants suggests that stomatal and apoplastic defenses are integrated in plants, but are genetically separable, and that COR is important for Pst DC3000 to overcome both stomatal guard cell- and apoplastic mesophyll cell-based defenses.

Of the six mutants defective in bacterium-triggered stomatal closure, three are defective in salicylic acid (SA)-induced stomatal closure, but exhibit normal stomatal closure in response to abscisic acid (ABA), and scord7 is compromised in both SA- and ABA-induced stomatal closure.

We have cloned SCORD3, which is required for salicylic acid (SA) biosynthesis, and SCORD5, which encodes an ATP-binding cassette (ABC) protein, AtGCN20/AtABCF3, predicted to be involved in stress-associated protein translation control. Identification of SCORD5 begins to implicate an important role of stress-associated protein translation in stomatal guard cell signaling in response to microbe-associated molecular patterns and bacterial infection.

Author Summary

Pathogen entry into host tissue is a critical first step in causing infection. For foliar bacterial plant pathogens, natural surface openings, such as stomata, are important entry sites into the leaf apoplast (internal intercellular spaces).

Recent studies have shown that plants respond to surface-inoculated bacterial pathogens by reducing stomatal aperture as part of the innate immune response to restrict bacterial invasion. Once inside plant tissue, bacteria encounter defenses in the apoplast.

To counter host defenses during invasion and in the apoplast, bacterial pathogens produce a variety of virulence factors, such as the polyketide toxin coronatine produced by Pseudomonas syringae pv. tomato (Pst) DC3000.

Coronatine-deficient Pst DC3000 mutants are compromised in virulence, especially when inoculated onto the plant surface.

In this study, we conducted a random genetic screen to identify Arabidopsis mutants that could rescue the virulence of coronatine-deficient mutant bacteria and obtained three classes of Arabidopsis mutants: those that are defective in stomatal closure only, those defective in apoplastic defense only, and those compromised in both stomatal closure and apoplastic defenses.

The isolation of these host mutants highlight the important role of COR, a molecular mimic of the plant hormone jasmonate, in overcoming both stomatal and apoplastic defenses during Pst DC3000 infection.

Zeaxanthin in blue light photoreception and stomata


Role of zeaxanthin in blue light photoreception and the modulation of light-CO2 interactions in guard cells

by Zeiger E., Zhu J. (1998)

Department of Biology,University of California,Los Angeles
CA 90095-1606,USA

in Journal of Experimental Botany 49: 433–442. – doi: 10.1093/jxb/49.Special_Issue.433 –

CrossRef Full Text | Google Scholar – Abstract/FREE Full Text



The stomatal response to blue light is an intrinsic component of the sensory transducing processes mediating light-stimulated stomatal movements. Guard cell chloroplasts have a specific blue light response with an action spectrum that resembles the action spectrum for blue light-stimulated stomatal opening, suggesting a role of guard cell chloroplasts in the sensory transduction of blue light.

The xanthophyll, zeaxanthin has recently been identified as a blue light photoreceptor in guard cells. The inhibitor of zeaxanthin formation, dithiothreitol, inhibits zeaxanthin formation and the stomatal response to blue light in a concentration-dependent fashion.

In greenhousegrown leaves, guard cell zeaxanthin content closely tracks incident radiation and it is positively correlated with stomatal apertures. The sensitivity of guard cells to blue light co-varies with guard cell zeaxanthin content. A zeaxanthin-less mutant of Arabidopsis is devoid of a typical stomatal response to blue light.

At constant light and temperature, changes in ambient [CO2] in a growth chamber caused large changes in stomata aperture and in guard cell zeaxanthin. The aperture zeaxanthin changes were linearly related over a wide range of [CO2].

Experiments with detached epidermis showed a similar relation among [CO2], stomatal apertures and guard cell zeaxanthin, and DTT inhibited the CO2 response in the light without altering the CO2 response in the dark.

These results indicate that blue light sensing by guard cell zeaxanthin has a regulatory role in the light response of stomata. Zeaxanthin also appears to mediate light-CO2 interactions in guard cells.