Analysis of Dehnel’s Phenomenon through Anti-apoptotic BCL-2L1 Knockdown in Mpf Cells

Presenter

Erin Theresa O'Neil

Campus

UMass Boston

Sponsor

Richard G. Hunter, Department of Psychology, UMass Boston

Schedule

Session 3, 1:30 PM - 2:15 PM [Schedule by Time][Poster Grid for Time/Location]

Location

Poster Board A81, Campus Center Auditorium, Row 5 (A81-A100) [Poster Location Map]

Abstract

Eurasian common shrews (Sorex Araneus) have been shown to reduce their skull and brain size by up to 30% in winter, and rapidly regrow to a second maximum in the spring. This process is known as Dehnel’s phenomenon (DP). It is unknown how or why this occurs, and many of the underlying mechanisms have yet to be understood. It is hypothesized that changes in brain size may be to reduce food requirement and energy use independent of environmental changes. This research focuses on the possibility that this system is genetically encoded in the genome. Preliminary data has identified BCL2L1 as a potential genetic mediator of DP. BCL2L1 is an anti-apoptotic protein which promotes cell survival. In this project, ferret neural cells (Mpf) will be used to observe the effects of BCL2L1 knockdown. Mpf cells are used because ferrets also exhibit this phenomenon and are phylogenetically the closest species to shrews, whose neuronal cells have no existing culture system. Mpf cells have been multiplied in culture media for future experimentation and analysis. BCL2L1 will be knocked down using small interfering RNA (siRNA) transfection, causing induced RNA interference to inactivate the protein. We will also examine activated Caspase 3, an apoptotic mark, to observe the role of BCL2L1 in an apoptotic mechanism. Understanding from this phenomenon has implications for possible treatment of neurodegenerative disorders, such as in Alzheimer’s and Parkinson’s disease. 

Keywords

apoptosis, neurogenesis, neural cell culture

Research Area

Neuroscience and Cognitive Science

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