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Fig. 4 | Molecular Brain

Fig. 4

From: The Rap activator Gef26 regulates synaptic growth and neuronal survival via inhibition of BMP signaling

Fig. 4

Altered dfmr1 expression and microtubule stability cause synaptic overgrowth in gef26 and rap1 mutants. a and b Transheterozygous interactions between gef26 or rap1 and dfmr1. a Confocal images of anti-HRP-labeled NMJ 6/7 in wild-type, gef26 6/+, dfmr1 Δ50M/+, and gef26 6/+; dfmr1 Δ50M /+ third-instar larvae. Scale bar, 20 μm. b Quantification of total bouton number and satellite bouton number at NMJ 6/7 in the following genotypes: wild-type, gef26 6/+, rap1 M/+, dfmr1 Δ50M/+, gef26 6/+; dfmr1 Δ50M /+, and rap1 M,+/+,dfmr1 Δ50M. c Quantification of dfmr1 RNA levels using quantitative real-time PCR in the CNS of wild-type, gef26 6/Df, and rap1 M/rap1 M third-instar larvae. rp49 was used as an internal control. d and e Levels of synaptic Futsch are increased in gef26 and rap1 mutants. d Confocal images of anti-Futsch and anti-HRP staining from NMJ 6/7 of wild-type, gef26 6/Df, and rap1 M/rap1 M third-instar larvae. Arrowheads indicate Futsch-positive terminal loops. Scale bar, 5 μm. e Quantification of the ratio of the average anti-Futsch to anti-HRP staining intensities. f and g Synaptic overgrowth in gef26 and rap1 mutants is suppressed by vinblastine administration. f Confocal images of NMJ 6/7 immunostained with anti-HRP are shown for gef26 6/Df mutants raised in the absence (-VB) or presence (+VB) of 1 μM vinblastine. Scale bar, 20 μm. g Quantification of total bouton number and satellite bouton number at NMJ 6/7 in the indicated genotypes. The number of NMJs analyzed is indicated in each bar. Data are expressed as mean ± SEM. All comparisons are made with wild-type unless otherwise indicated (*P < 0.001; **P < 0.01; ***P < 0.05; n.s., not significant)

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