miR-124 controls Drosophila behavior and is required for neural development

•miR-124 absence results in reduced motility and flawed female reproductivity of adult Drosophila. Behavioral phenotypes caused by mir-124 knock out could be rescued by elav-GAL driven over-expression.•Though miR-124 exhibits abundant expression in CNS, miR-124 absence does not cause developmental defects in the embryonic CNS.•Both miR-124 knock out and over-expression result in statistically reduced ddaE branch number.•Both miR-124 knock out and over-expression result in reduced NMJ 6/7 branch length and bouton number. The bouton number reduction attributes mainly to type Is terminal bouton number reduction.

MicroRNA-124 (miR-124) is an evolutionarily conserved, small, noncoding RNA molecule that participates in the central nervous system (CNS) developmental control of gene expression. In the current study, we found that Drosophila embryos lacking the mir-124 gene did not exhibit detectable defects in axon growth or CNS development. On the other hand, adult mutants showed severe problems in locomotion, flight, and female fertility. Furthermore, the deficits that we observed in the adult stage could be marginally rescued with elav-GAL4 driven expression of miR-124, making elav-GAL4 an excellently simulated driver to induce entopic over-expression of miR-124. Further developmental assessment in the third instar larval neuromuscular junction (NMJ) and dendritic arborization (DA) neurons was performed with miR-124 knock outs, flies over-expressing miR-124, and rescue models. Typically, the absence and over-abundance of a molecular signal exerts opposite effects on development or phenotype. However, we determined that both miR-124 knock-outs and over-expressing flies displayed reduced NMJ 6/7 bouton number and branch length. Similarly, reduced ddaE branching numbers were observed between the two mutant lines. As to ddaF, we found that branching number was not influenced by mir-124 knock out, but was statistically reduced by miR-124 over-expression. While we were not able to determine any causal relationship between behavioral defects and dysplasia of NMJs or DA neurons, there were some accompanying relationships among behavioral phenotypes, NMJ abnormalities, and ddaE/ddaF dendritic branching which were all controlled by miR-124.