Theses and Dissertations - UTB/UTPA

Date of Award


Document Type


Degree Name

Master of Science (MS)



First Advisor

Dr. Robert Gilkerson

Second Advisor

Dr. Megan Keniry

Third Advisor

Dr. Matthew Terry


Mitochondria are an organellar network involved in cellular bioenergetics and apoptosis, and dynamically balance their organization between fusion and fission events. Mitochondrial DNA (mtDNA) and nuclear DNA combine to encode polypeptides for the complexes of oxidative phosphorylation (OXPHOS) in the mitochondrial inner membrane, which generate a transmembrane potential (ΔΨm) to synthesize ATP. Loss of ΔΨm causes mitochondrial fission, which appears to be associated with the progression of apoptosis, a critical cell death mechanism that allows tissue homeostasis, developmental sculpturing, and the removal of unwanted cells. Using cultured human cell models of decreased ΔΨm (both genetic mtDNA-depleted ρ 0 and pharmacological Carbonyl cyanide m-chlorophenyl hydrazone (CCCP)-treated cell models), here we explore whether the loss of OXPHOS increases apoptosis. Based on current results, mtDNA-depleted ρ0 cells are more basally apoptotic compared to wild-type cells, and display loss of viability when challenged with galactose-containing medium. Based on current results, future research will determine whether this loss of viability is indeed apoptosis, as well as whether the bioenergetics defect or loss of fusion mediates the effect.


Copyright 2015 Alan M. Herrera. All Rights Reserved.

Granting Institution

University of Texas-Pan American

Included in

Biology Commons