Jean Smith, Graduate Student
Cell fusion is a ubiquitous process in eukaryotic organisms, yet little is known about the distinct molecular mechanisms that control how two cells fuse. During mating of the budding yeast, Saccharomyces cerevisiae, two cells of opposite mating types fuse to form a diploid zygote, making this organism an excellent model with which to study cell fusion. Fus2p, a pheromone-induced protein necessary for cell fusion, localizes to the shmoo tip and is thought to regulate the fusion of vesicles at the zone of cell fusion leading to cell wall breakdown. My work focuses on understanding how Fus2p functions by investigating the role of interacting partners and suppressors.
Matthew Remillard, Graduate Student
Junwon Kim, Postdoc
How higher eukaryotes regulate a protein important for differentiation to operate at the right time and place is a fundamental problem. In budding yeast pheromone-responsive Fus2p, a key regulator of cell fusion, remains sequestered in the nucleus until cell division is completed, after which it exits and moves to the mating tip. I am working to understand how pheromone signaling pathway and cell cycle regulators coordinate to ensure Fus2p exits the nucleus and becomes activated only after cell division.
Alumni and Visitors
Michael L. Smith
Kinnari Matheson, Graduate Student
Allison Hall, Graduate Student
Haploid yeast cells are able to respond to pheromone, polarize their growth toward a mating partner, and fuse to form a diploid zygote. The initial step in cell fusion is the degradation of the cell wall between the mating partners to allow plasma membrane fusion and eventual nuclear fusion. Because the improper timing or location of cell wall degradation would lead to cell lysis and death, this process is tightly regulated. The signal that indicates when cell wall degradation is appropriate has not been identified. My work focuses on identifying the signal for initial cell wall degradation during yeast mating using a combination of classic genetics and microscopy.
Leslie Alexis, Graduate Student
Irene N. Ojini, Graduate Student
The clinical consequences of chemoresistance underscore the need to discover novel treatments. Because of the elevated mutation rate, DNA mismatch repair defective tumors tend to be highly heterogeneous. Therefore, the most promising treating options should exploit the loss of function of mismatch repair rather than the diverse downstream pathways altered in the tumor. My research involves taking a “synthetic-lethal” approach to treating mismatch repair defective tumors. Since experimentation is difficult and expensive in mammals we employ yeast, an ideal experimental organism for studying eukaryotic mismatch repair.
May Husseini, Lab Manager 609-258-2709
Frontiers of Science