Mitochondria research areas: Difference between revisions

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http://www.piercenet.com/Products/Browse.cfm?fldID=45F252F7-2410-40C9-81CD-57B19AA095DB
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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.
* 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.
   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.
* Mitochondria: more than just a powerhouse. http://www.ncbi.nlm.nih.gov/pubmed/16860735
* Mitochondria: more than just a powerhouse. http://www.ncbi.nlm.nih.gov/pubmed/16860735
* Characterization of the human heart mitochondrial proteome. http://www.ncbi.nlm.nih.gov/pubmed/12592411
* Characterization of the human heart mitochondrial proteome. http://www.ncbi.nlm.nih.gov/pubmed/12592411

Revision as of 21:21, 29 April 2008

MIT 20.109 Spring 2008 Research Proposal

Red WF Team (Evan Hefner and Stephanie Yaung)

preliminary site -- ongoing updates within the next two weeks

Overview

Development of mitochondrial cultures

Background Information

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; uses for these cultures?
  • Mitochondrial diseases -- use genetic engineering to treat accelerated aging that arises from deletions accumulated in mitochondrial DNA; targeted gene therapy?
  • Nuclearize mitochondrial DNA
  • Future applications: mitochondrial model for toxicity tests

Statement of Research Problem and Goals

Create mitochondrial cultures as an enabling technology for critical research (e.g., toxicology

Details and Methods

  • isolating mitochondria
  • consequences of damaged mitochondria (mtDNA deletions, accelerated aging, early death)
  • cytosol-like materials; mimic environment around the mitochondria
  • mitochondrial genome, what's made inside and what's from outside (from nuclear DNA)
  • mitochondrial function, interaction with other elements of the eukaryotic cell

Predicted Outcomes

Resources Needed

  • mitochondria isolation kits
  • matrix with cytosol-like material properties

References

  • Mitochondria isolation kit

http://www.piercenet.com/Products/Browse.cfm?fldID=45F252F7-2410-40C9-81CD-57B19AA095DB

  • 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.
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