Mitochondria research areas: Difference between revisions

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* Mitochondrial diseases -- use genetic engineering to treat accelerated aging that arises from deletions accumulated in mitochondrial DNA; targeted gene therapy?
* Mitochondrial diseases -- use genetic engineering to treat accelerated aging that arises from deletions accumulated in mitochondrial DNA; targeted gene therapy?
* Nuclearize mitochondrial DNA
* Nuclearize mitochondrial DNA
* Future applications:
  - designs, such as Prof. Griffith's liver cell tox assay
  - candidate toxins to test the validity of the mitochondrial model


==Statement of Research Problem and Goals==
==Statement of Research Problem and Goals==
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* mitochondrial genome, what's made inside and what's from outside (from nuclear DNA)
* mitochondrial genome, what's made inside and what's from outside (from nuclear DNA)
* mitochondrial function, interaction with other elements of the eukaryotic cell
* mitochondrial function, interaction with other elements of the eukaryotic cell
* cell toxicity assays in general
*  
  * designs, such as Prof. Griffith's liver cell tox assay
 
  * candidate toxins to test the validity of the mitochondrial model


==Predicted Outcomes==
==Predicted Outcomes==
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==Resources Needed==
==Resources Needed==
* mitochondria isolation kits
* mitochondria isolation kits
* matrix with cytosol-like material properties


==References==
==References==
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* Vimentin supports mitochondrial morphology and organization. http://www.ncbi.nlm.nih.gov/pubmed/17983357
* Vimentin supports mitochondrial morphology and organization. http://www.ncbi.nlm.nih.gov/pubmed/17983357
* Protein transport into mitochondria. http://www.ncbi.nlm.nih.gov/pubmed/10744987
* Protein transport into mitochondria. http://www.ncbi.nlm.nih.gov/pubmed/10744987
* Mitochondrial toxicity of antiviral drugs. http://www.ncbi.nlm.nih.gov/pubmed/7585087
* Direct analysis of mitochondrial toxicity of antiretroviral drugs. http://www.ncbi.nlm.nih.gov/pubmed/11546944

Revision as of 14:25, 29 April 2008

MIT 20.109 Spring 2008 Research Proposal

Red WF Team (Evan Hefner and Stephanie Yaung)


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:
 - designs, such as Prof. Griffith's liver cell tox assay
 - candidate toxins to test the validity of the mitochondrial model

Statement of Research Problem and Goals

Create mitochondrial cultures as an enabling technology for critical research, such as 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

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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