Honors Program Theses

Award/Availability

Open Access Honors Program Thesis

First Advisor

Ira Simet

Abstract

Mitochondria are medium-sized organelles in which most cellular metabolic reactions are carried out. In postmitotic cells that are aged or diseased, such as myocardial, skeletal, and brain cells, abnormally large mitochondria ("giant mitochondria") are often observed. Mitochondrial size and shape are controlled by mitochondrial fusion and fission and disruption of this process may lead to their abnormally large size (Nauratil, Terman, Arriaga, 2008). These giant mitochondria exhibit variations from normal metabolism and altered membrane potentials (Nauratil et al., 2008). An increased number of giant mitochondria may therefore disrupt cell function (Nauratil et al., 2008). This accumulation may result either from the failure of macroautophagy to remove damaged organelles or from impaired fusion with normal mitochondria, which would allow repair by exchange of matrix contents. Since proteins such as mitofusin-1, mitofusin-2, and OP Al participate in fusion, their under- or overexpression could lead to the development of giant mitochondria (Nauratil et al., 2008). Measurement of the levels of these proteins in normal and giant mitochondria could provide insight into the development of giant mitochondria and their inability to fuse. This information could also be useful in understanding the aging of cells, in which giant mitochondria could play a prominent role.

Year of Submission

2009

Department

Department of Chemistry and Biochemistry

University Honors Designation

A thesis submitted in partial fulfillment of the requirements for the designation University Honors

Comments

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Date Original

11-2009

Object Description

1 PDF file (32 pages)

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