Event details

Proliferating cells must make an important cell fate choice with each cycle of cell division: to continue to divide, or to enter dormancy. The molecular mechanisms underpinning this cell fate choice are of fundamental and clinical interest.

My research group aims to address these mechanisms biochemically in vitro and in cells using human epithelial cell lines and primary T lymphocytes as model systems. In this seminar, I will present our work understanding how cyclin-dependent kinase (CDK1) substrate phosphorylation is ordered during cell cycle progression.

Using fixed cell kinase assays, identify a non-proline directed phosphorylation motif for CDK1 that is regulated by CDK1 subunit composition (1). I will also present our work understanding how aberrant cell size promotes senescence by inducing imbalanced proteome scaling and chemi-osmotic stress (2).

1) Cyclin A and Cks1 promote kinase consensus switching to non-proline directed CDK1 phosphorylation

2) Cell overgrowth during G1 arrest triggers an osmotic stress response and chronic p38 activation to promote cell cycle exit

About the speaker