Dr. Crestina Beites is an associate professor at the School of Midwifery where she teaches Life Sciences, Reproductive Physiology and Pharmacotherapeutics in both the English and French streams. She is also currently cross-appointed to the Dept of Biochemistry and Chemistry. After graduating with a BSc Hon in Biochemistry from LU, Crestina obtained her PhD at the University of Toronto where she studied synaptic transmission and completed a postdoctoral fellowship studying neural regeneration at the University of California, Irvine. Her current research focusses on understanding how growth factors instruct neural stem cells to either self-renew or redirect their fate to become any cell type in the brain. She is addressing this fundamental question using mouse models of brain development.
- Postdoctoral Fellowship, University of California, Irvine
- PhD, Programme in Cell Biology, Hospital for Sick Children and Dept of Biochem, University of Toronto
- BSc. Dept of Chemistry and Biochemistry, Laurentian University
During embryonic brain development, instructive factors secreted by neighboring cells influence neural stem cell behaviour. Stem cells interpret these factors as either self-renewing or differentiating programmes and consequently adopt specific fates: the stem cell either replenishes its undifferentiated stem cell pool or undergoes neurogenesis. Influential factors affecting disparate stem cell fate decisions play pivotal roles in normal brain development and repair. Not only do they control proper brain formation and function but aberrant signaling by these factors can also lead to 1) uncontrollable self-renewal as seen in neural cancers and 2) misdirected fate choices evident in pathologies involving abnormal organ formation and developmental disabilities of the nervous system. To understand the fundamental biology of neuron production, we are pursuing the role of the Transforming Growth Factor Beta (TGF-b) superfamily in directing neural stem cell fate. Using genetic and biochemical approaches in neural tissue from transgenic mice lacking certain TGF-b superfamily genes our goal is to specifically define stem cell regulatory networks affected by TGF-b signaling.