Abnormal mitochondrial morphology and dysfunction are often seen in neurodegenerative diseases, but the reason for this association is unclear. Now, Tsubouchi and colleagues report that the Drosophilamitochondrial protein Preli (protein of relevant evolutionary and lymphoid interest)-like (Prel), a member of the conserved PRELI/MSF1 family, is required for the development and maintenance of dendritic arbors in Drosophila sensory neurons (see ). The researchers identified Prel as a gene that affects the morphology of class IV (highly branched) dendritic arborization (da) sensory neurons in an overexpression screen. Both prel loss of function and overexpression,they report, abrogate mitochondrial structures and activity in Drosophila da neurons. Furthermore, when Prel function is impaired in vivo in class IV da neurons, the neurons simplify and downsize their dendritic arbors, and breakages appear in some of their major branches. These and other observations suggest that Prel-dependent regulation of mitochondrial activity prevents the regression of dendritic branches and that the human homologue of Prel may be mutated in some human neurodegenerative diseases.
