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. 2012 Nov 16;14(1):87–94. doi: 10.1038/embor.2012.181

Figure 1.

Figure 1

Loss of NMNAT causes loss of synaptic proteins and mislocalization of BRP. (A,B) MARCM analysis of adult brain lamina showing that synaptobrevin (A1), synaptotagmin (A3) and BRP (B3) levels are reduced in nmnat-null (GFP positive) lamina synaptic terminals. Dashed lines indicate nmnat-null (GFP positive) clones. Scale bars indicate 5 μm. (C) Midbrain structure of 2 days after eclosion control flies overexpressing UAS-Dicer with elav-GAL4C155 showing NMNAT in both cell bodies and synapses (C1) and BRP enriched at the synapses (C2). (D) In NMNAT–RNAi flies, BRP protein is drastically reduced in neuropil and forms clusters in the cell bodies. (D1′–D4′) Higher magnification of boxed areas in C reveals a high degree of colocalization of the remaining NMNAT with BRP clusters. Scale bars indicate 20 μm. BRP, Bruchpilot; DAPI, 4′6-diamidino-2-phenylindole; GFP, green fluorescent protein; MARCM, mosaic analysis with a repressible cell marker; NMNAT, nicotinamide mononucleotide adenylyltransferase; RNAi, RNA interference.