ArticleDevelopmental biology2010
Proteomic analysis reveals CCT is a target of Fragile X mental retardation protein regulation in Drosophila.
Article in Developmental biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 21 citations in OpenAlex.
- Loss of FMRP affects ovarian development and behaviour through multiple pathways in a zebrafish model of fragile X syndrome.Human molecular genetics · 2024Article
- Proteomics insights into fragile X syndrome: Unraveling molecular mechanisms and therapeutic avenues.Neurobiology of disease · 2024Review
- The regulatory role of endoplasmic reticulum chaperone proteins in neurodevelopment.Frontiers in neuroscience · 2022Review
- I-KCKT allows dissection-free RNA profiling of adultDevelopment (Cambridge, England) · 2021Article
- Altered mitochondrial function in cells carrying a premutation or unmethylated full mutation of the FMR1 gene.Human genetics · 2020Article
- Effects of Gene Dose, Chromatin, and Network Topology on Expression in Drosophila melanogaster.PLoS genetics · 2016Article
- Fmr1 deficiency promotes age-dependent alterations in the cortical synaptic proteome.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- 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
- Proteomic and functional analysis of the mitotic Drosophila centrosome.The EMBO journal · 2010Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Fragile X mental retardation protein (FMRP) is an RNA-binding protein that is required for the translational regulation of specific target mRNAs. Loss of FMRP causes Fragile X syndrome (FXS), the most common form of inherited mental retardation in humans. Understanding the basis for FXS has been limited because few in vivo targets of FMRP have been identified and mechanisms for how FMRP regulates physiological targets are unclear. We have previously demonstrated that Drosophila FMRP (dFMRP) is required in early embryos for cleavage furrow formation. In an effort to identify new targets of dFMRP-dependent regulation and new effectors of cleavage furrow formation, we used two-dimensional difference gel electrophoresis and mass spectrometry to identify proteins that are misexpressed in dfmr1 mutant embryos. Of the 28 proteins identified, we have identified three subunits of the Chaperonin containing TCP-1 (CCT) complex as new direct targets of dFMRP-dependent regulation. Furthermore, we found that the septin Peanut, a known effector of cleavage, is a likely conserved substrate of fly CCT and is mislocalized in both cct and in dfmr1 mutant embryos. Based on these results we propose that dFMRP-dependent regulation of CCT subunits is required for cleavage furrow formation and that at least one of its substrates is affected in dfmr1- embryos suggesting that dFMRP-dependent regulation of CCT contributes to the cleavage furrow formation phenotype.
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