Thomas Hall 3510, Box 7617
Raleigh, NC 27695
My lab studies cell cycle regulatory systems that are essential in maintaining genome stability and preventing mis-segregation of chromosomes during mitosis. We are studying the spindle assembly checkpoint using a combination of genetic and molecular genetic and cell biological approaches. The spindle assembly checkpoint is a regulatory mechanism that inhibits the onset of anaphase until all chromosomes achieve bipolar orientation on the spindle. We have recently identified complexity in the upstream signaling components that are evolutionarily conserved from yeast to humans. My lab, in collaboration with Todd Stukenberg’s lab (University of Virginia) has identified a conserved mechanism that moderates the spindle assembly checkpoint signal by controlling how the signal is extinguished. In addition, we have discovered crosstalk between the spindle assembly checkpoint and the DNA damage checkpoint that regulates the integrity of the response to DNA damage. Environmental agents in in addition to mutations that alter DNA replication induce the central protein kinases of the DNA damage response, ATM and ATR, to phosphorylate and activate spindle assembly checkpoint. We are using high throughput genetic screens to identify novel genes involved in both the spindle assembly and DNA damage checkpoints and gain new insights into how these are important.