Fig 8. Contribution of RPP1-like^Ler DM2h to autoimmunity.

A. Suppression of old3-1-induced autonecrosis by nde1-1. Col/Ler hybrids homozygous for old3-1 and either RPP1-like^Ler or RPP1-like^nde1-1 and control plants were grown at 28°C for three weeks. Plants were then shifted to 18°C or not (Ler old3-1 28°C), and phenotypes recorded at 8 d pts. F₃ families originating from crosses of old3-1 with two independent Col-RPP1-like^Ler or Col-RPP1-like^nde1-1 NILs were tested with similar results. Growth of Col plants was documented in the same experiment under the same conditions, but not in the same image, and is therefore separated by a dashed white line. B. PR1 and EDS1 gene expression in the lines shown in (A). RNA was extracted from the same plants at 24 h pts and cDNA used for transcript analysis by qRT-PCR. Gene expression was normalized to UBQ10. Standard deviation of three biological replicates is shown. Letters indicate statistically significant differences (ANOVA, Tukey’s Post-hoc test, p < 0,01). C. Suppression of SRF3^Kas/Kond-induced hybrid necrosis by nde1-1. Col NILs containing either RPP1-like^Ler or RPP1-like^nde1-1 were crossed to Kas and Kond, and occurrence of incompatible hybrids was recorded in 5-week-old F₂ plants grown at 14°C (the restrictive temperature for Ler x Kas-2/Kond HI [27]. Numbers of wild type-like or necrotic plants observed in different F₂ populations are indicated. Chi² values for the segregation hypothesis of 1/16 necrotic/wild-type plants are indicated for segregating F₂s.