Molecules and Cells

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Fig. 4.

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Fig. 4. Decrease in FMRP level is a neuronal compensatory response to the aberrant upregulation of ATX2. (A) Representative images of dendrites of C4da neurons of Control or expressing denoted transgenes (Genotype: Control, +/+; ppk1a> UAS-CD4-tdTom/UAS-luciferase; FMRP, +/+; ppk1a> UAS-CD4-tdTom/UAS-FMR1; FMRP RNAi, +/+; ppk1a> UAS-CD4-tdTom/UAS-FMRP RNAi, ATX2, UAS-ATX2/+; ppk1a> UAS-CD4-tdTom/UAS-luciferase; ATX2 + FMRP, UAS-ATX2/+; ppk1a> UAS-CD4-tdTom/UAS-FMR1; ATX2 + FMRP RNAi, UAS-ATX2/+; ppk1a> UAS-CD4-tdTom/UAS-FMRP RNAi). Scale bar = 100 µm. (B) Quantification of dendritic receptive fields of neurons expressing denoted transgenes described in Fig. 4A. Gray-dotted line indicates the differences in group II and III catagorized dendrite proportions of ATX2 and ATX2 + FMRP RNAi expressing C4da neurons. (C) A sholl analysis of C4da neuron dendrites in 3rd instar larvae expressing the denoted transgenes (Genotype: ATX2, UAS-ATX2/+; ppk1a> UAS-CD4-tdTom/UAS-luciferase; ATX2 + FMRP RNAi, UAS-ATX2/+; ppk1a> UAS-CD4-tdTom/UAS-FMRP RNAi). *P < 0.05 by two-tailed t-test; error bars ± SEM; n = 9 replicates.
Mol. Cells 2020;43:870~879 https://doi.org/10.14348/molcells.2020.0158
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