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Figure 2 | Neural Development

Figure 2

From: A chemical-genetic strategy reveals distinct temporal requirements for SAD-1 kinase in neuronal polarization and synapse formation

Figure 2

L123A SAD-1 is functional in vivo . (A, B) Polarity phenotype. Axons of VD neurons innervate ventral body wall muscles, forming presynaptic terminals exclusively on the ventral side (Ai). In wild-type (wt) animals, only few, if any, ectopic juIs1 puncta are observed on the dorsal side (Bi). In sad-1 LOF mutants, many ectopic juIs1 puncta are found (Aii, Bii). Expressing L123A SAD-1 partially rescued this phenotype, and fewer ectopic puncta were observed (Biii). DNC, dorsal nerve cord. VNC, ventral nerve cord. (C) Quantification of polarity phenotypes. Polarity defects were quantified by counting the number of ectopic juIs1 puncta per animal. Expressing L123A SAD-1 in sad-1 mutants reduced their polarity defect more than 50%, similar to expressing wild-type SAD-1. ***p < 0.001, Wilcoxon rank-sum test. Error bars indicate standard deviations. (D, E) Synaptic organization phenotype. In wild-type animals, juIs1 puncta in DD neurons appear round and discrete along the dorsal nerve cord (Di, Ei). In sad-1 mutants, diffuse or smaller puncta are observed (Dii, Eii). Expression of L123A SAD-1 rescued this phenotype and restored the juIs1 morphology (Eiii). (F) Quantification of synaptic organization phenotypes. Kernel density estimates of the punctum widths show a much wider distribution of punctum widths (that is, reduced kurtosis) in sad-1 mutants compared to wild-type animals. L123A SAD-1 rescued this sad-1 defect. Scale bar, 5 μm.

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