PgmNr D1367: Restoration of mitochondrial morphology rescues impaired axonal distribution caused by loss of Opa1 and Mitofusin in Drosophila melanogaster.

Authors:
T. Trevisan; A. Daga


Institutes
IRCSS E. Medea, Ass. La Nostra Famiglia, Conegliano, Italy.


Keyword: neural degeneration

Abstract:

Mitochondrial dynamics play a critical role in the control of organelle shape, size, number, function and quality control of mitochondria. It is regulated by several GTPases that play an important role in fusion and fission processes. In mammals, mitochondrial fusion is controlled by Mitofusin 1 (Mfn1), Mitofusin 2 (Mfn2) and Optic atrophy protein 1 (Opa1), while mitochondrial fission is regulated by Dynamin related protein 1 (Drp1). A significant imbalance of mitochondrial fusion and fission results in iperfused or fragmented mitochondria.

We use Drosophila melanogaster as model to study how loss of fusion and fission protein modify the axonal distribution and motility of mitochondria.

We demonstrate that loss of Marf (Mitochondrial associated regulatory factor) or Opa1 cause accumulation of mitochondria in the soma, a severe depletion of mitochondria in neuromuscular junctions (NMJs) and reduced mitochondrial motility. Loss of Drp1 rescue Marf and Opa1 phenotype. This suggests that restoring mitochondrial dimension and morphology is necessary to maintain normal mitochondrial trafficking in axons.  .



Flybase Genetic Index:
1. FlyBase gene symbol: Marf; FBgn: FBgn0029870
2. FlyBase gene symbol: Opa1; FBgn: FBgn0261276
3. FlyBase gene symbol: Drp1; FBgn: FBgn0026479