FB2019_05, released Oct 15, 2019

Allele: Dmel\Fmr1Δ50M

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General Information
Symbol
Dmel\Fmr1Δ50M
Species
D. melanogaster
Name
FlyBase ID
FBal0131033
Feature type
allele
Associated gene
Dmel\Fmr1
Associated Insertion(s)
Carried in Construct
Also Known As
dfmr150M, dfmr1Δ50M, Fmr1Δ50, dFmr1Δ50, dxfr150M
Allele class
amorphic allele - genetic evidence
loss of function allele
Mutagen
Nature of the Allele
Allele class
amorphic allele - genetic evidence
(Morales et al., 2002)
loss of function allele
(Bushey et al., 2009, Epstein et al., 2009, Zhang et al., 2001)
Mutagen
Delta2-3 transposase
(Zhang et al., 2001)
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DDBJ / EMBL / GenBank
DNA sequence
Protein sequence
 
UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
       
      Progenitor genotype
      Fmr1EP3517
      (Zhang et al., 2001)
      Cytology
      Nature of the lesion
      Statement
      Reference
      Deletion removing P{EP} and flanking DNA including the 5' non coding exons and the first coding exon of the Fmr1 gene.
      (Zhang et al., 2001)
      Expression Data
      Reporter Expression
      Additional Information
      Statement
      Reference
       
      Marker for
      Reflects expression of
      Reporter construct used in assay
      Human Disease Associations
      Disease Ontology (DO) Annotations
      Models Based on Experimental Evidence ( 1 )
      Modifiers Based on Experimental Evidence ( 1 )
      Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
       
      Phenotypic Data
      Phenotypic Class
      cell number defective (with Fmr13)
      (Epstein et al., 2009)
      cell number defective | adult stage (with Df(3R)Exel6265)
      (Tan et al., 2016)
      cell number defective | adult stage (with Fmr13)
      (Tan et al., 2016)
      decreased cell death
      (Gatto and Broadie, 2011)
      endomitotic cell cycle defective
      (Epstein et al., 2009)
      female semi-fertile (with Fmr1Δ113M)
      (Bozzetti et al., 2015)
      female semi-fertile | dominant
      (Bozzetti et al., 2015)
      female semi-fertile | recessive
      (Bozzetti et al., 2015)
      female semi-sterile (with Df(3R)Exel6265)
      (Tan et al., 2016)
      female semi-sterile (with Fmr13)
      (Tan et al., 2016)
      flight defective (with Df(3R)by62)
      (Zhang et al., 2001)
      increased occurrence of cell division (with Fmr13)
      (Epstein et al., 2009)
      learning defective | adult stage
      (Gatto et al., 2014, Coffee et al., 2012)
      lethal - all die before end of P-stage
      (Scantlebury et al., 2010, Morales et al., 2002)
      locomotor behavior defective
      (Pan et al., 2008)
      male semi-fertile | dominant
      (Bozzetti et al., 2015)
      male sterile
      (Coffee et al., 2010)
      male sterile (with Fmr1Δ113M)
      (Bozzetti et al., 2015)
      male sterile | recessive
      (Bozzetti et al., 2015)
      memory defective
      (Gross et al., 2015)
      memory defective | adult stage
      (Bienkowski et al., 2017)
      neuroanatomy defective
      (Gross et al., 2015, Kim et al., 2013, Gatto and Broadie, 2011, Coffee et al., 2010, Gatto and Broadie, 2009, Pan et al., 2008, Michel et al., 2004, Zhang et al., 2001)
      neuroanatomy defective, with Fmr1UAS.cZa, Scer\GAL4P2.4.Pdf
      (Gatto and Broadie, 2009)
      neuroanatomy defective (with Fmr1Δ113M)
      (Michel et al., 2004, Morales et al., 2002)
      neuroanatomy defective | adult stage
      (Bienkowski et al., 2017, Gatto et al., 2014)
      neuroanatomy defective | adult stage | recessive
      (Doll and Broadie, 2015)
      neuroanatomy defective | adult stage | somatic clone
      (Gatto et al., 2014, Tessier and Broadie, 2008)
      neuroanatomy defective | adult stage | somatic clone | conditional
      (Tessier and Broadie, 2008)
      neuroanatomy defective | larval stage
      (Nguyen et al., 2016, Scantlebury et al., 2010)
      neuroanatomy defective | pupal stage | somatic clone
      (Tessier and Broadie, 2008)
      neuroanatomy defective | somatic clone
      (Pan et al., 2004)
      neuroanatomy defective | somatic clone | third instar larval stage
      (Sterne et al., 2015)
      neuroanatomy defective | third instar larval stage
      (Friedman et al., 2013, Nahm et al., 2013, Xu et al., 2013, Coffee et al., 2012, Siller and Broadie, 2011)
      neurophysiology defective
      (Zhang et al., 2001)
      neurophysiology defective | adult stage | somatic clone
      (Gatto et al., 2014)
      neurophysiology defective | third instar larval stage
      (Friedman et al., 2013)
      partially lethal - majority die
      (Gross et al., 2015)
      semi-sterile
      (Zhang et al., 2004)
      size defective | adult stage | somatic clone
      (Tessier and Broadie, 2008)
      size defective | adult stage | somatic clone | conditional
      (Tessier and Broadie, 2008)
      size defective | pupal stage | somatic clone
      (Tessier and Broadie, 2008)
      sleep defective
      (van Alphen et al., 2013, Bushey et al., 2009)
      sleep defective (with Fmr1Δ113M)
      (Bushey et al., 2009)
      some die during pharate adult stage
      (Scantlebury et al., 2010, Morales et al., 2002)
      viable
      (Baumgartner et al., 2013, Zhang et al., 2001)
      viable | recessive
      (Bozzetti et al., 2015)
      Phenotype Manifest In
      adult mushroom body
      (Michel et al., 2004)
      adult mushroom body (with Fmr1Δ113M)
      (Michel et al., 2004)
      adult mushroom body beta-lobe
      (Gross et al., 2015)
      axon | adult stage | somatic clone
      (Tessier and Broadie, 2008)
      axon | adult stage | somatic clone | conditional
      (Tessier and Broadie, 2008)
      axon | pupal stage | somatic clone
      (Tessier and Broadie, 2008)
      axonemal microtubule
      (Coffee et al., 2010)
      bouton
      (Coffee et al., 2010, Gatto and Broadie, 2009)
      bouton, with Fmr1UAS.cZa, Scer\GAL4P2.4.Pdf
      (Gatto and Broadie, 2009)
      bouton | somatic clone
      (Pan et al., 2004)
      class IV dendritic arborizing neuron | somatic clone | third instar larval stage
      (Sterne et al., 2015)
      dendritic tree | adult stage
      (Doll and Broadie, 2015)
      dorsal cluster neuron (with Fmr1Δ113M)
      (Morales et al., 2002)
      dorsal cluster neuron & neurite (with Fmr1Δ113M)
      (Morales et al., 2002)
      egg chamber | adult stage (with Df(3R)Exel6265)
      (Tan et al., 2016)
      egg chamber | adult stage (with Fmr13)
      (Tan et al., 2016)
      embryonic/larval neuromuscular junction
      (Coffee et al., 2010, Scantlebury et al., 2010)
      embryonic/larval neuromuscular junction | third instar larval stage
      (Friedman et al., 2013, Xu et al., 2013, Coffee et al., 2012, Siller and Broadie, 2011)
      GABAergic neuron | adult stage | somatic clone
      (Gatto et al., 2014)
      gamma Kenyon cell | adult stage | somatic clone
      (Tessier and Broadie, 2008)
      gamma Kenyon cell | adult stage | somatic clone | conditional
      (Tessier and Broadie, 2008)
      gamma Kenyon cell | pupal stage | somatic clone
      (Tessier and Broadie, 2008)
      gamma-lobe & neuron | somatic clone
      (Pan et al., 2004)
      germarium | adult stage (with Df(3R)Exel6265)
      (Tan et al., 2016)
      germarium | adult stage (with Fmr13)
      (Tan et al., 2016)
      larval dorsal multidendritic neuron ddaC
      (Kim et al., 2013)
      LNv neuron (with Fmr1Δ113M)
      (Morales et al., 2002)
      mushroom body & neuron & dendrite | somatic clone
      (Pan et al., 2004)
      mushroom body & neuron | somatic clone
      (Pan et al., 2004)
      mushroom body | adult stage
      (Gatto et al., 2014)
      mushroom body alpha-lobe (with Fmr1Δ113M)
      (Michel et al., 2004)
      mushroom body alpha-lobe | adult stage
      (Bienkowski et al., 2017)
      mushroom body beta-lobe
      (Michel et al., 2004, Pan et al., 2004)
      mushroom body beta-lobe (with Fmr1Δ113M)
      (Michel et al., 2004)
      mushroom body beta-lobe | adult stage
      (Bienkowski et al., 2017)
      mushroom body intrinsic neuron
      (Pan et al., 2008)
      mushroom body pedunculus-medial lobe and vertical lobe arborizing neuron 2 | adult stage
      (Doll and Broadie, 2015)
      neuromuscular junction
      (Pan et al., 2008, Zhang et al., 2001)
      NMJ bouton
      (Scantlebury et al., 2010)
      NMJ bouton | supernumerary | third instar larval stage
      (Nahm et al., 2013, Coffee et al., 2012, Siller and Broadie, 2011)
      NMJ bouton | third instar larval stage
      (Xu et al., 2013)
      nurse cell (with Fmr13)
      (Epstein et al., 2009)
      nurse cell | adult stage (with Df(3R)Exel6265)
      (Tan et al., 2016)
      nurse cell | adult stage (with Fmr13)
      (Tan et al., 2016)
      nurse cell | supernumerary (with Fmr13)
      (Epstein et al., 2009)
      ovary | adult stage (with Df(3R)Exel6265)
      (Tan et al., 2016)
      ovary | adult stage (with Fmr13)
      (Tan et al., 2016)
      Pdf neuron close to tritocerebrum
      (Gatto and Broadie, 2011)
      peptidergic neuron
      (Gatto and Broadie, 2011)
      photoreceptor cell & synapse & lamina receptor cell
      (Zhang et al., 2001)
      presynaptic active zone
      (Pan et al., 2008)
      projection neuron | adult stage
      (Doll and Broadie, 2015)
      protocerebrum
      (Coffee et al., 2010)
      s-LNv Pdf neuron
      (Coffee et al., 2010)
      s-LNv Pdf neuron | supernumerary | third instar larval stage
      (Coffee et al., 2012)
      spermatid
      (Zhang et al., 2004)
      spermatid axoneme
      (Coffee et al., 2010, Zhang et al., 2004)
      spermatocyte | spermatogenesis
      (Bozzetti et al., 2015)
      spermatocyte | spermatogenesis (with Fmr1Δ113M)
      (Bozzetti et al., 2015)
      synapse
      (Kim et al., 2013, Gatto and Broadie, 2009, Pan et al., 2008)
      synapse, with Fmr1UAS.cZa, Scer\GAL4P2.4.Pdf
      (Gatto and Broadie, 2009)
      synaptic vesicle
      (Pan et al., 2008)
      synaptic vesicle | somatic clone | supernumerary
      (Pan et al., 2004)
      terminal bouton
      (Pan et al., 2008)
      testis
      (Zhang et al., 2004)
      type I bouton | larval stage
      (Nguyen et al., 2016)
      type I bouton | third instar larval stage
      (Friedman et al., 2013)
      Detailed Description
      Statement
      Reference
      Bouton numbers are unaffected at the NMJ of Fmr1Δ50M/+ third instar larvae.
      (Kim et al., 2019)
      Fmr1Δ50M adult heterozygotes do not display any overt eye morphology defects but display memory defects in an aversive olfactory conditioning assay (their olfactory perception however is not disrupted). Fmr1Δ50M homozygous adults exhibit mushroom body defects including missing or thinned mushroom body α-lobes and β-lobe fusion.
      (Bienkowski et al., 2017)
      Fmr1Δ50M/Fmr1Δ50M larvae show significant increases in the number of type I boutons at the neuromuscular junction, compared to controls.
      (Nguyen et al., 2016)
      Fmr1Δ50M/Df(3R)Exel6265 and Fmr1Δ50M/Fmr13 mutant females display a strong reduction in fertility. Ovaries of Fmr1Δ50M/Df(3R)Exel6265 mutants, and a subset of Fmr1Δ50M/Fmr13 mutants, display developmental defects, including fused egg chambers, aberrant nurse cell numbers, disorganized germaria often fused to an egg chamber, and occasional oocyte misspecification or multiple oocytes per egg chamber.
      (Tan et al., 2016)
      Fmr1Δ50M homozygotes are viable, male sterile and female semi-fertile. Fmr1Δ50M heterozygous males and females are semi-fertile. Fmr1Δ50M/Fmr1Δ113M transheterozygotes are male sterile and female semi-fertile. Fmr1Δ50M homozygosity and Fmr1Δ50M/Fmr1Δ113M transheterozygosity lead to the formation of crystalline aggregates (of Stellate protein) in spermatocytes, which are absent in Fmr1Δ50M heterozygotes and wild-type controls.
      (Bozzetti et al., 2015)
      Fmr1Δ50M/Fmr1Δ50M, but not Fmr1Δ50M/+, mutants display a striking expansion of dendritic arbors in MVP2 neurons at day 1 post-eclosion, as compared to controls, with a significant increase in total dendritic arbor volume; the central core of arbors is much wider than that of wild type, with less-pronounced anterior and posterior ends; homozygous mutant arbors occupy a greater dorsoventral depth as compared with wild type. Projection neuron dendritic arbors in Fmr1Δ50M/Fmr1Δ50M mutants also exhibit overgrowth, with a significant increase in total dendritic arbor volume, as compared to controls. These dendritic arbor expansion phenotypes are not observed at earlier developmental time points, measured at pupal day 4, and 1 hour post-eclosion.
      (Doll and Broadie, 2015)
      The presynaptic terminal length of class IV dendritic arborizing neurons in Fmr1Δ50M/Fmr1Δ50M MARCM somatic clones in third instar larvae is significantly increased compared to controls.
      (Sterne et al., 2015)
      Fmr1Δ50M/Fmr1Δ50M flies do not exhibit any significant difference in the number, distribution or density of GABAergic neurons, or the GABAergic mushroom body calyx innervation, but do show frequent mushroom body beta lobe crossing and fusion at the midline, and absence or loss of mushroom body lobes, most often the alpha lobe, as compared to controls. Fmr1Δ50M/Fmr1Δ50M flies exhibit a strong learning deficit in an associative learning assay. Fmr1Δ50M/Fmr1Δ50M GABAergic neuron clones do not show any significant difference in cumulative process length, as compared to control clones, but do exhibit a differential developmental trajectory in process elaboration, with a highly significant increase in process length between days 1 and 5 post-eclosion, and they also show altered depolarization-induced calcium signaling dynamics, in comparison to control neurons. Fmr1Δ50M/Fmr1Δ50M GABAergic neuron clones with only a primary process show a significant increase in total length at 5 days post-eclosion, and those with 5 or more processes show a significant decrease in total process length at 1 day post-eclosion, as compared to control neurons. Fmr1Δ50M/Fmr1Δ50M GABAergic neuron clones with 2-4 processes do not exhibit any significant difference in total process length as compared to controls. Fmr1Δ50M/Fmr1Δ50M GABAergic neuron clones with 5 or more processes show significantly shorter primary and secondary processes and fewer secondary and tertiary branches at 1 day post eclosion, as compared to controls, but these differences are not seen at 5 days post-eclosion.
      (Gatto et al., 2014)
      Homozygotes are viable and do not display obvious growth phenotypes. Fmr1Δ50M mutant eyes, generated by eyFLP/FRT-mediated mitotic recombination, do not show an increase in ommatidial number.
      (Baumgartner et al., 2013)
      Neuromuscular junctions in Fmr1Δ50M/Fmr1Δ50M mutant larvae exhibit significantly increased branch number and increased type I synaptic bouton number, and significantly increased amplitude of evoked junctional currents, as compared to controls.
      (Friedman et al., 2013)
      A Fmr1Δ50M mutant C4 ddaC neuron clones causes mild but significant overgrowth of presynaptic terminals.
      (Kim et al., 2013)
      Homozygous third instar larvae show an increase in bouton number and satellite bouton number at the neuromuscular junction compared to controls.
      (Nahm et al., 2013)
      Fmr1Δ50M mutant third instar larvae exhibit neuromuscular junction abnormalities in muscle 4. Their synaptic branch and bouton numbers are significantly higher than in wild type flies.
      (Xu et al., 2013)
      Mutant males and females show an increase in daytime sleep intensity compared to controls.
      (van Alphen et al., 2013)
      The Fmr1Δ50M mutant brain is unaltered in size and gross architecture compared with controls. However synaptogenesis defects can be seen including elevated synaptic area, increased synaptic branching and the formation of supernumerary synaptic boutons. Developmentally arrested satellite boutons also accumulate in Fmr1Δ50M mutant larvae. Futsch positive loops accumulate in Fmr1Δ50M mutant synaptic arbors. The brains of adult Fmr1Δ50M mutants exhibit strikingly abnormal small ventrolateral (sLN[[v]] neuron synaptic architecture with expanded terminals containing supernumerary synaptic boutons. Fmr1Δ50M mutant flies have approximately 70 Pdf positive boutons in the dorsal horn and protocerebrum compared to around 40 in controls. Fmr1Δ50M mutants display a highly significant decrease in olfactory learning compared to controls.
      (Coffee et al., 2012)
      A particularly prominent defect in Pdf neurons not reported previously is the aberrant appearance of a class of Pdf neurons in the central brain of Fmr1Δ50M mutants. This class of neurons is a developmentally-transient population of triocerebral Pdf neurons. These neurons are not observe in age-matched adult wild-type brains. In mutants, these neurons are often present at a bilaterally oriented pair with cell body positioning in the tritocerebrum, near the esophageal foramen. Mutant Pdf neurons project their axons upward beyond the posterior optic tract and elaborate a synaptic field in the protocerebral area adjacent to the sLN[[v]] synaptic arbors. Thus, in addition to connectivity defects within the s- and lLN[[v]] neurons, the PDF circuit may be compromised by the encroaching aberrant contributions of the midline PDF tritocerebral (PDF-TRI) neurons present only in Fmr1Δ50M mutants. Upon eclosion, wild-type and mutant brains show an indistinguishable array of PDF-TRI neurons. However, in the proceeding days, these cells are rapidly lost in control brains, while retained in Fmr1Δ50M mutants. The inappropriately retained Fmr1Δ50M mutant PDF-TRI neurons maintain synaptic connectivity at maturity as well as depolarization-dependent Ca[2+] transients. No evidence of increased proliferation for the abnormally retained neurons is found, but rather clear indication of impaired apoptosis in Fmr1Δ50M mutant brains. Examination of crustacean cardioactive peptide (CCAP) and bursicon circuits, which are developmentally-transient and normally eliminated immediately post-eclosion in wild-type, reveal significantly delayed clearance compared with wild-type, however, the CCAP/bursicon neurons are also subsequently eliminated in Fmr1Δ50M mutants.
      (Gatto and Broadie, 2011)
      The number of NMJ branches (defined as a process with two or more boutons), is significantly higher in Fmr1Δ50M mutant third instar larvae compared to controls. The number of mature type 1b boutons is significantly increased in the Fmr1Δ50M null synapse and the number of immature satellite boutons is similarly elevated. The increase in number of mature boutons and the accumulation of satellite neurons are both rescued when the larvae are fed >20uM minocycline. The increase in NMJ arbor branch number is not restored upon treatment with minocycline. Small ventrolateral (sLN[[v]]) clock neurons in Fmr1Δ50M brains at three days post eclosion have an increased number and density of synaptic boutons, with overextension of their spatial distribution extending from the dorsal horn bifurcation point. These phenotypes are completely rescued upon feeding with minocycline. However, minocycline-treated Fmr1Δ50M null sLN[[v]] neurons continue to display a somewhat dispersed bouton array. In young adult brains (0-4 hours post-eclosion), single cell Fmr1Δ50M mutant MARCM clones in the adult mushroom body γ lobe show increased axonal length and excess synaptic branching compared to controls. Both of these defects are rescued upon treatment with minocycline.
      (Siller and Broadie, 2011)
      Compared to wild-type, brain size and gross architecture of homozygous Fmr1Δ50M mutants appear unaltered. Dorsal projections into the protocerebrum in Fmr1Δ50M mutants exhibit a highly significant increase in the number of s-LNv Pdf neuron boutons compared with controls. Fmr1Δ50M mutants display defects on many levels of neuromuscular junction synaptic architecture, including grossly elevated synaptic area, increased synaptic branching, and the formation of supernumerary synaptic boutons. Most strikingly, developmentally arrested mini (or satellite) boutons accumulate int the mutants. Fmr1Δ50M males are completely sterile producing no viable progeny. In Fmr1Δ50M mutant spermatids, the central pair of axoneme microtubules is routinely lost, whereas the outer ring microtubule doublets are often deranged.
      (Coffee et al., 2010)
      There is an increase in the total number of branches and the total number of boutons at the neuromuscular junction in mutant larvae compared to controls.
      (Scantlebury et al., 2010)
      Fmr1Δ50M/Fmr1Δ50M, Fmr1Δ50M/Fmr1Δ113M and Fmr1Δ50M/Df(3R)Exel6265 adults sleep significantly longer each day than wild-type controls. The length of time they sleep each day increases with age up to some peak (for Fmr1Δ50M homozygotes: at 12 days in males, 42 days in females). Increased sleep in these animals is predominantly the result of increased number of sleep episodes and reduced number of brief awakenings, rather than increased average duration of sleep episodes. The increase in daily sleep in these mutants is also seen when animals are kept in permanent darkness. Fmr1Δ50M/Fmr1EP3517 adults sleep significantly longer per day than wild-type, although the effect is more subtle than in Fmr1Δ50M homozygotes and is more pronounced in females than in males. The increase in daily sleep in these flies is increased further by keeping them in permanent darkness. Under alternating 12 hours light and 12 hours dark conditions, Fmr1Δ50M/Fmr1Δ50M mutants show a circadian cycle of sleep. However, this differs from wild-type in having more sleep under light conditions and in lacking a reduction in sleep in anticipation of the end of dark conditions. Also unlike wild-type, under conditions of total darkness, Fmr1Δ50M/Fmr1Δ50M adults show no circadian rhythm in locomotor activity or sleep. Unlike wild-type flies, Fmr1Δ50M homozygotes do not recover significant amounts of sleep the day after 24 hours of sleep deprivation. However, following sleep deprivation they show reduced activity in response to a stimulus that causes arousal in wild-type or non-sleep deprived Fmr1Δ50M homozygotes. Fmr1Δ50M homozygotes have a reduced lifespan, with a steady death rate almost from eclosion, rather than a lag with few deaths in the first 28 days as seen in wild-type.
      (Bushey et al., 2009)
      Fmr13/Fmr1Δ50M ovaries contain aberrant egg chambers with both increased and decreased numbers of germ cells per chamber compared to the normal number of 16. Fmr13/Fmr1Δ50M mutant germaria contain significantly more mitotic cells than controls. None of the completely mutant egg chambers in Fmr1Δ50M mosaic ovaries surrounded by heterozygous follicle cells exhibit proliferation defects. They appear morphologically normal.
      (Epstein et al., 2009)
      Fmr1Δ50M mutant sLN[[v]] synaptic arbors display an overgrowth and over-elaboration phenotype. Fmr1Δ50M mutants exhibit an increased number of synaptic boutons throughout the sLN[[v]] terminal, projecting at minimum a further 20υm toward the midline and with a greatly increased average number of boutons beyond 50υm, compared to wild-type. Moreover, the number of synaptic boutons in every concentric ring is significantly elevated in Fmr1Δ50M mutants throughout the arbor. Both the number and spatial distribution of boutons in the sLN[[v]] synaptic arbor is altered in the absence of Fmr1, with more boutons occupying a larger territory beyond the normal extent of the sLN[[v]] arborization. Overexpression of Fmr1Scer\UAS.cZa at the earliest stage of pupal development, under the control of RU486-induced Scer\GAL4elav.Switch.PO exacerbates the Fmr1Δ50M mutant phenotype resulting in an elevated number of Pdf-positive synaptic boutons redistributed within 30% of the sLN[[v]] axonal arbor. Similarly, induction at pupal stage P2 provides no significant influence upon the synaptic arborization, with no change in the total number of Pdf-positive boutons. Overexpression of Fmr1Scer\UAS.cZa in the latter stage of pupal development, under the control of RU486-induced Scer\GAL4elav.Switch.PO ameliorates the Fmr1Δ50M mutant phenotype, restricting the number and specificity of synaptic connections.
      (Gatto and Broadie, 2009)
      Fmr1Δ50M mutants do not display defects in coordinated behavior (such as in a roll-over assay). Fmr1Δ50M mutants display significant overbranching in the neuromuscular synapse. Treatment of these mutants with the mGluR antagonist MPEP, which blocks mGluR signaling, suppresses the Fmr1Δ50M overbranching phenotype. Fmr1Δ50M mutant synaptic terminals display a significant increase in total area, compared to controls. Fmr1Δ50M mutants treated with the mGluR antagonist MPEP, which blocks mGluR signaling, display a significantly decreased synaptic area compared to non-treated mutants. However, MPEP-treated control animals display a similar decrease compared to non-treated controls, leading to the difference between the MPEP-treated wild-type control and the MPEP-treated Fmr1Δ50M mutant remaining significant, indicating that blocking mGluR signaling does not significantly rescue the increased synaptic terminal area characteristic of Fmr1Δ50M mutants. Fmr1Δ50M mutants display a significant increase in the number of synaptic boutons in the neuromuscular junction. Treatment of these mutants with the mGluR antagonist MPEP, which blocks mGluR signaling, does not rescue this increased bouton defect. At the ultrastructural level, the overall appearance of a bouton and the postsynaptic subsynaptic reticulum in Fmr1Δ50M mutants appears normal. Quantitatively, there is no significant difference in bouton size, mitochondria size, active zone size/number or the postsynaptic subsynaptic reticulum between Fmr1Δ50M mutants and control larvae. Fmr1Δ50M mutants display significant increases of synaptic vesicle density throughout the synaptic bouton clustered vesicle number surrounding active zones and docked vesicle number at the T-bar membrane. overall, Fmr1Δ50M mutants display a significant ~30% increase in overall vesicle number. Fmr1Δ50M mutants display a significant ~50% increase in the pool of clustered vesicles around the active zone. Fmr1Δ50M mutants display a significant ~85% increase in the number of docked vesicles at the active zone. Fmr1Δ50M mutant mushroom body neurons display axonal overgrowth, with both the axon branch number and the total axon branch length significantly increased in these mutants compared to controls. Treatment of these MARCM clone animals with the mGluR antagonist MPEP can effectively rescue the axon overgrowth and increased branching defects in these mutants.
      (Pan et al., 2008)
      At prepupal stage 4, but not stage 3, Fmr1Δ50M homozygous gamma neuron clones in a Fmr1Δ50M heterozygous background show longer axons with the same number of., but larger, branches, as compared to controls. Mutant neurons show a normal increase in size before eclose but show delayed pruning at eclosion, as they exhibit a decrease in axon branching only at day 4 after eclosion instead of at eclosion. In 4 days old adults reared under sensory deprivation, Fmr1Δ50M homozygous gamma neuron clones (in a Fmr1Δ50M heterozygous background) display a more pronounced increase in axon branch number, a significant increase in axon branch length and a failure in pruning, as compared to controls.
      (Tessier and Broadie, 2008)
      In just under 10% of homozygous Fmr1Δ50M mutants, the β lobe of the mushroom body is misdirected or missing. Just under 20% of homozygous Fmr1Δ50M mutants display a misdirected or missing α-lobe. In just under 70%, both the α- and β lobes of the mushroom body are either misdirected or missing. Where the β-lobe is present, just under 10% display severe midline crossing (defined as a densely strained band equal to or greater in width and thickness than those of the adjacent β-lobes), with approximately 25% displaying moderate midline crossing (defined as when the thickness of the fiber bundle crossing the midline is considerable but less than the width of the β-lobe termini). Just under 10% display mild midline crossing phenotypes in the β lobe (defined as when a thin band of fibers cross the midline). Approximately 10% of Fmr1Δ50M/Fmr1Δ113M transheterozygotes display misdirecting or missing α lobes. Approximately just over 70% of transheterozygous Fmr1Δ50M/Fmr1Δ113M mutants exhibit severe midline crossing in the β-lobe of the mushroom body (defined as a densely strained band equal to or greater in width and thickness than those of the adjacent β-lobes). The rest appear phenotypically normal. No sexual dimorphism in penetrance or expressivity is found.
      (Michel et al., 2004)
      Mutant adults have normal gross brain morphology, including an architecturally normal mushroom body. Mild β lobe overgrowth is seen at a slightly higher frequency than wild type. Single cell mutant clones in the mushroom body (in a wild-type background) produce additional cell body processes compared to wild-type single cell clones (converting the characteristic unipolar mushroom body neurons seen in wild-type into multipolar neurons); there is a 3-fold increase in the number of cell body processes in the mutant cells. The mutant cells show a more complex and disordered dendritic structure compared to wild type; primary dendrites display clear secondary branches and the fine dendritic processes that are normally restricted to the termini spread aberrantly along the primary branches. Single cell mutant γ neurons in the mushroom body always have significantly increased axonal branching and significantly more and longer axonal branches than control cells. The large, extra branches do not follow the main axon trajectory, but instead extend in apparently random directions to invade inappropriate territory. Neurons in large mutant clones in the mushroom body show a significantly enlarged average bouton area and more variable distribution of bouton sizes than wild type. The mutant presynaptic boutons are almost filled with vesicles; the average area of the bouton occupied by vesicles is increased 50% in mutant boutons to nearly 75% of the bouton.
      (Pan et al., 2004)
      When mutant female are mated with wild-type males, only 21% of the expected progeny produced. Mutant males have enlarged testes. The diameter of the tip of the testis is similar to controls, but the diameter in the middle of the testis is about 50% larger than wild-type. This phenotype is 100% penetrant in newly enclosed flies, but it abates with aging. Other than this the morphology of mutant testes appears normal. The testis phenotype appears to be caused by the accumulation of misarranged spermatid bundles within the testis lumen. The coiled spermatid bundles normally seen at the testis base are missing in mutants. Instead of mature spermatids, degenerated cell debris fill the base of mutant testes. The early individualisation process of spermatogenesis does appear to progress largely as normal (occasional defects are seen). However, the orientation of spermatid tails within a cyst is often arranged in an irregular fashion in mutants. In addition the configuration of mitochondria and axoneme within a sperm flagellum is variably skewed, as well as some unknown ring structures present at the inner-space between spermatid tails which is not seen in controls. There is also a specific disruption of the microtubule axoneme structure in the sperm flagellum which becomes progressively more pronounced at spermatid differentiation proceeds. The central pair microtubules are missing in mutant axonemes, although the outer microtubules are still present. this phenotype is progressive, 30% of early stage spermatids, and 56% of late-stage spermatid.
      (Zhang et al., 2004)
      Mutants show a fibre extension defect in the DC and LNv neurons. Extension of DC axons from the lobula to the medulla is incomplete, some axons show guidance errors. LNv neurons may over extend, show guidance defects or show aberrant morphology. The LVn defects are less consistent than those in the DC neurons. Stereotypical grid-like array of neurites entering the medulla is disrupted in mutant flies - short and thin branches fail to connect. This occurs even for neurons that do cross towards the distal medulla. Homozygotes show 0% eclosion from pupal case.
      (Morales et al., 2002)
      Mutants show no morphological defects. When tested for bang sensitivity, temperature sensitivity and phototaxis there is no detectable difference between wild type and mutant. However there are defects in coordination in a simple flight test. Synaptic transmission is reduced (as indicated by a reduction in off-transient mean amplitude as assayed by ERG). Null mutants show pronounced synaptic overgrowth and overelaboration of synaptic terminals. Muscle 4 has 51% increase in number of boutons over controls. Arboreal branching is increased - with muscle 4 showing 50% more branches than wild type. Evoked synaptic transmission at the NMJ is elevated. Mean EJC amplitude is increased. Average synaptic efficacy is upregulated.
      (Zhang et al., 2001)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Enhanced by
      Statement
      Reference
      Fmr1Δ50M has memory defective | adult stage phenotype, enhanceable by Nab2ex3/Nab2[+]
      (Bienkowski et al., 2017)
      NOT Enhanced by
      Statement
      Reference
      Fmr1Δ50M has neuroanatomy defective | larval stage phenotype, non-enhanceable by Scer\GAL4αTub84B.PL/TorsindsRNA.UAS.WIZ
      (Nguyen et al., 2016)
      Fmr1Δ50M has semi-sterile phenotype, non-enhanceable by futschN94
      (Zhang et al., 2004)
      Suppressed by
      Statement
      Reference
      Fmr1Δ50M has neuroanatomy defective | adult stage phenotype, suppressible | partially by Nab2ex3/Nab2[+]
      (Bienkowski et al., 2017)
      Fmr1Δ50M/Fmr13 has cell number defective | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8SM206
      (Tan et al., 2016)
      Fmr1Δ50M/Fmr13 has female semi-sterile phenotype, suppressible | partially by Zfrp8[+]/Zfrp8SM206
      (Tan et al., 2016)
      Fmr1Δ50M/Df(3R)Exel6265 has cell number defective | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8SM206
      (Tan et al., 2016)
      Fmr1Δ50M/Df(3R)Exel6265 has female semi-sterile phenotype, suppressible | partially by Zfrp8[+]/Zfrp8SM206
      (Tan et al., 2016)
      Fmr1Δ50M/Fmr1Δ113M has sterile phenotype, suppressible by aubsting-1/aub[+]
      (Bozzetti et al., 2015)
      Fmr1Δ50M has partially lethal - majority die phenotype, suppressible by CenG1A[+]/CenG1AEY01217
      (Gross et al., 2015)
      Fmr1Δ50M has neuroanatomy defective phenotype, suppressible by CenG1A[+]/CenG1AEY01217
      (Gross et al., 2015)
      Fmr1Δ50M has neuroanatomy defective | somatic clone | third instar larval stage phenotype, suppressible by Abl1/Abl[+]
      (Sterne et al., 2015)
      Fmr1Δ50M/Fmr1Δ113M, rinNP3248/rin2 has lethal - all die during pupal stage phenotype, suppressible by rinmCherry
      (Baumgartner et al., 2013)
      Fmr1Δ50M/Fmr1Δ113M, rinNP5420/rin2 has short lived phenotype, suppressible by rinmCherry
      (Baumgartner et al., 2013)
      Fmr1Δ50M has neuroanatomy defective | third instar larval stage phenotype, suppressible by dlp[+]/dlpA187
      (Friedman et al., 2013)
      Fmr1Δ50M has neuroanatomy defective | third instar larval stage phenotype, suppressible by dlp[+]/Sdc[+]/dlpA187/Sdc23
      (Friedman et al., 2013)
      Fmr1Δ50M has neurophysiology defective | third instar larval stage phenotype, suppressible by dlp[+]/Sdc[+]/dlpA187/Sdc23
      (Friedman et al., 2013)
      Fmr1Δ50M has neuroanatomy defective phenotype, suppressible by Dscam118
      (Kim et al., 2013)
      Fmr1Δ50M has neuroanatomy defective | third instar larval stage phenotype, suppressible | partially by Top3β26
      (Xu et al., 2013)
      Fmr1Δ50M has neuroanatomy defective | third instar larval stage phenotype, suppressible by Scer\GAL4elav.PU/Hsap\FMR1UAS.Tag:MYC
      (Coffee et al., 2012)
      Fmr1Δ50M has neuroanatomy defective | third instar larval stage phenotype, suppressible by Scer\GAL4elav.PU/Hsap\FMR1S500D.UAS.Tag:MYC
      (Coffee et al., 2012)
      Fmr1Δ50M has learning defective | adult stage phenotype, suppressible by Scer\GAL4ey-OK107/Hsap\FMR1UAS.Tag:MYC
      (Coffee et al., 2012)
      Fmr1Δ50M has learning defective | adult stage phenotype, suppressible by Scer\GAL4ey-OK107/Hsap\FMR1S500D.UAS.Tag:MYC
      (Coffee et al., 2012)
      Fmr1Δ50M has neuroanatomy defective | third instar larval stage phenotype, suppressible | partially by Scer\GAL4da.G32/TimpUAS.cPa
      (Siller and Broadie, 2011)
      Fmr1Δ50M has neuroanatomy defective | third instar larval stage phenotype, suppressible | partially by Mmp1Q112stop
      (Siller and Broadie, 2011)
      Fmr1Δ50M has neuroanatomy defective phenotype, suppressible by Scer\GAL4elav-C155/Hsap\FMR1UAS.Tag:MYC
      (Coffee et al., 2010)
      Fmr1Δ50M has male sterile phenotype, suppressible by Scer\GAL4VP16.nos.UTR/Hsap\FMR1UAS.Tag:MYC
      (Coffee et al., 2010)
      Fmr1Δ50M has male sterile phenotype, suppressible by Scer\GAL4VP16.nos.UTR/Hsap\FXR1UAS.Tag:MYC
      (Coffee et al., 2010)
      Fmr1Δ50M has male sterile phenotype, suppressible by Hsap\FXR2UAS.Tag:MYC/Scer\GAL4VP16.nos.UTR
      (Coffee et al., 2010)
      Fmr1Δ50M has neuroanatomy defective | larval stage phenotype, suppressible by RanBPMk05201/l(2)k05201[+]
      (Scantlebury et al., 2010)
      Fmr1Δ50M/Fmr13 has endomitotic cell cycle defective phenotype, suppressible | partially by CblF165/Cbl[+]
      (Epstein et al., 2009)
      Fmr1Δ50M has neuroanatomy defective phenotype, suppressible | partially by mGluR112b
      (Pan et al., 2008)
      Fmr1Δ50M has neurophysiology defective phenotype, suppressible by futschN94
      (Zhang et al., 2001)
      Fmr1Δ50M has neuroanatomy defective phenotype, suppressible by futschN94
      (Zhang et al., 2001)
      NOT suppressed by
      Enhancer of
      NOT Enhancer of
      Suppressor of
      Statement
      Reference
      Fmr1Δ50M/Fmr1[+] is a suppressor of visible | adult stage phenotype of Nab2EP3716, Scer\GAL4GMR.PU
      (Bienkowski et al., 2017)
      Fmr1Δ50M/Fmr1[+] is a suppressor of eye color defective phenotype of Nab2EP3716, Scer\GAL4GMR.PU
      (Bienkowski et al., 2017)
      Fmr1Δ50M/Fmr1[+] is a suppressor of size defective | adult stage phenotype of Nab2EP3716, Scer\GAL4GMR.PU
      (Bienkowski et al., 2017)
      Fmr1Δ50M is a suppressor | partially of neuroanatomy defective | third instar larval stage phenotype of Top3β26
      (Xu et al., 2013)
      Fmr1Δ50M is a suppressor of lethal - all die before end of pupal stage phenotype of Mmp1Q112stop
      (Siller and Broadie, 2011)
      Fmr1Δ50M is a suppressor of some die during pupal stage phenotype of Mmp1Q112stop
      (Siller and Broadie, 2011)
      Fmr1Δ50M is a suppressor of some die during third instar larval stage phenotype of Mmp1Q112stop
      (Siller and Broadie, 2011)
      Fmr1Δ50M is a suppressor | partially of lethal - all die before end of pupal stage phenotype of TimpUAS.cPa
      (Siller and Broadie, 2011)
      Fmr1Δ50M is a suppressor | partially of some die during embryonic stage phenotype of TimpUAS.cPa
      (Siller and Broadie, 2011)
      Fmr1Δ50M is a suppressor | partially of some die during larval stage phenotype of TimpUAS.cPa
      (Siller and Broadie, 2011)
      Fmr1Δ50M is a suppressor of locomotor behavior defective phenotype of mGluR112b
      (Pan et al., 2008)
      Fmr1Δ50M is a suppressor of neurophysiology defective phenotype of futschN94
      (Zhang et al., 2001)
      Fmr1Δ50M is a suppressor of neuroanatomy defective phenotype of futschN94
      (Zhang et al., 2001)
      NOT Suppressor of
      Other
      Phenotype Manifest In
      Enhanced by
      Statement
      Reference
      Fmr1Δ50M has terminal bouton phenotype, enhanceable by mGluR112b
      (Pan et al., 2008)
      NOT Enhanced by
      Suppressed by
      Statement
      Reference
      Fmr1Δ50M has mushroom body alpha-lobe | adult stage phenotype, suppressible | partially by Nab2ex3/Nab2[+]
      (Bienkowski et al., 2017)
      Fmr1Δ50M/Fmr13 has ovary | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8SM206
      (Tan et al., 2016)
      Fmr1Δ50M/Fmr13 has egg chamber | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8SM206
      (Tan et al., 2016)
      Fmr1Δ50M/Fmr13 has nurse cell | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8SM206
      (Tan et al., 2016)
      Fmr1Δ50M/Fmr13 has germarium | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8SM206
      (Tan et al., 2016)
      Fmr1Δ50M/Df(3R)Exel6265 has ovary | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8SM206
      (Tan et al., 2016)
      Fmr1Δ50M/Df(3R)Exel6265 has egg chamber | adult stage phenotype, suppressible | partially by Zfrp8[+]/Zfrp8SM206
      (Tan et al., 2016)
      Fmr1Δ50M/Df(3R)Exel6265 has nurse cell | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8SM206
      (Tan et al., 2016)
      Fmr1Δ50M/Df(3R)Exel6265 has germarium | adult stage phenotype, suppressible | partially by Zfrp8[+]/Zfrp8SM206
      (Tan et al., 2016)
      Fmr1Δ50M has spermatocyte | spermatogenesis phenotype, suppressible by aubsting-1/aub[+]
      (Bozzetti et al., 2015)
      Fmr1Δ50M has adult mushroom body beta-lobe phenotype, suppressible by CenG1A[+]/CenG1AEY01217
      (Gross et al., 2015)
      Fmr1Δ50M has class IV dendritic arborizing neuron | somatic clone | third instar larval stage phenotype, suppressible by Abl1/Abl[+]
      (Sterne et al., 2015)
      Fmr1Δ50M has type I bouton | third instar larval stage phenotype, suppressible by dlp[+]/dlpA187
      (Friedman et al., 2013)
      Fmr1Δ50M has type I bouton | third instar larval stage phenotype, suppressible by dlp[+]/Sdc[+]/dlpA187/Sdc23
      (Friedman et al., 2013)
      Fmr1Δ50M has larval dorsal multidendritic neuron ddaC phenotype, suppressible by Dscam118
      (Kim et al., 2013)
      Fmr1Δ50M has synapse phenotype, suppressible by Dscam118
      (Kim et al., 2013)
      Fmr1Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible | partially by Top3β26
      (Xu et al., 2013)
      Fmr1Δ50M has NMJ bouton | third instar larval stage phenotype, suppressible | partially by Top3β26
      (Xu et al., 2013)
      Fmr1Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible by Scer\GAL4elav.PU/Hsap\FMR1UAS.Tag:MYC
      (Coffee et al., 2012)
      Fmr1Δ50M has NMJ bouton | supernumerary | third instar larval stage phenotype, suppressible by Scer\GAL4elav.PU/Hsap\FMR1UAS.Tag:MYC
      (Coffee et al., 2012)
      Fmr1Δ50M has s-LNv Pdf neuron | supernumerary | third instar larval stage phenotype, suppressible by Scer\GAL4elav.PU/Hsap\FMR1UAS.Tag:MYC
      (Coffee et al., 2012)
      Fmr1Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible by Scer\GAL4elav.PU/Hsap\FMR1S500D.UAS.Tag:MYC
      (Coffee et al., 2012)
      Fmr1Δ50M has NMJ bouton | supernumerary | third instar larval stage phenotype, suppressible by Scer\GAL4elav.PU/Hsap\FMR1S500D.UAS.Tag:MYC
      (Coffee et al., 2012)
      Fmr1Δ50M has s-LNv Pdf neuron | supernumerary | third instar larval stage phenotype, suppressible by Scer\GAL4elav.PU/Hsap\FMR1S500D.UAS.Tag:MYC
      (Coffee et al., 2012)
      Fmr1Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible by Scer\GAL4da.G32/TimpUAS.cPa
      (Siller and Broadie, 2011)
      Fmr1Δ50M has NMJ bouton | supernumerary | third instar larval stage phenotype, suppressible | partially by Scer\GAL4da.G32/TimpUAS.cPa
      (Siller and Broadie, 2011)
      Fmr1Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible | partially by Mmp1Q112stop
      (Siller and Broadie, 2011)
      Fmr1Δ50M has NMJ bouton | supernumerary | third instar larval stage phenotype, suppressible by Mmp1Q112stop
      (Siller and Broadie, 2011)
      Fmr1Δ50M has s-LNv Pdf neuron phenotype, suppressible by Scer\GAL4elav-C155/Hsap\FMR1UAS.Tag:MYC
      (Coffee et al., 2010)
      Fmr1Δ50M has bouton phenotype, suppressible by Scer\GAL4elav-C155/Hsap\FMR1UAS.Tag:MYC
      (Coffee et al., 2010)
      Fmr1Δ50M has protocerebrum phenotype, suppressible by Scer\GAL4elav-C155/Hsap\FMR1UAS.Tag:MYC
      (Coffee et al., 2010)
      Fmr1Δ50M has embryonic/larval neuromuscular junction phenotype, suppressible by Scer\GAL4elav-C155/Hsap\FMR1UAS.Tag:MYC
      (Coffee et al., 2010)
      Fmr1Δ50M has spermatid axoneme phenotype, suppressible by Scer\GAL4VP16.nos.UTR/Hsap\FMR1UAS.Tag:MYC
      (Coffee et al., 2010)
      Fmr1Δ50M has axonemal microtubule phenotype, suppressible by Scer\GAL4VP16.nos.UTR/Hsap\FMR1UAS.Tag:MYC
      (Coffee et al., 2010)
      Fmr1Δ50M has spermatid axoneme phenotype, suppressible by Scer\GAL4VP16.nos.UTR/Hsap\FXR1UAS.Tag:MYC
      (Coffee et al., 2010)
      Fmr1Δ50M has axonemal microtubule phenotype, suppressible by Scer\GAL4VP16.nos.UTR/Hsap\FXR1UAS.Tag:MYC
      (Coffee et al., 2010)
      Fmr1Δ50M has spermatid axoneme phenotype, suppressible by Hsap\FXR2UAS.Tag:MYC/Scer\GAL4VP16.nos.UTR
      (Coffee et al., 2010)
      Fmr1Δ50M has axonemal microtubule phenotype, suppressible by Hsap\FXR2UAS.Tag:MYC/Scer\GAL4VP16.nos.UTR
      (Coffee et al., 2010)
      Fmr1Δ50M has embryonic/larval neuromuscular junction phenotype, suppressible by RanBPMk05201/l(2)k05201[+]
      (Scantlebury et al., 2010)
      Fmr1Δ50M has NMJ bouton phenotype, suppressible by RanBPMk05201/l(2)k05201[+]
      (Scantlebury et al., 2010)
      Fmr1Δ50M/Fmr13 has nurse cell phenotype, suppressible | partially by CblF165/Cbl[+]
      (Epstein et al., 2009)
      Fmr1Δ50M has neuromuscular junction phenotype, suppressible | partially by mGluR112b
      (Pan et al., 2008)
      Fmr1Δ50M has synaptic vesicle phenotype, suppressible by mGluR112b
      (Pan et al., 2008)
      Fmr1Δ50M has bouton phenotype, suppressible by futschN94
      (Zhang et al., 2001)
      Fmr1Δ50M has neuromuscular junction phenotype, suppressible by futschN94
      (Zhang et al., 2001)
      Fmr1Δ50M has synapse phenotype, suppressible by futschN94
      (Zhang et al., 2001)
      NOT suppressed by
      Statement
      Reference
      Fmr1Δ50M has mushroom body beta-lobe | adult stage phenotype, non-suppressible by Nab2ex3/Nab2[+]
      (Bienkowski et al., 2017)
      Fmr1Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype, non-suppressible by Scer\GAL4elav.PU/Hsap\FMR1S500A.UAS.Tag:MYC
      (Coffee et al., 2012)
      Fmr1Δ50M has NMJ bouton | supernumerary | third instar larval stage phenotype, non-suppressible by Scer\GAL4elav.PU/Hsap\FMR1S500A.UAS.Tag:MYC
      (Coffee et al., 2012)
      Fmr1Δ50M has s-LNv Pdf neuron | supernumerary | third instar larval stage phenotype, non-suppressible by Scer\GAL4elav.PU/Hsap\FMR1S500A.UAS.Tag:MYC
      (Coffee et al., 2012)
      Fmr1Δ50M has s-LNv Pdf neuron phenotype, non-suppressible by Scer\GAL4elav-C155/Hsap\FXR1UAS.Tag:MYC
      (Coffee et al., 2010)
      Fmr1Δ50M has bouton phenotype, non-suppressible by Scer\GAL4elav-C155/Hsap\FXR1UAS.Tag:MYC
      (Coffee et al., 2010)
      Fmr1Δ50M has protocerebrum phenotype, non-suppressible by Scer\GAL4elav-C155/Hsap\FXR1UAS.Tag:MYC
      (Coffee et al., 2010)
      Fmr1Δ50M has embryonic/larval neuromuscular junction phenotype, non-suppressible by Scer\GAL4elav-C155/Hsap\FXR1UAS.Tag:MYC
      (Coffee et al., 2010)
      Fmr1Δ50M has s-LNv Pdf neuron phenotype, non-suppressible by Scer\GAL4elav-C155/Hsap\FXR2UAS.Tag:MYC
      (Coffee et al., 2010)
      Fmr1Δ50M has bouton phenotype, non-suppressible by Scer\GAL4elav-C155/Hsap\FXR2UAS.Tag:MYC
      (Coffee et al., 2010)
      Fmr1Δ50M has protocerebrum phenotype, non-suppressible by Scer\GAL4elav-C155/Hsap\FXR2UAS.Tag:MYC
      (Coffee et al., 2010)
      Fmr1Δ50M has embryonic/larval neuromuscular junction phenotype, non-suppressible by Scer\GAL4elav-C155/Hsap\FXR2UAS.Tag:MYC
      (Coffee et al., 2010)
      Fmr1Δ50M/Fmr13 has nurse cell | supernumerary phenotype, non-suppressible by CblF165/Cbl[+]
      (Epstein et al., 2009)
      Fmr1Δ50M has synapse phenotype, non-suppressible by mGluR112b
      (Pan et al., 2008)
      Fmr1Δ50M has presynaptic active zone phenotype, non-suppressible by mGluR112b
      (Pan et al., 2008)
      Enhancer of
      Statement
      Reference
      Fmr1Δ50M/Fmr1[+] is an enhancer of mushroom body alpha-lobe | adult stage phenotype of Nab2ex3
      (Bienkowski et al., 2017)
      Fmr1Δ50M/Fmr1[+] is an enhancer of eye | adult stage phenotype of Hsap\TARDBPUAS.YFP.cEa, Scer\GAL4GMR.PU
      (Coyne et al., 2015)
      Fmr1Δ50M/Fmr1[+] is an enhancer of eye | adult stage phenotype of Hsap\TARDBPG298S.UAS.YFP, Scer\GAL4GMR.PU
      (Coyne et al., 2015)
      NOT Enhancer of
      Suppressor of
      Statement
      Reference
      Fmr1Δ50M/Fmr1[+] is a suppressor of eye phenotype of Nab2EP3716, Scer\GAL4GMR.PU
      (Bienkowski et al., 2017)
      Fmr1Δ50M/Fmr1[+] is a suppressor of ommatidium | adult stage phenotype of Nab2EP3716, Scer\GAL4GMR.PU
      (Bienkowski et al., 2017)
      Fmr1Δ50M is a suppressor | partially of embryonic/larval neuromuscular junction | third instar larval stage phenotype of Top3β26
      (Xu et al., 2013)
      Fmr1Δ50M is a suppressor | partially of NMJ bouton | third instar larval stage phenotype of Top3β26
      (Xu et al., 2013)
      Fmr1Δ50M is a suppressor of trachea phenotype of Scer\GAL4da.G32, TimpUAS.cPa
      (Siller and Broadie, 2011)
      Fmr1Δ50M is a suppressor of trachea phenotype of Mmp1Q112stop
      (Siller and Broadie, 2011)
      Fmr1Δ50M is a suppressor of synapse phenotype of futschN94
      (Zhang et al., 2001)
      Fmr1Δ50M is a suppressor of bouton phenotype of futschN94
      (Zhang et al., 2001)
      Fmr1Δ50M is a suppressor of neuromuscular junction phenotype of futschN94
      (Zhang et al., 2001)
      NOT Suppressor of
      Other
      Additional Comments
      Genetic Interactions
      Statement
      Reference
      The mushroom body α-lobe morphological defects characteristic for Fmr1Δ50M homozygous adults are ameliorated by combination with a single copy of Nab2ex3, whereas the reverse is true for Nab2ex3 homozygotes in which the combination with one copy of Fmr1Δ50M further worsens the α-lobe phenotype. The β-lobe fusion observed in either of the two homozygous mutants cannot be modified by heterozygosity of the other gene's allele. The mild memory defects displayed by the Fmr1Δ50M heterozygotes in an aversive olfactory conditioning assay are enhanced by Nab2ex3 heterozygosity. The eye defects (reduced size, partial depigmentation and disorganization of the ommatidial lattice) observed in adult flies expressing Nab2EP3716 under the control of Scer\GAL4GMR.PU can be suppressed by combination with a single copy of Fmr1Δ50M.
      (Bienkowski et al., 2017)
      Expression of TorsindsRNA.Scer\UAS.WIZ driven by Scer\GAL4αTub84B.PL does not enhance increased numbers of type I NMJ boutons seen in Fmr1Δ50M/Fmr1Δ50M larvae.
      (Nguyen et al., 2016)
      Zfrp8SM206/+ partially restores fertility and suppresses the majority of ovary defects in Fmr1Δ50M/Df(3R)Exel6265 mutants, restoring cell division in the germline, normal oogenesis, and normal egg chamber morphology and separation, although the first egg chamber often still appears fused to the germarium. Zfrp8SM206/+ partially restores fertility and restores ovary morphology to normal in Fmr1Δ50M/Fmr13 mutants.
      (Tan et al., 2016)
      The male sterility of Fmr1Δ50M/Fmr1Δ113M transheterozygotes and the crystalline aggregates observed in the spermatocytes of Fmr1Δ50M homozygotes are suppressed by aubsting-1/+ heterozygosity.
      (Bozzetti et al., 2015)
      Heterozygous CenG1AEY01217 increases the viability of flies homozygous for Fmr1Δ50M. Heterozygosity for CenG1AEY01217 suppresses the mushroom body phenotype of beta-lobe fusion and the impaired short-term memory defect in homozygous Fmr1Δ50M flies.
      (Gross et al., 2015)
      The increased presynaptic terminal length of class IV dendritic arborizing neurons in Fmr1Δ50M/Fmr1Δ50M MARCM somatic clones in third instar larvae is completely suppressed by combination with Abl1 in heterozygous state.
      (Sterne et al., 2015)
      rinNP3248/rin2, Fmr1Δ113M/Fmr1Δ50M animals reach a late pupal stage - pupae are long and slender. rinNP5420/rin2, Fmr1Δ113M/Fmr1Δ50M animals develop into adult flies that die soon after eclosion - pupae are long and slender. rinT:Disc\RFP-mCherry rescues the slender pupae phenotype and lethality associated with rinNP3248/rin2, Fmr1Δ113M/Fmr1Δ50M animals. rinT:Disc\RFP-mCherry rescues the slender pupae phenotype and lethality associated with rinNP5420/rin2, Fmr1Δ113M/Fmr1Δ50M animals.
      (Baumgartner et al., 2013)
      dlpA187/+, or both dlpA187/+ and Sdc23/+, suppresses the increase in NMJ branching and synaptic bouton number; and both Sdc23/+ and dlpA187/+ (but not dlpA187/+ alone) suppresses the increased amplitude of evoked junctional currents seen in Fmr1Δ50M/Fmr1Δ50M mutant larvae.
      (Friedman et al., 2013)
      The mild overgrowth of presynaptic terminals in Fmr1Δ50M mutant C4 ddaC neuron clones is completely abolished by a Dscam118 mutant background.
      (Kim et al., 2013)
      Fmr1Δ50M spartin1 and Fmr1Δ50M Dadj1E4 double heterozygous third instar larvae show an increase in bouton number and satellite bouton number at the neuromuscular junction compared to controls.
      (Nahm et al., 2013)
      The number of synaptic branches and boutons in muscle 4 neuromuscular junctions is significantly lower in Top3β26 Fmr1Δ50M double mutant third instar larvae than in either mutant alone.
      (Xu et al., 2013)
      Expression of TimpScer\UAS.cPa under the control of Scer\GAL4da.G32 suppresses the NMJ defects seen in Fmr1Δ50M mutant third instar larvae. The mutant over-branching and supernumerary bouton formation have been eliminated, and the accumulation of developmentally arrested satellite boutons is prevented. Flies expressing TimpScer\UAS.cPa under the control of Scer\GAL4da.G32 in a Fmr1Δ50M mutant background are robust, healthy and fully viable. Homozygous Fmr1Δ50M fully suppresses the tracheal defects seen when TimpScer\UAS.cPa is expressed under the control of Scer\GAL4da.G32. Homozygous Fmr1Δ50M fully suppresses the tracheal defects seen in Mmp1Q112stop mutant flies. Homozygous Mmp1Q112stop partially suppresses the NMJ defects seen in Fmr1Δ50M mutant third instar larvae. Synaptic bouton number is strongly rescued and increased number of synaptic branches is suppressed.
      (Siller and Broadie, 2011)
      The increased number of branches and of boutons at the neuromuscular junction of Fmr1Δ50M larvae is significantly suppressed by RanBPMk05201/+.
      (Scantlebury et al., 2010)
      CblF165 is a dominant suppressor of the germ cell proliferation defects in Fmr13/Fmr1Δ50M mutant ovaries. The fewer germ cell phenotype is largely suppressed by CblF165/+, while the supernumerary germ cell phenotype is not suppressed at all.
      (Epstein et al., 2009)
      7.7% of ban12/Fmr1Δ50M transheterozygous adult females are fertile. Double heterozygous adult females of ban12/Fmr1Δ50M display a significant increase in the number of germaria with one or no germline stem cells, compared to controls, that progressively worsens from day 2 post-eclosion to day 12.
      (Yang et al., 2009)
      A Fmr1Δ50M mutant background suppresses the behavioral/movement impairment seen in mGluR112b mutant larva. In these double mutants the roll-over behavioral response is smooth and efficient, with a significantly shorter 'struggle' time compared to mGluR112b single mutants. Quantitatively, the double mutant shows comparable behavior to the wild-type control. Fmr1Δ50M;mGluR112b double mutants display some suppression of the Fmr1Δ50M single mutant synaptic overbranching phenotype but the level of overbranching is still significant compared to wild-type controls. Fmr1Δ50M;mGluR112b double mutants do not show any suppression of the increased neuromuscular junction synaptic area characteristic of Fmr1Δ50M single mutants. Fmr1Δ50M;mGluR112b double mutants display a synergistic increase in synaptic bouton number compared to Fmr1Δ50M single mutants. Fmr1Δ50M;mGluR112b double mutants show a significant rescue of the elevated vesicle density phenotype seen in Fmr1Δ50M single mutants. This includes the clustered vesicles around the active zone.
      (Pan et al., 2008)
      Xenogenetic Interactions
      Statement
      Reference
      The depigmentation phenotype in the adult eye and the lengthened time it takes for larvae to roll over in a turning assay characteristic for animals expressing Hsap\TARDBPScer\UAS.T:Avic\GFP-YFP.cEa under the control of Scer\GAL4GMR.PU or Scer\GAL4Toll-6-D42 respectively, are exacerbated further by combination with Fmr1Δ50M in heterozygous state. The depigmentation phenotype in the adult eye and the lengthened time it takes for larvae to roll over in a turning assay characteristic for animals expressing Hsap\TARDBPG298S.Scer\UAS.T:Avic\GFP-YFP under the control of Scer\GAL4GMR.PU or Scer\GAL4Toll-6-D42 respectively, are exacerbated further by combination with Fmr1Δ50M in heterozygous state.
      (Coyne et al., 2015)
      Expression of Hsap\FMR1Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4elav.PU rescues the neuromuscular junction synapse architecture defects seen in Fmr1Δ50M mutant third instar larvae. The increase in Futsch-positive loops is also fully rescued. Expression of Hsap\FMR1S500D.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4elav.PU rescues the neuromuscular junction synapse architecture defects seen in Fmr1Δ50M mutant third instar larvae. The increase in Futsch-positive loops is also fully rescued. Expression of Hsap\FMR1S500A.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4elav.PU is unable to rescue the neuromuscular junction synapse architecture defects seen in Fmr1Δ50M mutant third instar larvae. The increase in Futsch-positive loops is also not rescued. Expressing Hsap\FMR1Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4elav.PU rescues the expanded terminals and supernumerary synaptic boutons seen in the small ventrolateral neurons of Fmr1Δ50M mutant adults. Expressing Hsap\FMR1S500D.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4elav.PU rescues the expanded terminals and supernumerary synaptic boutons seen in the small ventrolateral neurons of Fmr1Δ50M mutant adults. Expressing Hsap\FMR1S500A.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4elav.PU fails to rescue the expanded terminals and supernumerary synaptic boutons seen in the small ventrolateral neurons of Fmr1Δ50M mutant adults. Expression of Hsap\FMR1Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4ey-OK107 rescues the decreases in olfactory learning seen in Fmr1Δ50M mutants. Expression of Hsap\FMR1S500D.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4ey-OK107 rescues the decreases in olfactory learning seen in Fmr1Δ50M mutants. Expression of Hsap\FMR1S500A.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4ey-OK107 fails to rescue the decreases in olfactory learning seen in Fmr1Δ50M mutants.
      (Coffee et al., 2012)
      Expression of Hsap\FMR1Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4elav-C155 completely suppresses the synaptic overgrowth defects characterising Fmr1Δ50M mutants. Expression of Hsap\FXR1Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4elav-C155 fails to suppress the synaptic overgrowth defects characterising Fmr1Δ50M mutants. Expression of Hsap\FXR2Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4elav-C155 fails to suppress the synaptic overgrowth defects characterising Fmr1Δ50M mutants. Expression of Hsap\FMR1Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4elav-C155 fully rescues both the enlarged neuromuscular junctional area and increased synaptic branching that characterise Fmr1Δ50M mutants. Expression of Hsap\FXR1Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4elav-C155 fails to suppress the enlarged neuromuscular junctional area and increased synaptic branching that characterise Fmr1Δ50M mutants. Expression of Hsap\FXR2Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4elav-C155 fails to suppress the enlarged neuromuscular junctional area and increased synaptic branching that characterise Fmr1Δ50M mutants. Pre-synaptic expression of Hsap\FMR1Scer\UAS.T:Hsap\MYC using Scer\GAL4elav-C155 completely restores bouton number to control levels in Fmr1Δ50M mutants. Pre-synaptic expression of Hsap\FXR1Scer\UAS.T:Hsap\MYC using Scer\GAL4elav-C155 is totally incapable of restoring bouton number to control levels in Fmr1Δ50M mutants. Pre-synaptic expression of Hsap\FXR2Scer\UAS.T:Hsap\MYC using Scer\GAL4elav-C155 is totally incapable of restoring bouton number to control levels in Fmr1Δ50M mutants. Scer\GAL4elav-C155>Hsap\FMR1Scer\UAS.T:Hsap\MYC can strongly rescue the mini-bouton number in Fmr1Δ50M mutants back to wild-type levels. Scer\GAL4elav-C155>Hsap\FXR1Scer\UAS.T:Hsap\MYC is totally incapable of restoring the elevated mini-bouton number in Fmr1Δ50M mutants. Scer\GAL4elav-C155>Hsap\FXR2Scer\UAS.T:Hsap\MYC is totally incapable of restoring the elevated mini-bouton number in Fmr1Δ50M mutants. Expression of Hsap\FMR1Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 completely suppresses the male fecundity phenotype that characterises Fmr1Δ50M mutants. Expression of Hsap\FXR1Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 completely suppresses the male fecundity phenotype that characterises Fmr1Δ50M mutants. Expression of Hsap\FXR2Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 completely suppresses the male fecundity phenotype that characterises Fmr1Δ50M mutants. Expression of Hsap\FMR1Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 can fully restore the spermatid axoneme architecture in Fmr1Δ50M mutants. Expression of Hsap\FXR1Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 can fully restore the spermatid axoneme architecture in Fmr1Δ50M mutants. Expression of Hsap\FXR2Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 can fully restore the spermatid axoneme architecture in Fmr1Δ50M mutants.
      (Coffee et al., 2010)
      The rough eye phenotype caused by expression of Hsap\MAPTV337M.Scer\UAS under the control of Scer\GAL4GMR.PF is not modified if the flies are also carrying Fmr1Δ50M.
      (Shulman and Feany, 2003)
      Complementation and Rescue Data
      Rescued by
      Fmr1Δ50M/Fmr1Δ113M is rescued by Fmr1UAS.cZa/Scer\GAL4T76
      (Bozzetti et al., 2015)
      Fmr1Δ50M/Fmr1[+] is rescued by Fmr1UAS.cZa/Scer\GAL4T76
      (Bozzetti et al., 2015)
      Fmr1Δ50M is rescued by Fmr1UAS.cZa/Scer\GAL4T76
      (Bozzetti et al., 2015)
      Fmr1Δ50M is rescued by Fmr1UAS.cZa/Scer\GAL4T76
      (Bozzetti et al., 2015)
      Fmr1Δ50M is rescued by Fmr1UAS.cZa/Scer\GAL4GMR12G04
      (Doll and Broadie, 2015)
      Fmr1Δ50M is rescued by Fmr1UAS.cZa/Scer\GAL4GMR12G04
      (Doll and Broadie, 2015)
      Fmr1Δ50M is rescued by Fmr1UAS.cZa/Scer\GAL4GMR65G01
      (Doll and Broadie, 2015)
      Fmr1Δ50M is rescued by Fmr1UAS.cZa/Scer\GAL4GMR65G01
      (Doll and Broadie, 2015)
      Fmr1Δ50M is rescued by Fmr1+t14
      (Gatto and Broadie, 2011)
      Fmr1Δ50M is rescued by Fmr1UAS.Tag:MYC,Tag:HA
      (Coffee et al., 2010)
      Fmr1Δ50M is rescued by Fmr1+t14
      (Epstein et al., 2009)
      Fmr1Δ50M/Fmr13 is rescued by Fmr1+t14
      (Epstein et al., 2009)
      Not rescued by
      Fmr1Δ50M is not rescued by Scer\GAL4elav.Switch.PO/Fmr1UAS.cZa
      (Gatto and Broadie, 2009)
      Comments
      The expression of Fmr1Scer\UAS.cZa under the control of Scer\GAL4T76 partially rescues the male sterility of Fmr1Δ50M homozygotes and of Fmr1Δ50M/Fmr1Δ113M transheterozygotes, and partially rescues the decreased fertilities of Fmr1Δ50M heterozygous males, of Fmr1Δ50M homozygous and heterozygous females, and of Fmr1Δ50M/Fmr1Δ113M transheterozygous females.
      (Bozzetti et al., 2015)
      Expression of Fmr1Scer\UAS.cZa under the control of Scer\GAL4GMR12G04 (either in combination with a Gal80[ts] transgene to restrict expression to the period including pupal day 4 to 1 day post-eclosion, or without a Gal80[ts] for expression throughout development) significantly rescues the MVP2 dendritic arbor overgrowth seen in Fmr1Δ50M/Fmr1Δ50M mutants. Expression of Fmr1Scer\UAS.cZa under the control of Scer\GAL4GMR65G01 (either in combination with a Gal80[ts] transgene to restrict expression to the period including pupal day 4 to 1 day post-eclosion, or without a Gal80[ts] for expression throughout development) significantly rescues the projection neuron dendritic arbor overgrowth seen in Fmr1Δ50M/Fmr1Δ50M mutants.
      (Doll and Broadie, 2015)
      Expression of Fmr1+t14 strongly diminishes PDF-TRI neuron retention in Fmr1Δ50M mutants.
      (Gatto and Broadie, 2011)
      Expression of Fmr1Scer\UAS.T:Hsap\MYC,T:Ivir\HA1 under the control of Scer\GAL4elav-C155 completely rescued the synaptic overgrowth characterising the Fmr1Δ50M mutant, and the terminals become clearly more restricted in extent and refined in the number of synaptic boutons. Expression of Fmr1Scer\UAS.T:Hsap\MYC,T:Ivir\HA1 under the control of Scer\GAL4elav-C155 fully rescues both the enlarged neuromuscular junctional area and increased synaptic branching that characterise Fmr1Δ50M mutants. Pre-synaptic expression of Fmr1Scer\UAS.T:Hsap\MYC,T:Ivir\HA1 using Scer\GAL4elav-C155 completely rescues bouton number back to control levels in Fmr1Δ50M mutants. Scer\GAL4elav-C155>Fmr1Scer\UAS.T:Hsap\MYC,T:Ivir\HA1 can strongly rescue the mini-bouton number in Fmr1Δ50M mutants back to wild-type levels. Expression of Fmr1Scer\UAS.T:Hsap\MYC,T:Ivir\HA1 under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 completely rescues the male fecundity defect that characterises Fmr1Δ50M mutants. Expression of Fmr1Scer\UAS.T:Hsap\MYC,T:Ivir\HA1 under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 can strongly rescue the spermatid axoneme defects that characterise Fmr1Δ50M mutants.
      (Coffee et al., 2010)
      Provision of Fmr1 transiently during the early stages of neural development, through expression of Fmr1Scer\UAS.cZa under the RU486-induced control of Scer\GAL4elav.Switch.PO in a Fmr1Δ50M mutant background is not sufficient to correct the characteristic synaptic defects caused by the loss of Fmr1 as assayed at maturity. Provision of Fmr1 at maturity, following completion of neural development, is not sufficient to rescue the synaptic defects found in Fmr1Δ50M mutants.
      (Gatto and Broadie, 2009)
      Images (0)
      Mutant
      Wild-type
      Stocks (1)
      Notes on Origin
      Discoverer
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (27)
      Reported As
      Symbol Synonym
      FMR1D50M
      (Baumgartner et al., 2013)
      Fmr1null
      (Cvetkovska et al., 2013)
      Fmr1Δ50
      (Gross et al., 2015, Michel et al., 2004, Morales et al., 2002)
      Fmr1Δ50M
      (Tan et al., 2016, Andlauer et al., 2014, van Alphen et al., 2013, Bushey et al., 2009)
      d50
      (van Alphen et al., 2013)
      dFMR150M
      (Cziko et al., 2009)
      dFMR1Δ50
      (Kashima et al., 2017)
      dFMR1Δ50M
      (Kashima et al., 2017)
      dFMRP50M
      (Kim et al., 2013)
      dFMRPΔ50M
      (Sterne et al., 2015)
      dFmr150M
      (Epstein et al., 2009)
      dFmr1Δ50
      (Bozzetti et al., 2015)
      dFmr1Δ50M
      (Kim et al., 2019, Gross et al., 2015)
      dfmr150
      (Scantlebury et al., 2010)
      dfmr150M
      (Kang et al., 2019, Sears et al., 2019, Doll et al., 2017, Kennedy and Broadie, 2017, Vita and Broadie, 2017, Doll and Broadie, 2016, Coyne et al., 2015, Doll and Broadie, 2015, Gatto et al., 2014, Sudhakaran et al., 2014, Friedman et al., 2013, Coffee et al., 2012, Gatto and Broadie, 2011, Tessier and Broadie, 2011, Yao et al., 2011, Coffee et al., 2010, Gatto and Broadie, 2009, Pan et al., 2008, Reeve et al., 2008, Tessier and Broadie, 2008)
      dfmr1delta50
      (Zhang et al., 2014)
      dfmr1delta5
      (Yang et al., 2009)
      dfmr1Δ50
      (Bienkowski et al., 2017)
      dfmr1Δ50M
      (Xu et al., 2013, Siller and Broadie, 2011)
      dfmr50M
      (Pan et al., 2004)
      dfmrdel50
      (Mutsuddi et al., 2004)
      dfmrΔ50
      (Yang et al., 2009)
      dfmrΔ50M
      (Nahm et al., 2013)
      dfxr null
      (Zhang et al., 2001)
      dxfr150M
      (Zhang et al., 2004, Shulman and Feany, 2003)
      fmr1Δ50
      (Tadros et al., 2007)
      fmr1Δ50M
      (Mansilla et al., 2017, Nguyen et al., 2016, Wan et al., 2015, Scantlebury et al., 2010)
      Name Synonyms
      Secondary FlyBase IDs
        References (53)