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  • Friday, November 13, 2015
  • 1:30 PM–2:30 PM
  • Science Building 010

Stephan Buiter, JR biology and biochemistry major Megan Van Baren, Jr biology major

Stephan Buiter's talk is titled: Profilin and Its Effects on Cytokinesis in Fission Yeast


Schizosaccharomyces pombe yeast has three actin cytoskeleton structures: patches, cables, and contractile rings. Actin is distributed to these structures from one common pool. One regulatory protein of this distribution is the actin binding protein profilin. Profilin activates the production of rings and cables while inhibiting patch formation. Microscopy is used to study profilin’s roles in fission yeast cytokinesis in a strain where endogenous profilin can be depleted. This strain (cdc30-124) is used to integrate different profilin constructs: WT profilin and two mutant profilins (Y5D and K81E). When these constructs are integrated and expressed weakly in cdc3-124 and endogenous profilin is depleted, most cells have 2 or more nuclei and abnormal septa present, indicating defects in cytokinesis. These results show that profilin’s function is vital for contractile ring formation allowing proper cytokinesis to occur in fission yeast. The results also show the weakest expression level of WT profilin is inadequate to counter the depletion of endogenous profilin, so constructs of higher expression must be studied in the future.

Megan Van Baren will talk about: When Broken Brakes are a Problem: Developing a TSC Cell-Based Screen for Compound Sensitivity


Tuberous Sclerosis Complex, or TSC, is a genetic autosomal dominant disorder characterized by non-malignant tumors in multiple organ systems including the heart, brain, lungs, and kidneys. TSC affects 1 in 6,000 people, and there are approximately one million people worldwide who suffer from the disease. TSC is caused by mutations in the TSC1 or TSC2 genes, which lead to aberrant mTOR signaling and uncontrolled cell growth. Although interventions, such as mTOR inhibitors or surgical resection of tumors, are possible for some aspects of the disease, no cure for TSC is currently known. To better understand the disease and increase potential treatment options, we aim to develop a cell-based screen in order to test compounds for use in treating TSC. The  patient-derived renal angiomyolipoma (AML) cell line, TRI102, which lacks TSC2, and its TSC2-rescued counterpart cell line, TRI103, were chosen to develop the cell-based screen. To better simulate the tumor environment in the physiological conditions of the body, a gradient of growth serums was tested to determine the amount of growth serum needed to allow the TSC null (disease relevant) cells, but not the TSC wildtype cells, to grow. Once developed, this cell-based screen will be used to test a library of FDA approved compounds that potentially could be used to treat TSC.

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