ArticleFrontiers in neural circuits2010
Fragile x mental retardation 1 and filamin a interact genetically in Drosophila long-term memory.
Article in Frontiers in neural circuits, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- Do metabolic deficits contribute to sleep disruption in monogenic intellectual disability syndromes?Trends in neurosciences · 2024Review
- Insights into the role of intracellular calcium signaling in the neurobiology of neurodevelopmental disorders.Frontiers in neuroscience · 2023Review
- Fragile X mental retardation protein modulates somatic D-type KJournal of neurophysiology · 2020Article
- Stress-Sensitive Protein Rac1 and Its Involvement in Neurodevelopmental Disorders.Neural plasticity · 2020Review
- A molecular war: convergent and ontogenetic evidence for adaptive host manipulation in related parasites infecting divergent hosts.Proceedings. Biological sciences · 2019Article
- Review
- Filamin actin-binding and titin-binding fulfill distinct functions in Z-disc cohesion.PLoS genetics · 2017Article
- The Oxygen Sensor PHD2 Controls Dendritic Spines and Synapses via Modification of Filamin A.Cell reports · 2016Article
- Deciphering discord: How Drosophila research has enhanced our understanding of the importance of FMRP in different spatial and temporal contexts.Experimental neurology · 2015Review
- Rcan1 deficiency impairs neuronal migration and causes periventricular heterotopia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- From Learning to Memory: What Flies Can Tell Us about Intellectual Disability Treatment.Frontiers in psychiatry · 2015Review
- Insulin signaling is acutely required for long-term memory in Drosophila.Frontiers in neural circuits · 2015Article
- Lithium: a promising treatment for fragile X syndrome.ACS chemical neuroscience · 2014Review
- GABAergic circuit dysfunction in the Drosophila Fragile X syndrome model.Neurobiology of disease · 2014Article
- Impaired activity-dependent neural circuit assembly and refinement in autism spectrum disorder genetic models.Frontiers in cellular neuroscience · 2014Review
- Microdomains in forebrain spines: an ultrastructural perspective.Molecular neurobiology · 2013Review
- The role of the actin cytoskeleton in regulating Drosophila behavior.Reviews in the neurosciences · 2013Review
- 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
- Extracellular matrix and its receptors in Drosophila neural development.Developmental neurobiology · 2011Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
The last decade has witnessed the identification of single-gene defects associated with an impressive number of mental retardation syndromes. Fragile X syndrome, the most common cause of mental retardation for instance, results from disruption of the FMR1 gene. Similarly, Periventricular Nodular Heterotopia, which includes cerebral malformation, epilepsy and cognitive disabilities, derives from disruption of the Filamin A gene. While it remains unclear whether defects in common molecular pathways may underlie the cognitive dysfunction of these various syndromes, defects in cytoskeletal structure nonetheless appear to be common to several mental retardation syndromes. FMR1 is known to interact with Rac, profilin, PAK and Ras, which are associated with dendritic spine defects. In Drosophila, disruptions of the dFmr1 gene impair long-term memory (LTM), and the Filamin A homolog (cheerio) was identified in a behavioral screen for LTM mutants. Thus, we investigated the possible interaction between cheerio and dFmr1 during LTM formation in Drosophila. We show that LTM specifically is defective in dFmr1/cheerio double heterozygotes, while it is normal in single heterozygotes for either dFmr1 or cheerio. In dFmr1 mutants, Filamin (Cheerio) levels are lower than normal after spaced training. These observations support the notion that decreased actin cross-linking may underlie the persistence of long and thin dendritic spines in Fragile X patients and animal models. More generally, our results represent the first demonstration of a genetic interaction between mental retardation genes in an in vivo model system of memory formation.
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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.