Despite the importance of the
mitochondria in disease, suitable mouse models to study
mitochondrial dysfunction have proved difficult to generate because classical genetic techniques cannot be applied to the thousands of individual
mitochondria in a single cell. Now, a team of researchers reports the introduction of these organelles from one mouse species into another, generating a
mitochondrial mutant model that could be used to elucidate
mitochondria-related disease mechanisms.
In the January 26 PNAS, Matthew McKenzie and colleagues at the University of Melbourne demonstrate the successful transfer of species-specific
mitochondria into mouse embryos using
mitochondrial DNA–depleted embryonic stem cells and cytoplast fusions that results in homoplasmy for the introduced
mitochondrial background (PNAS, DOI:10.1073/pnas.0303184101, January 26, 2004).