Newly published Boulder research reveals previously unknown qualities of a gene vital to a cell’s mitochondrial structure and function
A key takeaway from first-year biology is that mitochondria are the powerhouses of cells—it’s the thing most people know about them.
However, mitochondria perform a large array of functions for cells beyond generating the chemical energy that powers a cell’s biochemical reactions. They play a role calcium signaling and storage, signaling between cells and cell death. And through these various and vital mitochondrial functions, a master regulator is the OPA1 gene.
For a long time, researchers have known that OPA1 plays a crucial role in mitochondria. For example, OPA1 helps maintain the architecture of the mitochondria’s inner membrane. Without that maintenance, a protein, cytochrome c, can leak into the cell and trigger cell death at the wrong time.
While researchers have long known that OPA1 is vital to mitochondria and mitochondrial membranes in human cells, not much has been known about how OPA1 does its work. But in the journal Nature sheds new lights on how OPA1 helps reshape mitochondrial membranes and how that translates to cellular health.
Halil Aydin, a Boulder assistant professor of biochemistry, led research that discovered surprising plasticity in the vital OPA1 gene.
“We’ve known for a long time that this gene exists, we know that it’s important in a variety of diseases, including cardiovascular disease, cancer, neurodegenerative disease,” says principal investigator Halil Aydin, a University of Colorado Boulder assistant professor of biochemistry. “What we didn’t know is how it functions. Our goal is to understand how it works and then in the future use that as a blueprint for developing therapeutic strategies or drugs.”
Read more in Rachel Sauer's article in Arts and Sciences Magazine...