Forcing contacts between mitochondria and the endoplasmic reticulum extends lifespan in a Drosophila model of Alzheimer’s disease.
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Journal Title
Biology Open
ISSN
2046-6390
Publisher
Company of Biologists
Number
bio.047530
Type
Article
This Version
VoR
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Martins, L., & Loh, S. (2019). Forcing contacts between mitochondria and the endoplasmic reticulum extends lifespan in a Drosophila model of Alzheimer’s disease.. Biology Open, (bio.047530)https://doi.org/10.1242/bio.047530
Abstract
cells are complex systems containing internal compartments with specialised
functions. Among these compartments, the endoplasmic reticulum (ER) plays a major role in
processing proteins for modification and delivery to other organelles, whereas mitochondria
generate energy in the form of ATP. Mitochondria and the ER form physical interactions,
defined as mitochondria-ER contact sites (MERCS) to exchange metabolites such as calcium
ions (Ca2+) and lipids. Sites of contact between mitochondria and the ER can regulate
biological processes such as ATP generation and mitochondrial division. The interactions
between mitochondria and the ER are dynamic and respond to the metabolic state of cells.
Changes in MERCS have been linked to metabolic pathologies such as diabetes,
neurodegenerative diseases and sleep disruption.
Here we explored the consequences of increasing contacts between mitochondria and the ER
in flies using a synthetic linker. We showed that enhancing MERCS increases locomotion
and extends lifespan. We also showed that, in a Drosophila model of Alzheimer’s disease
linked to toxic amyloid beta (Aβ), linker expression can suppress motor impairment and
extend lifespan. We conclude that strategies for increasing contacts between mitochondria
and the ER may improve symptoms of diseases associated with mitochondria dysfunction.
Sponsorship
MRC RG94521
Identifiers
External DOI: https://doi.org/10.1242/bio.047530
This record's URL: https://www.repository.cam.ac.uk/handle/1810/300750
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