Mitochondria research areas: Difference between revisions
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Areas of interest regarding mitochondria research and regenerative medicine | Areas of interest regarding mitochondria research and regenerative medicine | ||
* Mitochondria cell cultures -- Self-sustaining mitochondria may require cytoskeletal-like scaffolds and modified plasmids with necessary proteins encoded by nuclear and not mitochondrial DNA. | * Mitochondria "cell" cultures -- Self-sustaining mitochondria may require cytoskeletal-like scaffolds and modified plasmids with necessary proteins encoded by nuclear and not mitochondrial DNA. | ||
* Mitochondrial diseases -- use genetic engineering to treat accelerated aging that arises from deletions accumulated in mitochondrial DNA | * Mitochondrial diseases -- use genetic engineering to treat accelerated aging that arises from deletions accumulated in mitochondrial DNA | ||
Revision as of 19:53, 25 April 2008
20.109 Spring 2008 Research Proposal
Red WF Team (Evan Hefner and Stephanie Yaung)
Areas of interest regarding mitochondria research and regenerative medicine
- Mitochondria "cell" cultures -- Self-sustaining mitochondria may require cytoskeletal-like scaffolds and modified plasmids with necessary proteins encoded by nuclear and not mitochondrial DNA.
- Mitochondrial diseases -- use genetic engineering to treat accelerated aging that arises from deletions accumulated in mitochondrial DNA
Current methods and publications:
- Mitochondria isolation
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- Vermulst M, Wanagat J, Kujoth GC, Bielas JH, Rabinovitch PS, Prolla TA, Loeb LA. (2008) DNA deletions and clonal mutations drive premature aging in mitochondrial mutator mice. Nature Genetics 40 , 392-394.
Mutant polymerase gamma (PolgA) that contains a proofreading-deficient subunit causes an increase in mitochondrial DNA (mtDNA) mutations by hindering homology-directed DNA repair mechanisms. mtDNA mutations play a role in aging that may vary among different tissues, where deletions accumulate the most in the brain and heart. With defective PolgA, there are more mtDNA mutations, the deletions accumulate at an accelerated rate, and the mice have a shortened lifespan.
