Poster
Laura Alexandra Randarevitch
Department of Population Genetics, Heinrich Heine University, Dusseldorf
Düsseldorf, NRW, GERMANY
Zahra Zangishei
PhD Student
Institute for Biological Data Science, Heinrich Heine University, Dusseldorf.
Duesseldorf, Nordrhein-Westfalen, Germany
Björn Usadel
Principal Investigator
Institute for Biological Data Science, Heinrich Heine University, Dusseldorf
Duesseldorf, Nordrhein-Westfalen, Germany
Laura Rose
Principal Investigator
Department of Population Genetics, Heinrich Heine University, Dusseldorf.
Dusseldorf, Nordrhein-Westfalen, Germany
Plants lack a circulatory immune system and must therefore rely on cell-autonomous mechanisms to recognize pathogens and initiate defence responses. This defence relies on resistance (R) genes, which can be broadly classified into those responsible for pathogen detection and those involved in executing the defence response. In many cases, the defence response results in localized programmed cell death, known as the hypersensitive response, to restrict pathogen spread. We evaluated the genetic variation of resistance genes and a subset of housekeeping genes within and between individuals of Solanum pennellii. Given the diversity of resistance gene classes, we focused on a subset of genes belonging to the nucleotide-binding leucine-rich repeat (NLR) gene family, including homologs of the ZAR1 gene in Arabidopsis thaliana. The ZAR1 protein forms a pentameric structure, termed the resistosome, upon pathogen detection. It functions as a calcium channel, triggering immune signalling and promoting cell death. By performing population genetic analyses, we evaluated these genes for deviations from neutrality, signatures of selection and the potential impact of purifying selection due to functional constraints. Furthermore, by integrating gene expression levels, measured as TPM, we explored the relationship between gene expression and evolutionary pressures, providing deeper insights into the adaptive significance of resistance genes in S. pennellii.