Extensive use of RNA-binding proteins in Drosophila sensory neuron dendrite morphogenesis.

TitleExtensive use of RNA-binding proteins in Drosophila sensory neuron dendrite morphogenesis.
Publication TypeJournal Article
Year of Publication2014
AuthorsOlesnicky, EC, Killian, DJ, Garcia, E, Morton, MC, Rathjen, AR, Sola, IE, Gavis, ER
JournalG3 (Bethesda)
Volume4
Issue2
Pagination297-306
Date Published2014 Feb 19
ISSN2160-1836
KeywordsAnimals, Dendrites, Drosophila, Drosophila Proteins, Larva, Morphogenesis, Neurogenesis, Protein Biosynthesis, RNA-Binding Proteins, Sensory Receptor Cells
Abstract

<p>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.</p>

DOI10.1534/g3.113.009795
Alternate JournalG3 (Bethesda)
PubMed ID24347626
PubMed Central IDPMC3931563
Grant ListF32 HD056779 / HD / NICHD NIH HHS / United States
R01 GM061107 / GM / NIGMS NIH HHS / United States
R01 GM084947 / GM / NIGMS NIH HHS / United States
R01-GM084947 / GM / NIGMS NIH HHS / United States