Investigating molecular modes of heat stress effects on immune response using the Sclerotinia-Arabidopsis pathosystem as a model
Abstract of Ph.D Project
Plants depend on a specific temperature range for optimal growth and development. While moderate increases above this range can accelerate growth, heat stress impairs generative and reproductive development and decreases resistance against bacterial and fungal pathogens, thereby reducing yield stability in crops. The suppressive effects of heat on biotic stress resistance are mediated by genetic and epigenetic modifications in immune-responsive genes and emerging evidence suggests that the plant hormones brassinosteroids (BRs) play a role in this regulatory process. This thesis investigates whether the BR-controlled bHLH transcription factor CESTA and its homologs, BEE1-3, induce DNA methylation changes that suppress resistance to the necrotrophic fungus Sclerotinia sclerotiorum and whether heat stress activates this signaling cascade in Arabidopsis thaliana. Molecular genetic studies using mutants are complemented by a proteomics approach aimed at defining the heat stress-regulated proteome and identifying putative subgroups involved in plant immunity. This proteomics analysis will be conducted in both A. thaliana and Helianthus annuus (sunflower) to evaluate whether findings from the model plant can be translated to sunflower, an oilseed crop with high importance in Europe that’s significantly affected by Sclerotinia.