dSarm plays a crucial role in the execution of axon degeneration after injury. Here, Arnau shows that the accumulation of NMN results in the activation of dSarm in Drosophila.
With the help of the Coleman and Wu labs, this article demonstrates that low levels of NMN fail to execute axon degeneration, while increased NMN synthesis results in faster axon degeneration after injury. NMN activates dSarm to initiate NAD+ depletion, an essential mechanism of axon death signaling in Drosophila.
The article is accessible on eLife.
