From stress signal to coordinated cell-cycle arrest

The Engeland laboratory studies transcriptional networks that determine whether a cell continues dividing or enters arrest. A central focus is the p53–p21–DREAM–E2F/CHR pathway: p53 activates p21, cyclin-dependent kinase activity falls, and RB-family pocket proteins assemble repressor complexes that silence broad programmes of cell-cycle genes. The group combines promoter dissection, genome-scale expression and binding analysis, gene editing, protein-complex biology and quantitative cell-cycle assays to distinguish the contributions of DREAM, RB:E2F and activating MuvB–MYB complexes. Current work extends this framework to BRCA1/2 and DNA-repair genes, A-MYB/B-MYB redundancy, and new assays that track cell death and division in the same population.