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. Author manuscript; available in PMC: 2012 Dec 8.
Published in final edited form as: Neuron. 2011 Dec 8;72(5):760–775. doi: 10.1016/j.neuron.2011.09.031

Figure 6. Dcp-1 Is Necessary and Sufficient for Prodegenerative Signaling.

Figure 6

(A and B) Representative immunofluorescence images of NMJs at muscle 6/7 in larva expressing full-length Dcp-1 in neurons. NMJs are stained with the presynaptic marker Brp (green), the postsynaptic marker Dlg (red), and the neuronal membrane marker HRP (blue). A range of phenotypes exists when Dcp-1 is expressed in neurons, including significant synaptic degeneration (A) and complete presynaptic degeneration resulting in discontinuous HRP staining (B).

(C) Membrane-bound GFP expression (green) in single motoneurons being driven by the EveRRa-GAL4 driver within an otherwise wild-type nerve bundle. A single axon is visualized.

(D) Expression of full-length Dcp-1 and membrane-bound GFP (green) in single motoneurons by the EveRRa-GAL4 driver within a nerve bundle. Expression of Dcp-1 causes motoneurons to degenerate along their length.

(E) Quantification of degeneration frequency as measured by the average percentage of NMJs retracted per animal in wild-type, dcp-1 homozygous mutants, ank2, and in larva expressing Dcp-1 in all neurons or in a subset of peripheral glia with egr-GAL4. wt = w1118 (n = 129 NMJs); dcp-1 = dcp-1Prev1/dcp-1Prev1 (n = 130 NMJs); ank2 = ank22001/ank22001 (n = 122 NMJs); C155 > UAS-Dcp1 = elavC155-GAL4; UAS-Dcp-1/+ (n = 96 NMJs); egrG4 > UAS-Dcp-1 = egr-GAL4/UAS-Dcp-1 (n = 80). Dcp-1 expression in neurons causes significantly more synaptic degeneration events that have >1 bouton, >7 boutons retracted, >20 boutons retracted, and complete synaptic eliminations (*p < 0.05; ***p < 0.001). Expression of Dcp-1 in Eiger expressing peripheral glia causes no degeneration.

(F) Quantification of degeneration frequency as measured above in wild-type and neuronal overexpression of Drice, Dredd, Dronc, or Dcp-1. wt = w1118 (n = 59 NMJs); elavC155-GAL4; UAS-Drice (n = 100 NMJs); elavC155-GAL4; UAS-Dredd (n = 40 NMJs); elavC155-GAL4; UAS-Dronc (n = 50 NMJs); elavC155-UAS-Dcp-1 (n = 106 NMJs). Only expression of Dronc and Dcp-1 causes significantly more synaptic degeneration than in wild-type (p < 0.001). Note that data for C155-dependent UAS-Dcp-1 are the same data as are presented in (E), reproduced to highlight specific comparisons.

(G and H) Quantification of degeneration severity as in Figures 2E and 2F. wt = w1118 (n = 129 NMJs); dcp-1 = dcp-1Prev1/dcp-1Prev1 (n = 130 NMJs); ank2 = ank22001/ank22001 (n = 122 NMJs); dcp-1/+; ank2/ank2 = dcp-1Prev1/+; ank22001/ank22001 (n = 40 NMJs); dcp-1/dcp-1; ank2/ank2 = dcp-1Prev1/dcp-1Prev1; ank22001/ank22001 (n = 127 NMJs). Mutant dcp-1 as either a heterozygote or a homozygote significantly reduces the number of ank2-dependent synaptic degeneration events (p < 0.001). Error bars represent SEM. p values were determined using one-way ANOVA with post hoc Tukey-Kramer: ***p < 0.001. Statistical differences remain when comparisons are made using Student’s t test. n.s., not significant.