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How SENS is tackling mitochondrial DNA damage

Amutha Boominathan presented her work on MitoSENS project at Ending Age-Related Diseases 2019

17-Jan-2020

Key points from article :

Mitochondria has own DNA and able to synthesise proteins.

Has inefficient DNA repair mechanisms.

1in 200 people born with mitochondrial DNA defect.

Current treatments (typically small molecule) only address symptoms.

SENS approach is to express mtDNA in the nucleus (allotopic expression).

Codon optimisation aids efficiency of gene expression.

mRNA levels higher that their recorded counterparts.

8 of 13 genes can be expressed stably.

ATP8 is smallest of these proteins.

Aerobic and anaerobic respiration return to normal.

Allotopic ND1 incorporates into Complex I monomers.

Few animal models available for mitochondria.

Validated safe harbour allotropic expression.

Mentioned in this article:

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Amutha Boominathan

Group Lead for the MitoSENS program at SENS Research Foundation

SENS Research Foundation

Non-profit organization focused on transforming the way the world researches and treats age-related diseases

Topics mentioned on this page:
Mitochondria