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Mouse Tmem135 mutation reveals a mechanism involving mitochondrial dynamics that leads to age-dependent retinal pathologies.

eLife | Nov 15, 2016

While the aging process is central to the pathogenesis of age-dependent diseases, it is poorly understood at the molecular level. We identified a mouse mutant with accelerated aging in the retina as well as pathologies observed in age-dependent retinal diseases, suggesting that the responsible gene regulates retinal aging, and its impairment results in age-dependent disease. We determined that a mutation in the transmembrane 135 (Tmem135) is responsible for these phenotypes. We observed localization of TMEM135 on mitochondria, and imbalance of mitochondrial fission and fusion in mutant Tmem135 as well as Tmem135 overexpressing cells, indicating that TMEM135 is involved in the regulation of mitochondrial dynamics. Additionally, mutant retina showed higher sensitivity to oxidative stress. These results suggest that the regulation of mitochondrial dynamics through TMEM135 is critical for protection from environmental stress and controlling the progression of retinal aging. Our study identified TMEM135 as a critical link between aging and age-dependent diseases.

Pubmed ID: 27863209 RIS Download

Mesh terms: Adaptor Proteins, Signal Transducing | Aging | Animals | Mice | Mitochondria | Mitochondrial Dynamics | Mutant Proteins | Nuclear Proteins | Retinal Diseases

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Associated grants

  • Agency: NICHD NIH HHS, Id: P30 HD003352
  • Agency: NEI NIH HHS, Id: P30 EY016665
  • Agency: NEI NIH HHS, Id: R01 EY022086
  • Agency: NIMH NIH HHS, Id: U01 MH061915
  • Agency: NIGMS NIH HHS, Id: T32 GM007133
  • Agency: NEI NIH HHS, Id: R21 EY023061
  • Agency: Howard Hughes Medical Institute, Id:

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