ArticlePloS one2009
Argonaute2 suppresses Drosophila fragile X expression preventing neurogenesis and oogenesis defects.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- piRNAs and endo-siRNAs: Small molecules with large roles in the nervous system.Neurochemistry international · 2021Review
- Review
- Modeling Fragile X Syndrome inFrontiers in molecular neuroscience · 2018Review
- Insulin signaling misregulation underlies circadian and cognitive deficits in a Drosophila fragile X model.Molecular psychiatry · 2017Article
- Drosophila Syncrip modulates the expression of mRNAs encoding key synaptic proteins required for morphology at the neuromuscular junction.RNA (New York, N.Y.) · 2014Article
- Concise review: Fragile X proteins in stem cell maintenance and differentiation.Stem cells (Dayton, Ohio) · 2014Review
- Unlocking epigenetic codes in neurogenesis.Genes & development · 2014Review
- Impact of age-associated increase in 2'-O-methylation of miRNAs on aging and neurodegeneration in Drosophila.Genes & development · 2014Article
- Sustained miRNA-mediated knockdown of mutant AAT with simultaneous augmentation of wild-type AAT has minimal effect on global liver miRNA profiles.Molecular therapy : the journal of the American Society of Gene Therapy · 2012Article
- Article
- Molecular and genetic analysis of the Drosophila model of fragile X syndrome.Results and problems in cell differentiation · 2012Article
- Drosophila modeling of heritable neurodevelopmental disorders.Current opinion in neurobiology · 2011Review
- Modulation of dADAR-dependent RNA editing by the Drosophila fragile X mental retardation protein.Nature neuroscience · 2011Article
- A Drosophila model of FUS-related neurodegeneration reveals genetic interaction between FUS and TDP-43.Human molecular genetics · 2011Article
- A non-canonical start codon in the Drosophila fragile X gene yields two functional isoforms.Neuroscience · 2011Article
- Ablation of Fmrp in adult neural stem cells disrupts hippocampus-dependent learning.Nature medicine · 2011Article
- Natural variation of the amino-terminal glutamine-rich domain in Drosophila argonaute2 is not associated with developmental defects.PloS one · 2010Article
- Fragile X syndrome and model organisms: identifying potential routes of therapeutic intervention.Disease models & mechanismsReview
- Development and plasticity of the Drosophila larval neuromuscular junction.Wiley interdisciplinary reviews. Developmental biologyReview
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Fragile X Syndrome is caused by the silencing of the Fragile X Mental Retardation gene (FMR1). Regulating dosage of FMR1 levels is critical for proper development and function of the nervous system and germ line, but the pathways responsible for maintaining normal expression levels are less clearly defined. Loss of Drosophila Fragile X protein (dFMR1) causes several behavioral and developmental defects in the fly, many of which are analogous to those seen in Fragile X patients. Over-expression of dFMR1 also causes specific neuronal and behavioral abnormalities. We have found that Argonaute2 (Ago2), the core component of the small interfering RNA (siRNA) pathway, regulates dfmr1 expression. Previously, the relationship between dFMR1 and Ago2 was defined by their physical interaction and co-regulation of downstream targets. We have found that Ago2 and dFMR1 are also connected through a regulatory relationship. Ago2 mediated repression of dFMR1 prevents axon growth and branching defects of the Drosophila neuromuscular junction (NMJ). Consequently, the neurogenesis defects in larvae mutant for both dfmr1 and Ago2 mirror those in dfmr1 null mutants. The Ago2 null phenotype at the NMJ is rescued in animals carrying an Ago2 genomic rescue construct. However, animals carrying a mutant Ago2 allele that produces Ago2 with significantly reduced endoribonuclease catalytic activity are normal with respect to the NMJ phenotypes examined. dFMR1 regulation by Ago2 is also observed in the germ line causing a multiple oocyte in a single egg chamber mutant phenotype. We have identified Ago2 as a regulator of dfmr1 expression and have clarified an important developmental role for Ago2 in the nervous system and germ line that requires dfmr1 function.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.