CELL CYCLE CHECKPOINT AND MAP KINASE SIGNALING


Research in our group deals with the mechanisms (called checkpoints) by which a eukaryotic cell signals the presence of conditions that should stop or delay cell cycle progression. Examples of such conditions are DNA damage (will delay entry into mitosis or S phase) and unreplicated DNA (will prevent mitosis). If this signalling is somehow perturbed, such as in mutants affected in any of several genes essential for these pathways, progression in the cell cycle will continue in spite of e.g. DNA damage. As a result, such mutant cells will acquire a higher number of mutations. Humans with the cell cycle checkpoint disorder Ataxia telangiectasia are hypersensitive to ionizing radiation and have an increased cancer risk. In our lab, we work mainly with the yeasts Schizosaccharomyces pombe (fission yeast) and Saccharomyces cerevisiae (budding yeast) as genetic model organisms. We try to work out the mechanisms of action and relationships between individual checkpoint gene products. Among the issues we are studying are:  

 EU-funded QUASI project

Yeast genes of interest:

S. cerevisiae:
RCK1, RCK2, RAD17, RAD24, MEC1, TEL1, HOG1
Sz. pombe: rad1+, rad3+, rad9+, rad17+, rad26+, hus1+