Honors: All College Participants

Title

Characterization of gene expression, glucose responsiveness, and cell proliferation in a pancreatic beta cell hybridoma cell line stably overexpressing the transcription factor Glis3

Academic Level at Time of Presentation

Senior

Major

Exercise Science

Minor

Biology

List all Project Mentors & Advisor(s)

Dr. Gary ZeRuth

Presentation Format

Oral Presentation

Abstract/Description

The transcription factor Gli-similar 3 (Glis3) is important for the specification of insulin-producing beta cells during development and is required for the production of insulin in the mature pancreas. Genetic variants of Glis3 have been implicated in the development of diabetes, however the precise etiology remains unclear. Over the course of the semester, a series of experiments will be conducted to characterize a pancreatic hybridoma cell line that lacks insulin expression. Stable overexpression of Glis3 restores insulin expression in this cell line. The phenotype of the stable cells will be characterized focusing on gene activation levels, glucose responsiveness, and their ability to proliferate. Collectively, these studies may provide insight into Glis3 function and how dysfunction of Glis3 signaling leads to diabetes.

Location

Classroom 211, Waterfield Library

Start Date

November 2016

End Date

November 2016

Affiliations

Honors Thesis

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Nov 15th, 1:30 PM Nov 15th, 3:30 PM

Characterization of gene expression, glucose responsiveness, and cell proliferation in a pancreatic beta cell hybridoma cell line stably overexpressing the transcription factor Glis3

Classroom 211, Waterfield Library

The transcription factor Gli-similar 3 (Glis3) is important for the specification of insulin-producing beta cells during development and is required for the production of insulin in the mature pancreas. Genetic variants of Glis3 have been implicated in the development of diabetes, however the precise etiology remains unclear. Over the course of the semester, a series of experiments will be conducted to characterize a pancreatic hybridoma cell line that lacks insulin expression. Stable overexpression of Glis3 restores insulin expression in this cell line. The phenotype of the stable cells will be characterized focusing on gene activation levels, glucose responsiveness, and their ability to proliferate. Collectively, these studies may provide insight into Glis3 function and how dysfunction of Glis3 signaling leads to diabetes.