Extensive use of RNA-binding proteins in Drosophila sensory neuron dendrite morphogenesis. Author Eugenia Olesnicky, Darrell Killian, Evelyn Garcia, Mary Morton, Alan Rathjen, Ismail Sola, Elizabeth Gavis Publication Year 2014 Type Journal Article Abstract The large number of RNA-binding proteins and translation factors encoded in the Drosophila and other metazoan genomes predicts widespread use of post-transcriptional regulation in cellular and developmental processes. Previous studies identified roles for several RNA-binding proteins in dendrite branching morphogenesis of Drosophila larval sensory neurons. To determine the larger contribution of post-transcriptional gene regulation to neuronal morphogenesis, we conducted an RNA interference screen to identify additional Drosophila proteins annotated as either RNA-binding proteins or translation factors that function in producing the complex dendritic trees of larval class IV dendritic arborization neurons. We identified 88 genes encoding such proteins whose knockdown resulted in aberrant dendritic morphology, including alterations in dendritic branch number, branch length, field size, and patterning of the dendritic tree. In particular, splicing and translation initiation factors were associated with distinct and characteristic phenotypes, suggesting that different morphogenetic events are best controlled at specific steps in post-transcriptional messenger RNA metabolism. Many of the factors identified in the screen have been implicated in controlling the subcellular distributions and translation of maternal messenger RNAs; thus, common post-transcriptional regulatory strategies may be used in neurogenesis and in the generation of asymmetry in the female germline and embryo. Keywords Animals, Dendrites, Drosophila, Drosophila Proteins, Larva, Morphogenesis, Neurogenesis, Protein Biosynthesis, RNA-Binding Proteins, Sensory Receptor Cells Journal G3 (Bethesda) Volume 4 Issue 2 Pages 297-306 Date Published 2014 Feb 19 ISSN Number 2160-1836 DOI 10.1534/g3.113.009795 Alternate Journal G3 (Bethesda) PMCID PMC3931563 PMID 24347626 PubMedPubMed CentralGoogle ScholarBibTeXEndNote X3 XML