Genetic Modifiers ofdFMR1Encode RNA Granule Components in Drosophila Journal Article uri icon

Overview

abstract

  • AbstractMechanisms of neuronal mRNA localization and translation are of considerable biological interest. Spatially regulated mRNA translation contributes to cell-fate decisions and axon guidance during development, as well as to long-term synaptic plasticity in adulthood. The Fragile-X Mental Retardation protein (FMRP/dFMR1) is one of the best-studied neuronal translational control molecules and here we describe the identification and early characterization of proteins likely to function in the dFMR1 pathway. Induction of the dFMR1 in sevenless-expressing cells of the Drosophila eye causes a disorganized (rough) eye through a mechanism that requires residues necessary for dFMR1/FMRP's translational repressor function. Several mutations in dco, orb2, pAbp, rm62, and smD3 genes dominantly suppress the sev-dfmr1 rough-eye phenotype, suggesting that they are required for dFMR1-mediated processes. The encoded proteins localize to dFMR1-containing neuronal mRNPs in neurites of cultured neurons, and/or have an effect on dendritic branching predicted for bona fide neuronal translational repressors. Genetic mosaic analyses indicate that dco, orb2, rm62, smD3, and dfmr1 are dispensable for translational repression of hid, a microRNA target gene, known to be repressed in wing discs by the bantam miRNA. Thus, the encoded proteins may function as miRNA- and/or mRNA-specific translational regulators in vivo.

publication date

  • August 1, 2009

has restriction

  • bronze

Date in CU Experts

  • February 20, 2014 11:11 AM

Full Author List

  • Cziko A-MJ; McCann CT; Howlett IC; Barbee SA; Duncan RP; Luedemann R; Zarnescu D; Zinsmaier KE; Parker RR; Ramaswami M

author count

  • 10

Other Profiles

Electronic International Standard Serial Number (EISSN)

  • 1943-2631

Additional Document Info

start page

  • 1051

end page

  • 1060

volume

  • 182

issue

  • 4