Optimizing the Allotopic Expression of ATP6 to Mitochondria in Mutant Cells
Jasmine Zhao joined us this summer from UCLA where she will be a senior this fall. In Jasmine's words:
"This summer, my project will be conducted under the mentorship of Dr. Amutha Boominathan and Dr. Matthew O’Connor at the SRF Research Center in Mountain View. The goal of this project is to design and test different constructs that can potentially improve the allotopic expression of ATP6 to mitochondria in mutant cell lines. Mitochondria are double-membrane bound organelles that provide energy in the form of ATP to power the biochemical reactions of a cell. Unlike other organelles, however, mitochondria have their own DNA separate from the nucleus, and 13 out of those 37 genes encode for oxidative phosphorylation complex proteins. Due to possible leakage of the high-energy electrons of the respiratory chain, which results in the formation of reactive oxygen species, the oxidative stress mitochondrial-DNA (mtDNA) is subjected to can lead to mutations, aging, and cell death. For instance, the ATP6 gene encodes for subunit a of the Fo structural domain of ATP synthase, also known as Complex V. The Fo structural domain is embedded in the inner membrane of the mitochondria and contains the membrane proton channel that allows for the synthesis of ATP. Mutations of ATP6 have been implicated in different human diseases that affect neural development, vision, and motor movement such as Leigh syndrome and Neuropathy, Ataxia, and Retinitis Pigmentosa (NARP)."
Read more here! http://www.sens.org/...le-jasmine-zhao
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Matthew S. O'Connor, Ph.D.
Head of Research
SENS Research Foundation - www.sens.org
reimagine aging
Edited by caliban, 22 September 2017 - 03:18 AM.
