High impact information on Nsf2

• We now report the identification of a second homolog of NSF, called dNSF-2 within this species and report evidence that this ubiquitous and widely utilized fusion protein belongs to a multigene family [1].
• Drosophila that express a neural transgene encoding a dominant-negative form of NSF2 show an 80% reduction in the size of releasable synaptic vesicle pool, but no change in the number of vesicles in nerve terminal boutons [2].
• Using a combination of genetics, pharmacology, and imaging we find a substantial reduction in vesicle mobility within the nerve terminal boutons of Drosophila NSF2 mutant larvae [2].
• Here we report the identification of the Drosophila homologue of syntaxin 16. dsyntaxin 16 binds SNAP in a concentration-dependent fashion and genetically interacts with NSF2 [3].
• A genetic screen for suppressors of Drosophila NSF2 neuromuscular junction overgrowth [4].

Biological context of Nsf2

• Additional evidence suggests that dNSF1 and dNSF2 may play redundant roles during embryonic development and in the larval nervous system [5].
• This collection of genes that suppress the NSF2 neuromuscular junction overgrowth phenotype is a valuable resource in our efforts to further understand the role of NSF at the synapse [4].

Anatomical context of Nsf2

• Intriguingly, we also found that expression of mutant dNSF2 induced pronounced overgrowth of the neuromuscular junction and some misrouting of axons [6].
• Results of this analysis indicate that dNSF1 function is required in the nervous system beginning at the adult stage of development and that dNSF2 function is required in mesoderm beginning at the first instar larval stage of development [5].
• Interaction of cytoskeleton genes with NSF2-induced neuromuscular junction overgrowth [7].

Other interactions of Nsf2

• First, we tested for loss-of-function interaction and, indeed, we found that the combination of flies heterozygous for Act5C and NSF2 alleles led to reduced viability [7].

References