Drosophila fragile X-related gene regulates the MAP1B homolog Futsch to control synaptic structure and function.

By Yong Q. Zhang, A. Bailey, Heinrich J.G. Matthies, Robert B. Renden, Mark A. Smith, Sean D. Speese, Gerald M. Rubin, K. Broadie. Cell, 2001

658 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/32e7766826b233c0a215eb8f041ca3672f4e087b

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Citations in the corpus

• Fragile X-related protein and VIG associate with the RNA interference machinery. (2002, background): “In Drosophila, a bona fide dFXR regulatory target has been identified as Futsch, a Map1B homolog (Zhang et al. 2001).”
• The role of the Rho GTPases in neuronal development. (2005, background): “In addition, FMRP inversely regulates mRNA translation of Futsch, the Drosophila homolog of MAP1B, shown to be required for dendritic, axonal, and synaptic development (Zhang et al. 2001).”
• A Drosophila fragile X protein interacts with components of RNAi and ribosomal proteins. (2002, background): “Importantly, genetic studies demonstrate that dFMR1 has a role in the regulation of synapse growth and functions (Zhang et al. 2001; Dockendorff et al. 2002; Morales et al. 2002; Inoue et al. 2002), probably by acting as a translational repressor of an mRNA encoding Futsch, which is the fly homolog…”
• Role of Purα in targeting mRNA to sites of translation in hippocampal neuronal dendrites (2006, background): “, 2003), a dendrite-specific protein, and Map1B (Zhang et al., 2001), an embryonic protein present in neurites, have been observed in dendrites in various systems.”
• Drosophila strategies to study psychiatric disorders. (2013, background): “to mammalian FMR1, containing identical protein domains that mediate in RNA binding [186].”
• Fragile X syndrome: loss of local mRNA regulation alters synaptic development and function. (2008, positive): “Although futsch (MAP1b) is one dFMRP target whose translational impairment is already known to account for the synaptic overgrowth phenotype in Drosophila (Zhang et al., 2001), it is unclear whether this is caused by loss of local translational regulation in axons.”
• Diseases of Unstable Repeat Expansion: Mechanisms and Common Principles (2005, positive): “fcgi?db=gene&cmd=Retrieve&dopt=Graphics&list_uids=44443"> futsch , a MAP1B homologu”
• Fragile X Mental Retardation Protein Regulates New Neuron Differentiation in the Adult Olfactory Bulb (2011, background): “This alteration is thought to be due to loss of translational suppression of cytoskeleton regulators, either of actin filaments, as mentioned above, or of microtubules, through Map1B/Futsch (Zhang et al., 2001).”
• Biochemical and genetic interaction between the fragile X mental retardation protein and the microRNA pathway (2004, background): “It has been shown that overexpression of dFMR1 causes neuronal cell death and leads to apoptosi”
• The Fly as a Model for Neurodegenerative Diseases: Is It Worth the Jump? (2007, positive): “Functionally relevant RNA targets of dFMR1 were found to include futsch , which encodes for a microtubule-associated protein with homology to mammalian MAP1B [”