Adina Brett Morris, Ph.D
Kyle Whiddon, Ph.D.
Maria Stoll: firstname.lastname@example.org
Elizabeth Akinbiyi: email@example.com
Brianna Bauer: firstname.lastname@example.org
Kristy Rochon: email@example.com
Yuli Buckley: firstname.lastname@example.org
Jasmine Liu: email@example.com
The central goal of the Mears Lab is to examine macromolecular interactions in cells that impact health. Our group has a particular interest on mitochondrial structure and function, and we have focused on large membrane complexes that regulate mitochondrial fission and fusion. These dynamic interactions govern mitochondrial health and function, including energy production, calcium homeostasis and regulation of programmed cell death (apoptosis). In fact, a delicate balance of fission and fusion is needed to prevent morphological changes that impair organelle redistribution and function, and alterations in mitochondrial dynamics has recently come to the forefront as a therapeutic target in several diseases, including neurodegeneration, cancer, and aging.
The lack of mechanistic insight into mitochondrial membrane remodeling remains a major limitation for developing new therapies. To address this shortcoming, our group has focused on defining the functional roles of proteins in the mitochondrial fission complex using diverse strategies, including structural, biochemical and cellular methods. This multifaceted approach seeks to investigate proteins that interact on membranes and alter their morphologies. Since membranes provide a platform for biochemical interactions that drive cell physiology, structural reorganization can alter signaling networks and functional organization of bioenergetic complexes.
As mitochondrial morphology is linked to metabolic capacity and lineage specification, we are investigating the role of mitochondrial dynamics in driving metabolic changes that provide energy to promote cancer stem cell growth and proliferation. Our goal is investigate and improve novel therapies that target mitochondrial dynamics as a selective point of vulnerability for glioma stem cells.
PI: Jason Mears, Ph.D.