B Baumeister C. elegans

1. find the gene of interest that is associated with the human disease

2. Identify the C. elegans homologue

3. Manipulate the gene in C- elegans

   • RNAi

   • CRISPR / CAS9 + Non homologues end joining or insertions with homology direct repair

4. Identify the phenotype

5. use the results for pharma research, search fr modifier genes or reaseach the mode of action

6. Translate the findings into human (or mouse) context

Example used = Muscular Dystrophy -> mutant in C. elegans analyszed and the knockdown of one gene (sup-1) rescued the degrading muscles -> simple assay with C. elegans

serum-and-glucocorticoid-inducible Kinase

SGK-1 + SKN-1 have distinct roles in nervous system (food sensing) and intestine (stress signaling) -> 2 phase detoxification

ENDU-2 is expressed in somatic tissues (incl . the uterus)

-> may encode a secreted protein

-> stress & pathogens activate secretion of ENDU-2 from the soma to the germline

-> germline effects of ENDU-2 depend on secretion

ENDU-2 can both positively and negatively affect mRNA abundance -> class 1 (germline genes) upregulated and class 2 (somatic genes) down

endu-2 null mutants loose germline/stem cell immortality