Identification and screening of other esr1 alleles/insertion lines conferring increased resistance to Fusarium oxysporum.

(a-b) Disease phenotypes of F. oxysporum inoculated wild-type (WT) GSTF8:LUC and esr1-2 plants. Values are averages ± SE (n>15). (c) At5g53060/ESR1, LUCIFERASE (LUC) and GSTF8 expression in 12 day old WT and esr1-2 seedlings (values are averages ± SE of 3 biological replicates consisting of pools of 20 seedlings). Gene expression levels are relative to the internal control β-actin genes. (d-g) Disease phenotypes of F. oxysporum inoculated (d-e) Col-0 and SALK_09566, and (f-g) WT GSTF8:LUC and esr1-3 and esr1-4 plants. Values are averages ± SE (n>15). (h) esr1-1, esr1-3 and esr1-4 mutants were crossed and F₁ progeny screened for complementation of the GSTF8:LUC constitutive expression phenotype. Crosses to wild-type (WT) GSTF8:LUC were included as controls. (i) Next Generation Mapping identified esr1-3 and esr1-4 mutations at splice site junctions in At5g53060/ESR1. For Fusarium disease assays, diseased leaves was measured at 14 days post inoculation and survival at 21 days post inoculation. Asterisks indicate values that are significantly different (**P<0.01, *P<0.05 Student’s t-test) from WT or Col-0.