Mon, Oct 1, 2018
The Biology Monday Seminar for September 24th will feature presentations by Honors students in Biology, BCBP, and Chemistry who are working with a Biology mentor. The following students are presenting today:
Rachel Cohen Biology Advisor: Michael Hood
Augusta Hollers Biology Advisor: Sarah Goodwin
Jocelyn Hunyadi Biology Advisor: Ethan Clotfelter
Elisa Bello BCBP Advisor: Alexandra Purdy
David Brinkley BCBP Advisor: Caroline Goutte
Sophia Doerr BCBP Advisor: Katerina Ragkousi
Erik Zhang BCBP Advisor: Marc Edwards
Mon, Oct 15, 2018
Biology Monday Seminar
Katie Kindt, Ph.D.
National Institutes of Health
National Institute on Deafness and other Communication Disorders
"Using transgenic zebrafish to light up hair-cell synapse formation and function"
Sensory hair-cells are required to reliably transmit auditory and vestibular information to the brain. While the majority of hearing loss is due to damage of sensory hair cells, there is accumulating evidence that in cases of noise-induced hearing loss, the pathology may be due to damage of hair-cell synapses rather than hair cells. Therefore, to restore hearing loss after synapse damage is it critical to understand 1) the molecular requirements and 2) the function and assembly of synapses in vivo. Our research studies leverage the strengths of the zebrafish model system by using genetics and in vivo imaging to dissect the molecular and functional requirements underlying hair-cell synapse function and assembly. Recently we examined how ensembles of sensory hair cells function in vivo using optical indicators in intact zebrafish. Our imaging unexpectedly revealed that the majority of hair cells are synaptically silent. Latent hair cells can be rapidly recruited after damage, demonstrating that they are synaptically competent. Therefore synaptically silent hair cells may be an important reserve that acts to maintain sensory function. Although it is not yet known, it will be exciting to see if our data are generalizable to other hair-cell organs and model systems.
Refreshments at 3:45 PM in Science Center A011
Mon, Oct 22, 2018
Allen Hurlbert '94, PhD
Department of Biology
University of North Carolina
In the Hurlbert Lab, we ask questions about the structure of ecological communities and the processes that are responsible for determining the patterns of diversity, composition, turnover and relative abundance both within local assemblages and around the globe. Our work spans vertebrate, invertebrate and plant communities, and we use a variety of approaches from manipulative experiments to modeling to working with global-scale data sets.
Mon, Oct 29, 2018
Barbara A. Osborne, Ph.D.
Professor, Veterinary and Animal Sciences
Co-director, Center for Bioactive Delivery, Institute for Applied Life Sciences
University of Massachusetts, Amherst
Research in the Osborne Lab
The Osborne laboratory focuses on the differentiation and function of mature CD4+ lymphocytes. In particular, we are interested in the role of Notch proteins in CD4+ maturation and function. Over the past several years, we have demonstrated that Notch plays a critical role in the differentiation of the T-helper 1 (Th1) and T-helper17 (Th17) subsets of T cells. Both Th1 and Th17 cells have been implicated in several diseases, including experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis. Using gamma-secretase inhibitors (GSIs), compounds that block the activation of Notch, we have found that we can block the development of EAE in mice, suggesting that GSIs may be a possible therapeutic for the treatment of MS. Our current studies are focused on determining how Notch signaling influences the development of EAE, as well as determining which Notch family member is important in the development of disease. In mammals, there are four Notch family members, and it is unclear which Notch family member is most important in driving EAE.
Notch signaling is initiated by two enzymatic cleavages. The first cleavage, driven by ADAM proteases, is required for the second cleavage, mediated by gamma-secretase, which results in the release of the intra-cellular domain of Notch and initiates the Notch signaling cascade. Notch signaling can be blocked by gamma-secretase inhibitors, and our lab, in collaboration with colleagues at UMass, UFlorida and LSU Medical School, investigates how gamma-secretase inhibition may be used to modulate immune responses. We also are actively investigating whether Notch signaling in CD4+ T cells is mediated through canonical Notch signaling. Our data suggest Notch signaling in T cells occurs through a non-canonical pathway and current research is focused on a clearer description of this non-canonical pathway.