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

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

eLife digest

Affiliation details

University of Wisconsin-Madison, United States; Morgridge Institute for Research, United States; Northwestern University, United States; University of Iowa, United States; Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, United States

Older people have an increased risk of developing many diseases, such as diabetes and age-related macular degeneration (which is often shortened to AMD). This suggests that changes that occur during normal aging may some how be linked to how such diseases develop. However, the molecular mechanisms responsible for these links are not clear.

AMD causes damage to the retina of the eye, which can lead to visual loss in older people. To investigate the link between aging and age-dependent diseases, Lee et al. used mutant mice whose retina of the eye ages more quickly than normal mice and are prone to developing an eye condition that is similar to AMD. The experiments show that these mice have a mutation in a gene called Tmem135 that is responsible for these visual problems. Tmem135 regulates the size of cell compartments called mitochondria, which produce energy for the cell. This affects the ability of the mitochondria to work properly and makes the cells more sensitive to environmental stress, which in turn makes the retina age more quickly.

The findings of Lee et al. show that Tmem135 is a critical link between aging and an AMD-like condition in mice. Furthermore, the experiments suggest that defects in mitochondria may accelerate the normal pace of aging and lead to AMD and other age-dependent diseases. Further studies are needed to find out exactly what role Tmem135 plays in mitochondria and whether it also contributes to the aging of other parts of the body.

DOI: http://dx.doi.org/10.7554/eLife.19264.002