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FB2026_01
,
released March 12, 2026
dfmr1, FMRP, dFMRP, dfxr, dfmr
KH domain RNA-binding protein - homolog of mammalian Fragile X mental retardation gene - represses Futsch translation - mutants have synaptic structural defects
Please see the JBrowse view of Dmel\Fmr1 for information on other features
To submit a correction to a gene model please use the Contact FlyBase form
AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Gene model reviewed during 6.02
Gene model reviewed during 5.47
Low-frequency RNA-Seq exon junction(s) not annotated.
Annotated transcripts do not represent all supported alternative splices within 5' UTR.
Annotated transcripts do not represent all possible combinations of alternative exons and/or alternative promoters.
Unconventional translation start (CUG) postulated; FBrf0213401.
Gene model reviewed during 5.55
Gene model reviewed during 6.04
Homodimer (PubMed:11046149). Interacts with AGO2, Dcr-1, Rm62, vig, RpL5 and RpL11; these interactions form the RNA-induced silencing complex (RISC), a messenger ribonucleoprotein particle (RNP) complex involved in translation regulation (PubMed:12368261, PubMed:14508492). As part of the RISC complex, interacts with Tudor-SN (PubMed:14508492). Component of a neuronal RNP at least composed of Fmr1, tral and me31B (PubMed:17178403). Interacts with piwi and vas; these interactions occur in the polar granules (PubMed:16949822). Interacts with Cyfip (PubMed:12818175). Associates with polyribosome (PubMed:12368261). Interacts with Ythdf; the interaction is RNA independent (PubMed:33428246).
The C-terminal disordered region undergoes liquid-liquid phase separation (LLPS) for the formation of a membraneless compartment that concentrates mRNAs with associated regulatory factors.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Fmr1 using the Feature Mapper tool.
The testis specificity index was calculated from modENCODE tissue expression data by Vedelek et al., 2018 to indicate the degree of testis enrichment compared to other tissues. Scores range from -2.52 (underrepresented) to 5.2 (very high testis bias).
Comment: assayed 0-16 hr AEL; peak at 0-3 hr AEL for short isoform, 6-12 hr AEL for long isoform
At embryonic stage 5 Fmr1 is ubiquitously expressed at low levels, and enriched in pole cells. By stage 9, expression is observed in the central nervous system and, at a lower level, in the somatic musculature. Expression increases in somatic musculature, and by stage 12 is visible in lateral stripes corresponding to the somatic muscles.
Comment: NOT terminal epithelial cell of testis
Comment: NOT terminal epithelial cell of testis
Comment: assayed 0-18 hr AEL
Fmr1 levels appear to be slightly higher in enteroblasts relative to intestinal stem cells.
Fmr1 protein is distributed granularly in the cytoplasm of embryonic muscles, and is accumulated in the muscle tip, where the muscle attaches to the tendon cell.
Fmr1 protein expression is ubiquitous within neurons and relatively uniform between neurons throughout adult brain
Fmr1 protein expression is enriched in the brain. It is expressed specifically in neurons and is excluded from glia. In pupal and adult brains, it is expressed in most, if not all neurons.
The 85 kD band is detectable via Western blot at all embryonic stages and in S2 cells. THe 82 kD band is observed in S2 cells and in embryos colleced 9-12 hours AEL. Embryonic expression of Fmr1 protein is first detectable in the somatic musculature at embryonic stage 9. By stage 12, Fmr1 protein accumulates in the brain and ventral nerve cord. In late embryos high levels of expression are observed in the pharyngeal muscle, gonads, visceral muscle and hindgut. Expression is also observed in the tips of scolopidial dendrites in thoracic and abdominal segments, and at muscle attachment sites. In first instar larvae, the expression in scolopidial neurons extend to the entire scolopidial dendrite. In third instar larvae, expression persists in muscles, but is primarily localized to the central nervous system. Fmr1 protein is heavily expressed in the larval mushroom body, and accumulates in the cell bodies, dendrites, and axons of Kenyon cells. Expression is widespread in the ventral nerve cord, where it is cytoplasmically localized. In the larval testis, expression is localized cytoplasmically in spermatocytes, but is excluded from spermatogonia. In the eye disc, Fmr1 protein is observed at the morphogenetic furrow, in the axon of the Bolwig nerve, and in maturing ommatidia. Ommatidial expression appears to be restricted to photoreceptor cell R8.
JBrowse - Visual display of RNA-Seq signals
View Dmel\Fmr1 in JBrowse3-49
3-46.6
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see JBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
monoclonal
polyclonal
Fmr1 plays a developmentally restricted role in sculpting synaptic architecture in these neurons that cannot be compensated for by later reintroduction of the protein at maturity.
One of 42 Drosophila genes identified as being most likely to reveal molecular and cellular mechanisms of nervous system development or plasticity relevant to human Mental Retardation disorders.
Fmr1 mutants exhibit developmental defects in the mushroom bodies, of which the most common is a failure of β-lobes to stop at the brain midline.
Fmr1 mutants are highly sensitive to genetic background.
Fmr1 is a negative regulator of neuronal architecture and synaptic differentiation.
Fmr1 has a role in dendritic development.
Mutant flies show normal central clock function, though have arrhythmic circadian activity and erratic patterns of locomotor activity and show failure to maintain courtship interest. Neurons required for normal circadian behavior show subtle abnormalities.
Fmr1 plays a critical role in the circadian output pathway regulating locomotor activity.
Fmr1 mutants show strong eclosion failure and circadian rhythm defects. Different neuronal cell types show different phenotypes.
Area matching Drosophila ESTS AA438987 and AA264877. These ESTs have sequence similarity to Human FXR1 gene.
Source for merge of: Fmr1 BcDNA:GM08679
Source for merge of Fmr1 BcDNA:GM08679 was a shared cDNA ( date:030206 ).
