Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2069109 | Mitochondrion | 2009 | 10 Pages |
Abstract
Tafazzin is a conserved mitochondrial protein that is required to maintain normal content and composition of cardiolipin. We used electron tomography to investigate the effect of tafazzin deletion on mitochondrial structure and found that cellular differentiation plays a crucial role in the manifestation of abnormalities. This conclusion was reached by comparing differentiated cardiomyocytes with embryonic stem cells from mouse and by comparing different tissues from Drosophila melanogaster. The data suggest that tafazzin deficiency affects cardiolipin in all mitochondria, but significant alterations of the ultrastructure, such as remodeling and aggregation of inner membranes, will only occur after specific differentiation.
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Authors
Devrim Acehan, Zaza Khuchua, Riekelt H. Houtkooper, Ashim Malhotra, Johanna Kaufman, Frédéric M. Vaz, Mindong Ren, Howard A. Rockman, David L. Stokes, Michael Schlame,