Supplementary MaterialsS1 Fig: Autoimmune mutants exhibit temperature-dependent disease resistance against DC3000. indicate statistically significant variations between indicated plant lines (in guard cells reduces autoimmunity in transgenic lines grown at 22C, 12h/12h L/D. White arrows point to the flat young leaves of plants with transgene in their guard cells compared to the twisted young leaves of -/plants without transgene (Scale bar = 1 cm).(TIF) ppat.1008094.s004.tif (1.9M) GUID:?7D74E480-FFB7-493C-BA30-7378AE43037C S5 Fig: Stomatal aperture in Col-0 and chimeras at 10 am and 12 pm. Shown are stomatal apertures measured at 10 am and 12 pm in the indicated plant lines at 22C. Results are from one replica representing three biological repeats, error bars indicate SDs (n = 30 stomata). Statistical analysis was performed with one-way ANOVA followed by Tukey-Kramer test (and assayed by qPCR in enriched guard cells (G) and whole leaves (L) with (+) or without (-) DC 3000 infection. Total RNAs were isolated from enriched guard cell preps and whole rosette leaves of 5-week-old plants. The expression was normalized to the expression of a reference Smoc1 gene and relative to their expression in Col-0 Values are arithmetic means S.E., different letters indicate statistically significant differences between indicated plant lines (DC3000. Stomatal apertures in response to buffer alone (mock) and DC3000 strains (with or without indicated effectors) in the Col-0 (a, left panel of b) and (right panel of b). Results are from one set of experiment, error bars indicate Phenytoin sodium (Dilantin) SDs (n = 30 stomata). Asterisks indicate statistically significant differences in stomata aperture between DC3000 and avirulent DC3000 treatment (*, . Recent genetic screens using a pathogen strain deficient in coronatine production and thus disarmed of combating stomatal defense revealed positive regulators affecting only stomatal defense or only apoplastic defense . Surprisingly, some immune regulators are found to have opposite effects on stomatal closure response and whole plant disease resistance. For example, mutants defective in ABA biosynthesis are compromised in stomatal defense  but could gain enhanced whole plant disease resistance . This opposing function of ABA is reconciled by temporal Phenytoin sodium (Dilantin) separation in distinct pre-invasion and post-invasion phases of pathogen infection . One other potential example is the NLR gene whose constitutive active form induces enhanced apoplastic defense  but inhibits stomatal closure response to ABA although the stomatal defense in response to pathogen has not been tested . The more established examples are calcium pumps ACA10 and ACA8 as well as their interacting calcium binding protein BON1, Phenytoin sodium (Dilantin) all of which possess contrasting tasks in stomatal protection and whole vegetable disease level of resistance. The LOF mutants of and so are faulty in stomatal closure response to pathogens but show enhanced level of resistance to the virulent bacterial pathogen (usually do not close stomata in response to pathogens but are even more resistant to DC3000 compared to the crazy type [22,23]. The mutants of are called autoimmune mutants because protection reactions for restricting pathogen development are fired up in the lack of pathogen disease. This upregulation of protection reactions in or mutants can be conferred by or connected with upregulation of gene actions. The Col-0 accession particular gene can be upregulated in the mutant under regular development condition and confers improved disease level of resistance. A No-0 particular gene that confers a constitutive protection response in the mutant is also.