FlyBase Allele Report: Dmel\Fmr1[Δ50M]

General Information

Symbol

Dmel\Fmr1^Δ50M

Species

D. melanogaster

Name

FlyBase ID

FBal0131033

Feature type

allele

Associated gene

Dmel\Fmr1

Associated Insertion(s)

Carried in Construct

Also Known As

dfmr1^50M, dfmr1^Δ50M, Fmr1^Δ50, dFmr1^Δ50, dxfr1^50M, dFMRP^Δ50M, fmr1^Delta50M

Key Links

Allele class

loss of function allele

amorphic allele - genetic evidence

Mutagen

Delta2-3 transposase

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)

Progenitor genotype

Fmr1^EP3517

(Zhang et al., 2001)

Cytology

Description

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)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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 )

Disease

Evidence

References

model of fragile X syndrome

CEA with Fmr1^Δ113M

(Starke et al., 2022, Luhur et al., 2017, Michel et al., 2004)

CEA with Fmr1^Δ3

(Kang et al., 2019)

CEA with Fmr1³

(Zhao et al., 2021, Kennedy et al., 2020, Greenblatt and Spradling, 2018)

CEA with Fmr1²

(Russo and DiAntonio, 2019)

Modifiers Based on Experimental Evidence ( 1 )

Disease

Interaction

References

exacerbates amyotrophic lateral sclerosis

modeled by Hsap\TARDBP^UAS.YFP.cEa

(Coyne et al., 2015)

modeled by Hsap\TARDBP^{G298S.UAS.YFP}

(Coyne et al., 2015)

exacerbates Troyer syndrome

modeled by spartin¹

(Nahm et al., 2013)

model of fragile X syndrome

is ameliorated by futsch^N94

(Zhang et al., 2001)

is ameliorated by Timp^UAS.cPa

(Siller and Broadie, 2011)

is ameliorated by Mmp1^Q112stop

(Siller and Broadie, 2011)

is ameliorated by mGluR^112b

(Pan et al., 2008)

is ameliorated by Fmr1^UAS.cZa

(Doll and Broadie, 2015)

is ameliorated by dlp^A187

(Dear et al., 2017, Friedman et al., 2013)

is ameliorated by shrb⁴

(Vita and Broadie, 2017)

is ameliorated by Nab2^ex3

(Bienkowski et al., 2017)

is ameliorated by rg^FDD

(Sears et al., 2019)

is ameliorated by wnd¹

(Russo and DiAntonio, 2019)

is ameliorated by bsk^HMS04479

(Russo and DiAntonio, 2019)

is ameliorated by kay^Fbz.UAS

(Russo and DiAntonio, 2019)

is ameliorated by wnd³

(Russo and DiAntonio, 2019)

is ameliorated by wnd^GL00282

(Russo and DiAntonio, 2019)

is exacerbated by stau¹

(Song et al., 2022)

is ameliorated by stau^UAS.GFP

(Song et al., 2022)

is ameliorated by CenG1A^KG00800

(Matsumoto et al., 2018)

is ameliorated by InR^del.UAS

(Vita et al., 2021)

is ameliorated by drpr^Δ5

(Vita et al., 2021)

is ameliorated by drpr^I.UAS

(Vita et al., 2021)

is ameliorated by Hsap\DISC1^UAS.Tag:HA

(Honda et al., 2024)

is ameliorated by Abl¹

(Sterne et al., 2015)

is ameliorated by CenG1A^EY01217

(Gross et al., 2015)

ameliorates autosomal recessive intellectual developmental disorder

modeled by Nab2^EP3716

(Bienkowski et al., 2017)

exacerbates autosomal recessive intellectual developmental disorder

modeled by Nab2^ex3

(Bienkowski et al., 2017)

ameliorates autism spectrum disorder

modeled by CenG1A^KG00800

(Matsumoto et al., 2018)

ameliorates schizophrenia 9

modeled by Hsap\DISC1^UAS.Tag:HA

(Honda et al., 2024)

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal cell number (with Fmr1³)

(Epstein et al., 2009)

abnormal cell number | adult stage (with Df(3R)Exel6265)

(Tan et al., 2016)

abnormal cell number | adult stage (with Fmr1³)

(Tan et al., 2016)

abnormal circadian rhythm | adult stage (with Fmr1³)

(Zhao et al., 2021)

abnormal endomitotic cell cycle

(Epstein et al., 2009)

abnormal flight (with Df(3R)by62)

(Zhang et al., 2001)

abnormal grooming behavior | progressive

(Russo and DiAntonio, 2019)

abnormal grooming behavior | progressive (with Df(3R)Exel6265)

(Russo and DiAntonio, 2019)

abnormal learning | adult stage

(Gatto et al., 2014, Coffee et al., 2012)

abnormal locomotor behavior

(Pan et al., 2008)

abnormal memory

(Gross et al., 2015)

abnormal memory | adult stage

(Bienkowski et al., 2017)

abnormal neuroanatomy

(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)

abnormal neuroanatomy, with Fmr1^UAS.cZa, Scer\GAL4^P2.4.Pdf

(Gatto and Broadie, 2009)

abnormal neuroanatomy (with Fmr1^Δ113M)

(Michel et al., 2004, Morales et al., 2002)

abnormal neuroanatomy | adult stage

(Bienkowski et al., 2017, Gatto et al., 2014)

abnormal neuroanatomy | adult stage (with Df(3R)Exel6265)

(Russo and DiAntonio, 2019)

abnormal neuroanatomy | adult stage (with Fmr1³)

(Zhao et al., 2021)

abnormal neuroanatomy | adult stage | recessive

(Doll and Broadie, 2015)

abnormal neuroanatomy | adult stage | somatic clone

(Gatto et al., 2014, Tessier and Broadie, 2008)

abnormal neuroanatomy | adult stage | somatic clone | conditional

(Tessier and Broadie, 2008)

abnormal neuroanatomy | larval stage

(Nguyen et al., 2016, Scantlebury et al., 2010)

abnormal neuroanatomy | larval stage | progressive

(Li and Gavis, 2022)

abnormal neuroanatomy | pupal stage | somatic clone

(Tessier and Broadie, 2008)

abnormal neuroanatomy | somatic clone

(Pan et al., 2004)

abnormal neuroanatomy | somatic clone | third instar larval stage

(Sterne et al., 2015)

abnormal neuroanatomy | third instar larval stage

(Song et al., 2022, Russo and DiAntonio, 2019, Friedman et al., 2013, Nahm et al., 2013, Xu et al., 2013, Coffee et al., 2012, Siller and Broadie, 2011)

abnormal neuroanatomy | third instar larval stage (with Df(3R)Exel6265)

(Russo and DiAntonio, 2019)

abnormal neurophysiology

(Zhang et al., 2001)

abnormal neurophysiology | adult stage | somatic clone

(Gatto et al., 2014)

abnormal neurophysiology | larval stage

(Yuan et al., 2020)

abnormal neurophysiology | third instar larval stage

(Song et al., 2022, Russo and DiAntonio, 2019, Friedman et al., 2013)

abnormal size | adult stage (with Df(3R)Exel6265)

(Russo and DiAntonio, 2019)

abnormal size | adult stage | somatic clone

(Tessier and Broadie, 2008)

abnormal size | adult stage | somatic clone | conditional

(Tessier and Broadie, 2008)

abnormal size | pupal stage | somatic clone

(Tessier and Broadie, 2008)

abnormal sleep

(van Alphen et al., 2013, Bushey et al., 2009)

abnormal sleep (with Fmr1^Δ113M)

(Bushey et al., 2009)

decreased cell death

(Gatto and Broadie, 2011)

female semi-fertile (with Fmr1^Δ113M)

(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)

increased occurrence of cell division (with Fmr1³)

(Epstein et al., 2009)

increased size | larval stage

(Yuan et al., 2020)

lethal - all die before end of P-stage

(Scantlebury et al., 2010, Morales et al., 2002)

lethal - all die during embryonic stage (with Fmr1^Δ113M), with Fmr1^{KH1mut.UAS.EGFP}, Scer\GAL4^futsch-C380, Scer\GAL80^ChAT.3.3P

(Starke et al., 2022)

lethal - all die during embryonic stage (with Fmr1^Δ113M), with Fmr1^{KH2mut.UAS.EGFP}, Scer\GAL4^futsch-C380, Scer\GAL80^ChAT.3.3P

(Starke et al., 2022)

male semi-fertile | dominant

(Bozzetti et al., 2015)

male sterile

(Coffee et al., 2010)

male sterile (with Fmr1^Δ113M)

(Bozzetti et al., 2015)

male sterile | recessive

(Bozzetti et al., 2015)

partially lethal - majority die

(Gross et al., 2015)

semi-sterile

(Zhang et al., 2004)

some die during pharate adult stage

(Scantlebury et al., 2010, Morales et al., 2002)

viable

(Baumgartner et al., 2013, Zhang et al., 2001)

viable (with Fmr1^Δ113M)

(Starke et al., 2022)

viable | recessive

(Bozzetti et al., 2015)

Phenotype Manifest In

A1-7 ventral longitudinal muscle cell | third instar larval stage

(Song et al., 2022)

adult mushroom body

(Michel et al., 2004)

adult mushroom body (with Fmr1^Δ113M)

(Michel et al., 2004)

adult mushroom body alpha-lobe (with Df(3R)Exel6265)

(Russo and DiAntonio, 2019)

adult mushroom body alpha-lobe (with Fmr1^Δ113M)

(Michel et al., 2004)

adult mushroom body alpha-lobe | adult stage

(Bienkowski et al., 2017)

adult mushroom body beta-lobe

(Gross et al., 2015, Michel et al., 2004, Pan et al., 2004)

adult mushroom body beta-lobe (with Fmr1^Δ113M)

(Michel et al., 2004)

adult mushroom body beta-lobe | adult stage

(Bienkowski et al., 2017)

adult s-LNv neuron (with Fmr1³)

(Zhao et al., 2021)

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)

axon collateral | adult stage (with Fmr1³)

(Zhao et al., 2021)

axonemal microtubule

(Coffee et al., 2010)

axon terminus | adult stage (with Fmr1³)

(Zhao et al., 2021)

bouton

(Coffee et al., 2010, Gatto and Broadie, 2009)

bouton, with Fmr1^UAS.cZa, Scer\GAL4^P2.4.Pdf

(Gatto and Broadie, 2009)

bouton | somatic clone

(Pan et al., 2004)

dendritic branch | increased number | larval stage

(Li and Gavis, 2022)

dendritic tree | adult stage

(Doll and Broadie, 2015)

dorsal cluster neuron & neurite (with Fmr1^Δ113M)

(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 | larval stage

(Yuan et al., 2020)

embryonic/larval neuromuscular junction | third instar larval stage

(Song et al., 2022, Russo and DiAntonio, 2019, 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)

larval multidendritic class IV neuron

(Li and Gavis, 2022)

larval multidendritic class IV neuron | somatic clone | third instar larval stage

(Sterne et al., 2015)

l-LNv neuron (with Fmr1³)

(Zhao et al., 2021)

LNv neuron (with Fmr1^Δ113M)

(Morales et al., 2002)

lobula columnar neuron LC14 (with Fmr1^Δ113M)

(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 intrinsic neuron

(Pan et al., 2008)

mushroom body output neuron 11 | adult stage

(Doll and Broadie, 2015)

neuromuscular junction

(Pan et al., 2008, Zhang et al., 2001)

NMJ bouton

(Scantlebury et al., 2010)

NMJ bouton | increased number | third instar larval stage

(Song et al., 2022, Russo and DiAntonio, 2019, Nahm et al., 2013, Coffee et al., 2012, Siller and Broadie, 2011)

NMJ bouton | increased number | third instar larval stage (with Df(3R)Exel6265)

(Russo and DiAntonio, 2019)

NMJ bouton | larval stage

(Yuan et al., 2020)

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 | increased number (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 | increased number | 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 Fmr1^Δ113M)

(Bozzetti et al., 2015)

synapse

(Kim et al., 2013, Gatto and Broadie, 2009, Pan et al., 2008)

synapse, with Fmr1^UAS.cZa, Scer\GAL4^P2.4.Pdf

(Gatto and Broadie, 2009)

synaptic vesicle

(Pan et al., 2008)

synaptic vesicle | somatic clone | increased number

(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

Fmr1^Δ50M mutants show supernumerary boutons (total and satellite) in the third instar larval neuromuscular junction; ventral longitudinal muscles exhibit increased evoked EJC amplitude and increased spontaneous EJC frequency.

(Song et al., 2022)

Fmr1³/Fmr1^Δ50M adults show circadian arrhythmicity. Their sLNvs show over-elaborated axon terminals in the dorsal protocerebrum, and collateral branches. Their l-LNvs show a split POT.

(Zhao et al., 2021)

Bouton numbers are unaffected at the NMJ of Fmr1^Δ50M/+ third instar larvae.

(Kim et al., 2019)

Fmr1^Δ50M and Fmr1^Δ50M/Df(3R)Exel6265 third instar larvae exhibit increased number of presynaptic boutons, namely satellite boutons, at the third instar larval neuromuscular junction, as compared to controls. In Fmr1^Δ50M larval neuromuscular junction, there is a significant decrease in mEPSP amplitude and significant increase in quantal content, but unchanged EPSP amplitude, as compared to controls; there are no apparent changes in active zones and postsynaptic densities, as compared to controls.

Fmr1^Δ50M and Fmr1^Δ50M/Df(3R)Exel6265 transheterozygotes show a progressive increase in grooming behavior (observed in 25-days old individuals, but not in 10-days old individuals). The mushroom bodies of Fmr1^Δ50M/Df(3R)Exel6265 transheterozygotes show highly penetrant defects (α-lobe thinning and malformation), as compared to controls.

(Russo and DiAntonio, 2019)

Fmr1^Δ50M 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). Fmr1^Δ50M homozygous adults exhibit mushroom body defects including missing or thinned mushroom body α-lobes and β-lobe fusion.

(Bienkowski et al., 2017)

Fmr1^Δ50M/Fmr1^Δ50M larvae show significant increases in the number of type I boutons at the neuromuscular junction, compared to controls.

(Nguyen et al., 2016)

Fmr1^Δ50M/Df(3R)Exel6265 and Fmr1^Δ50M/Fmr1³ mutant females display a strong reduction in fertility. Ovaries of Fmr1^Δ50M/Df(3R)Exel6265 mutants, and a subset of Fmr1^Δ50M/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)

Fmr1^Δ50M homozygotes are viable, male sterile and female semi-fertile. Fmr1^Δ50M heterozygous males and females are semi-fertile. Fmr1^Δ50M/Fmr1^Δ113M transheterozygotes are male sterile and female semi-fertile.

Fmr1^Δ50M homozygosity and Fmr1^Δ50M/Fmr1^Δ113M transheterozygosity lead to the formation of crystalline aggregates (of Stellate protein) in spermatocytes, which are absent in Fmr1^Δ50M heterozygotes and wild-type controls.

(Bozzetti et al., 2015)

Fmr1^Δ50M/Fmr1^Δ50M, but not Fmr1^Δ50M/+, 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 Fmr1^Δ50M/Fmr1^Δ50M 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 Fmr1^Δ50M/Fmr1^Δ50M MARCM somatic clones in third instar larvae is significantly increased compared to controls.

(Sterne et al., 2015)

Fmr1^Δ50M/Fmr1^Δ50M 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. Fmr1^Δ50M/Fmr1^Δ50M flies exhibit a strong learning deficit in an associative learning assay.

Fmr1^Δ50M/Fmr1^Δ50M 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. Fmr1^Δ50M/Fmr1^Δ50M 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. Fmr1^Δ50M/Fmr1^Δ50M GABAergic neuron clones with 2-4 processes do not exhibit any significant difference in total process length as compared to controls. Fmr1^Δ50M/Fmr1^Δ50M 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. Fmr1^Δ50M mutant eyes, generated by eyFLP/FRT-mediated mitotic recombination, do not show an increase in ommatidial number.

(Baumgartner et al., 2013)

Neuromuscular junctions in Fmr1^Δ50M/Fmr1^Δ50M 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 Fmr1^Δ50M 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)

Fmr1^Δ50M 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 Fmr1^Δ50M 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 Fmr1^Δ50M mutant larvae. Futsch positive loops accumulate in Fmr1^Δ50M mutant synaptic arbors.

The brains of adult Fmr1^Δ50M mutants exhibit strikingly abnormal small ventrolateral (sLN[[v]] neuron synaptic architecture with expanded terminals containing supernumerary synaptic boutons. Fmr1^Δ50M mutant flies have approximately 70 Pdf positive boutons in the dorsal horn and protocerebrum compared to around 40 in controls.

Fmr1^Δ50M 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 Fmr1^Δ50M 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 Fmr1^Δ50M 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 Fmr1^Δ50M mutants. The inappropriately retained Fmr1^Δ50M 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 Fmr1^Δ50M 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 Fmr1^Δ50M mutants.

(Gatto and Broadie, 2011)

The number of NMJ branches (defined as a process with two or more boutons), is significantly higher in Fmr1^Δ50M mutant third instar larvae compared to controls. The number of mature type 1b boutons is significantly increased in the Fmr1^Δ50M 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 Fmr1^Δ50M 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 Fmr1^Δ50M null sLN[[v]] neurons continue to display a somewhat dispersed bouton array.

In young adult brains (0-4 hours post-eclosion), single cell Fmr1^Δ50M 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 Fmr1^Δ50M mutants appear unaltered.

Dorsal projections into the protocerebrum in Fmr1^Δ50M mutants exhibit a highly significant increase in the number of s-LNv Pdf neuron boutons compared with controls.

Fmr1^Δ50M 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.

Fmr1^Δ50M males are completely sterile producing no viable progeny.

In Fmr1^Δ50M 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)

Fmr1^Δ50M/Fmr1^Δ50M, Fmr1^Δ50M/Fmr1^Δ113M and Fmr1^Δ50M/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 Fmr1^Δ50M 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.

Fmr1^Δ50M/Fmr1^EP3517 adults sleep significantly longer per day than wild-type, although the effect is more subtle than in Fmr1^Δ50M 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, Fmr1^Δ50M/Fmr1^Δ50M 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, Fmr1^Δ50M/Fmr1^Δ50M adults show no circadian rhythm in locomotor activity or sleep.

Unlike wild-type flies, Fmr1^Δ50M 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 Fmr1^Δ50M homozygotes.

Fmr1^Δ50M 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/Fmr1^Δ50M ovaries contain aberrant egg chambers with both increased and decreased numbers of germ cells per chamber compared to the normal number of 16. Fmr1³/Fmr1^Δ50M mutant germaria contain significantly more mitotic cells than controls.

None of the completely mutant egg chambers in Fmr1^Δ50M mosaic ovaries surrounded by heterozygous follicle cells exhibit proliferation defects. They appear morphologically normal.

(Epstein et al., 2009)

Fmr1^Δ50M mutant sLN[[v]] synaptic arbors display an overgrowth and over-elaboration phenotype.

Fmr1^Δ50M 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 Fmr1^Δ50M 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 Fmr1^Scer\UAS.cZa at the earliest stage of pupal development, under the control of RU486-induced Scer\GAL4^{elav.Switch.PO} exacerbates the Fmr1^Δ50M 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 Fmr1^Scer\UAS.cZa in the latter stage of pupal development, under the control of RU486-induced Scer\GAL4^{elav.Switch.PO} ameliorates the Fmr1^Δ50M mutant phenotype, restricting the number and specificity of synaptic connections.

(Gatto and Broadie, 2009)

Fmr1^Δ50M mutants do not display defects in coordinated behavior (such as in a roll-over assay).

Fmr1^Δ50M mutants display significant overbranching in the neuromuscular synapse. Treatment of these mutants with the mGluR antagonist MPEP, which blocks mGluR signaling, suppresses the Fmr1^Δ50M overbranching phenotype.

Fmr1^Δ50M mutant synaptic terminals display a significant increase in total area, compared to controls.

Fmr1^Δ50M 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 Fmr1^Δ50M mutant remaining significant, indicating that blocking mGluR signaling does not significantly rescue the increased synaptic terminal area characteristic of Fmr1^Δ50M mutants.

Fmr1^Δ50M 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 Fmr1^Δ50M mutants appears normal. Quantitatively, there is no significant difference in bouton size, mitochondria size, active zone size/number or the postsynaptic subsynaptic reticulum between Fmr1^Δ50M mutants and control larvae.

Fmr1^Δ50M 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, Fmr1^Δ50M mutants display a significant ~30% increase in overall vesicle number. Fmr1^Δ50M mutants display a significant ~50% increase in the pool of clustered vesicles around the active zone. Fmr1^Δ50M mutants display a significant ~85% increase in the number of docked vesicles at the active zone.

Fmr1^Δ50M 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, Fmr1^Δ50M homozygous gamma neuron clones in a Fmr1^Δ50M 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, Fmr1^Δ50M homozygous gamma neuron clones (in a Fmr1^Δ50M 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 Fmr1^Δ50M mutants, the β lobe of the mushroom body is misdirected or missing. Just under 20% of homozygous Fmr1^Δ50M 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 Fmr1^Δ50M/Fmr1^Δ113M transheterozygotes display misdirecting or missing α lobes.

Approximately just over 70% of transheterozygous Fmr1^Δ50M/Fmr1^Δ113M 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

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

Fmr1^Δ50M has abnormal memory | adult stage phenotype, enhanceable by Nab2^ex3/Nab2[+]

(Bienkowski et al., 2017)

NOT Enhanced by

Statement

Reference

Fmr1^Δ50M has abnormal neuroanatomy | larval stage phenotype, non-enhanceable by Scer\GAL4^αTub84B.PL/Torsin^RNAi.UAS.WIZ

(Nguyen et al., 2016)

Fmr1^Δ50M has semi-sterile phenotype, non-enhanceable by futsch^N94

(Zhang et al., 2004)

Suppressed by

Statement

Reference

Fmr1^Δ50M/Fmr1³ has abnormal circadian rhythm | adult stage phenotype, suppressible | partially by Scer\GAL4^elav-C155/CRMP^TH02545.N

(Zhao et al., 2021)

Fmr1^Δ50M/Fmr1³ has abnormal circadian rhythm | adult stage phenotype, suppressible | partially by Scer\GAL4^elav-C155/CRMP^KK108924

(Zhao et al., 2021)

Fmr1^Δ50M/Fmr1³ has abnormal neuroanatomy | adult stage phenotype, suppressible | partially by Scer\GAL4^elav-C155/CRMP^TH02545.N

(Zhao et al., 2021)

Fmr1^Δ50M/Fmr1³ has abnormal neuroanatomy | adult stage phenotype, suppressible | partially by Scer\GAL4^elav-C155/CRMP^KK108924

(Zhao et al., 2021)

Fmr1^Δ50M/Fmr1³ has abnormal circadian rhythm | adult stage phenotype, suppressible | partially by CRMP^TH02545.N/Scer\GAL4^Ilp2.PR

(Zhao et al., 2021)

Fmr1^Δ50M/Fmr1³ has abnormal circadian rhythm | adult stage phenotype, suppressible | partially by Scer\GAL4^Ilp2.PR/CRMP^KK108924

(Zhao et al., 2021)

Fmr1^Δ50M has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by wnd³

(Russo and DiAntonio, 2019)

Fmr1^Δ50M has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by wnd^GL00282/Scer\GAL4^elav.PU

(Russo and DiAntonio, 2019)

Fmr1^Δ50M has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by Scer\GAL4^elav.PU/bsk^HMS04479

(Russo and DiAntonio, 2019)

Fmr1^Δ50M has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by Scer\GAL4^elav.PU/kay^Fbz.UAS

(Russo and DiAntonio, 2019)

Fmr1^Δ50M has abnormal neurophysiology | third instar larval stage phenotype, suppressible by wnd³

(Russo and DiAntonio, 2019)

Fmr1^Δ50M has abnormal neurophysiology | third instar larval stage phenotype, suppressible by wnd^GL00282/Scer\GAL4^elav.PU

(Russo and DiAntonio, 2019)

Fmr1^Δ50M/Df(3R)Exel6265 has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by wnd³/wnd¹

(Russo and DiAntonio, 2019)

Fmr1^Δ50M/Df(3R)Exel6265 has abnormal neuroanatomy | adult stage phenotype, suppressible by wnd³/wnd¹

(Russo and DiAntonio, 2019)

Fmr1^Δ50M/Df(3R)Exel6265 has abnormal size | adult stage phenotype, suppressible by wnd³/wnd¹

(Russo and DiAntonio, 2019)

Fmr1^Δ50M/Df(3R)Exel6265 has abnormal grooming behavior | progressive phenotype, suppressible by wnd³/wnd¹

(Russo and DiAntonio, 2019)

Fmr1^Δ50M has abnormal neuroanatomy | adult stage phenotype, suppressible by Nab2^ex3/Nab2[+]

(Bienkowski et al., 2017)

Fmr1^Δ50M/Df(3R)Exel6265 has abnormal cell number | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8^SM206

(Tan et al., 2016)

Fmr1^Δ50M/Fmr1³ has abnormal cell number | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8^SM206

(Tan et al., 2016)

Fmr1^Δ50M/Df(3R)Exel6265 has female semi-sterile phenotype, suppressible | partially by Zfrp8[+]/Zfrp8^SM206

(Tan et al., 2016)

Fmr1^Δ50M/Fmr1³ has female semi-sterile phenotype, suppressible | partially by Zfrp8[+]/Zfrp8^SM206

(Tan et al., 2016)

Fmr1^Δ50M/Fmr1^Δ113M has sterile phenotype, suppressible by aub^sting-1/aub[+]

(Bozzetti et al., 2015)

Fmr1^Δ50M has partially lethal - majority die phenotype, suppressible by CenG1A[+]/CenG1A^EY01217

(Gross et al., 2015)

Fmr1^Δ50M has abnormal neuroanatomy phenotype, suppressible by CenG1A[+]/CenG1A^EY01217

(Gross et al., 2015)

Fmr1^Δ50M has abnormal neuroanatomy | somatic clone | third instar larval stage phenotype, suppressible by Abl¹/Abl[+]

(Sterne et al., 2015)

Fmr1^Δ50M/Fmr1^Δ113M, rin^NP3248/rin² has lethal - all die during pupal stage phenotype, suppressible by rin^mCherry

(Baumgartner et al., 2013)

Fmr1^Δ50M/Fmr1^Δ113M, rin^NP5420/rin² has short lived phenotype, suppressible by rin^mCherry

(Baumgartner et al., 2013)

Fmr1^Δ50M has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by dlp[+]/dlp^A187

(Friedman et al., 2013)

Fmr1^Δ50M has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by dlp[+]/Sdc[+]/dlp^A187/Sdc²³

(Friedman et al., 2013)

Fmr1^Δ50M has abnormal neurophysiology | third instar larval stage phenotype, suppressible by dlp[+]/Sdc[+]/dlp^A187/Sdc²³

(Friedman et al., 2013)

Fmr1^Δ50M has abnormal neuroanatomy phenotype, suppressible by Dscam1¹⁸

(Kim et al., 2013)

Fmr1^Δ50M has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by Top3β²⁶

(Xu et al., 2013)

Fmr1^Δ50M has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by Scer\GAL4^elav.PU/Hsap\FMR1^UAS.Tag:MYC

(Coffee et al., 2012)

Fmr1^Δ50M has abnormal learning | adult stage phenotype, suppressible by Scer\GAL4^ey-OK107/Hsap\FMR1^UAS.Tag:MYC

(Coffee et al., 2012)

Fmr1^Δ50M has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by Scer\GAL4^elav.PU/Hsap\FMR1^{S500D.UAS.Tag:MYC}

(Coffee et al., 2012)

Fmr1^Δ50M has abnormal learning | adult stage phenotype, suppressible by Scer\GAL4^ey-OK107/Hsap\FMR1^{S500D.UAS.Tag:MYC}

(Coffee et al., 2012)

Fmr1^Δ50M has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by Scer\GAL4^da.G32/Timp^UAS.cPa

(Siller and Broadie, 2011)

Fmr1^Δ50M has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by Mmp1^Q112stop

(Siller and Broadie, 2011)

Fmr1^Δ50M has abnormal neuroanatomy phenotype, suppressible by Scer\GAL4^elav-C155/Hsap\FMR1^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M has male sterile phenotype, suppressible by Scer\GAL4^{VP16.nanos.UTR}/Hsap\FMR1^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M has male sterile phenotype, suppressible by Scer\GAL4^{VP16.nanos.UTR}/Hsap\FXR1^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M has male sterile phenotype, suppressible by Hsap\FXR2^UAS.Tag:MYC/Scer\GAL4^{VP16.nanos.UTR}

(Coffee et al., 2010)

Fmr1^Δ50M has abnormal neuroanatomy | larval stage phenotype, suppressible by RanBPM^k05201/l(2)k05201[+]

(Scantlebury et al., 2010)

Fmr1^Δ50M/Fmr1³ has abnormal endomitotic cell cycle phenotype, suppressible | partially by Cbl^F165/Cbl[+]

(Epstein et al., 2009)

Fmr1^Δ50M has abnormal neuroanatomy phenotype, suppressible by mGluR^112b

(Pan et al., 2008)

Fmr1^Δ50M has abnormal neurophysiology phenotype, suppressible by futsch^N94

(Zhang et al., 2001)

Fmr1^Δ50M has abnormal neuroanatomy phenotype, suppressible by futsch^N94

(Zhang et al., 2001)

NOT suppressed by

Statement

Reference

Fmr1^Δ50M/Fmr1³ has abnormal circadian rhythm | adult stage phenotype, non-suppressible by Scer\GAL4^Pdf.PU/CRMP^TH02545.N

(Zhao et al., 2021)

Fmr1^Δ50M/Fmr1³ has abnormal circadian rhythm | adult stage phenotype, non-suppressible by Scer\GAL4^Pdf.PU/CRMP^KK108924

(Zhao et al., 2021)

Fmr1^Δ50M has abnormal neurophysiology | third instar larval stage phenotype, non-suppressible by dlp[+]/dlp^A187

(Friedman et al., 2013)

Fmr1^Δ50M has abnormal neuroanatomy | third instar larval stage phenotype, non-suppressible by Scer\GAL4^elav.PU/Hsap\FMR1^{S500A.UAS.Tag:MYC}

(Coffee et al., 2012)

Fmr1^Δ50M has abnormal learning | adult stage phenotype, non-suppressible by Scer\GAL4^ey-OK107/Hsap\FMR1^{S500A.UAS.Tag:MYC}

(Coffee et al., 2012)

Fmr1^Δ50M has abnormal neuroanatomy phenotype, non-suppressible by Scer\GAL4^elav-C155/Hsap\FXR1^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M has abnormal neuroanatomy phenotype, non-suppressible by Scer\GAL4^elav-C155/Hsap\FXR2^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M has semi-sterile phenotype, non-suppressible by futsch^N94

(Zhang et al., 2004)

Enhancer of

Statement

Reference

Fmr1^Δ50M/Fmr1[+] is an enhancer of abnormal neuroanatomy | adult stage phenotype of Nab2^ex3

(Bienkowski et al., 2017)

Fmr1^Δ50M/Fmr1[+] is an enhancer of abnormal eye color | adult stage phenotype of Hsap\TARDBP^UAS.YFP.cEa, Scer\GAL4^GMR.PU

(Coyne et al., 2015)

Fmr1^Δ50M/Fmr1[+] is an enhancer of abnormal locomotor behavior | third instar larval stage phenotype of Hsap\TARDBP^UAS.YFP.cEa, Scer\GAL4^Toll-6-D42

(Coyne et al., 2015)

Fmr1^Δ50M/Fmr1[+] is an enhancer of abnormal eye color | adult stage phenotype of Hsap\TARDBP^{G298S.UAS.YFP}, Scer\GAL4^GMR.PU

(Coyne et al., 2015)

Fmr1^Δ50M/Fmr1[+] is an enhancer of abnormal locomotor behavior | third instar larval stage phenotype of Hsap\TARDBP^{G298S.UAS.YFP}, Scer\GAL4^Toll-6-D42

(Coyne et al., 2015)

NOT Enhancer of

Statement

Reference

Fmr1^Δ50M/Df(3R)by62 is a non-enhancer of abnormal neuroanatomy phenotype of Hsap\ATXN8OS^CTG112.UAS, Scer\GAL4^GMR.PF

(Mutsuddi et al., 2004)

Fmr1^Δ50M is a non-enhancer of visible phenotype of Hsap\MAPT^V337M.UAS, Scer\GAL4^GMR.PF

(Shulman and Feany, 2003)

Suppressor of

Statement

Reference

Fmr1^Δ50M/Fmr1[+] is a suppressor of visible | adult stage phenotype of Nab2^EP3716, Scer\GAL4^GMR.PU

(Bienkowski et al., 2017)

Fmr1^Δ50M/Fmr1[+] is a suppressor of abnormal eye color phenotype of Nab2^EP3716, Scer\GAL4^GMR.PU

(Bienkowski et al., 2017)

Fmr1^Δ50M/Fmr1[+] is a suppressor of abnormal size | adult stage phenotype of Nab2^EP3716, Scer\GAL4^GMR.PU

(Bienkowski et al., 2017)

Fmr1^Δ50M is a suppressor | partially of abnormal neuroanatomy | third instar larval stage phenotype of Top3β²⁶

(Xu et al., 2013)

Fmr1^Δ50M is a suppressor of lethal - all die before end of pupal stage phenotype of Mmp1^Q112stop

(Siller and Broadie, 2011)

Fmr1^Δ50M is a suppressor of some die during pupal stage phenotype of Mmp1^Q112stop

(Siller and Broadie, 2011)

Fmr1^Δ50M is a suppressor of some die during third instar larval stage phenotype of Mmp1^Q112stop

(Siller and Broadie, 2011)

Fmr1^Δ50M is a suppressor of lethal - all die before end of pupal stage phenotype of Timp^UAS.cPa

(Siller and Broadie, 2011)

Fmr1^Δ50M is a suppressor of some die during embryonic stage phenotype of Timp^UAS.cPa

(Siller and Broadie, 2011)

Fmr1^Δ50M is a suppressor of some die during larval stage phenotype of Timp^UAS.cPa

(Siller and Broadie, 2011)

Fmr1^Δ50M is a suppressor of abnormal locomotor behavior phenotype of mGluR^112b

(Pan et al., 2008)

Fmr1^Δ50M is a suppressor of abnormal neurophysiology phenotype of futsch^N94

(Zhang et al., 2001)

Fmr1^Δ50M is a suppressor of abnormal neuroanatomy phenotype of futsch^N94

(Zhang et al., 2001)

NOT Suppressor of

Statement

Reference

Fmr1^Δ50M/Df(3R)by62 is a non-suppressor of abnormal neuroanatomy phenotype of Hsap\ATXN8OS^CTG112.UAS, Scer\GAL4^GMR.PF

(Mutsuddi et al., 2004)

Fmr1^Δ50M is a non-suppressor of visible phenotype of Hsap\MAPT^V337M.UAS, Scer\GAL4^GMR.PF

(Shulman and Feany, 2003)

Other

Statement

Reference

Fmr1^Δ50M/Fmr1[+], stau¹ has viable phenotype

(Song et al., 2022)

Fmr1^Δ50M/Fmr1[+], stau¹ has abnormal neuroanatomy | third instar larval stage phenotype

(Song et al., 2022)

Fmr1^Δ50M, stau¹ has lethal - all die before end of larval stage phenotype

(Song et al., 2022)

Abl⁴, Fmr1^Δ50M has abnormal neuroanatomy | third instar larval stage phenotype

(Kim et al., 2019)

Fmr1^Δ50M, Rac1^J11 has abnormal neuroanatomy | third instar larval stage phenotype

(Kim et al., 2019)

Abi⁵, Fmr1^Δ50M has abnormal neuroanatomy | third instar larval stage phenotype

(Kim et al., 2019)

Fmr1^Δ50M/Fmr1^Δ113M, rin^NP5420/rin² has abnormal size | pupal stage phenotype

(Baumgartner et al., 2013)

Fmr1^Δ50M/Fmr1^Δ113M, rin^NP3248/rin² has lethal - all die during pupal stage phenotype

(Baumgartner et al., 2013)

Fmr1^Δ50M/Fmr1^Δ113M, rin^NP5420/rin² has short lived phenotype

(Baumgartner et al., 2013)

Fmr1^Δ50M, spartin[+]/spartin¹ has abnormal neuroanatomy | dominant | third instar larval stage phenotype

(Nahm et al., 2013)

Dad^j1E4/Dad[+], Fmr1^Δ50M has abnormal neuroanatomy | dominant | third instar larval stage phenotype

(Nahm et al., 2013)

Fmr1^Δ50M, Scer\GAL4^da.G32, Timp^UAS.cPa has viable phenotype

(Siller and Broadie, 2011)

Fmr1^Δ50M, mir-ban¹² has sterile phenotype

(Yang et al., 2009)

Fmr1^Δ50M, ban[+]/mir-ban¹² has female sterile phenotype

(Yang et al., 2009)

Phenotype Manifest In

Enhanced by

Statement

Reference

Fmr1^Δ50M has terminal bouton phenotype, enhanceable by mGluR^112b

(Pan et al., 2008)

NOT Enhanced by

Statement

Reference

Fmr1^Δ50M has type I bouton | larval stage phenotype, non-enhanceable by Scer\GAL4^αTub84B.PL/Torsin^RNAi.UAS.WIZ

(Nguyen et al., 2016)

Fmr1^Δ50M has protocerebrum phenotype, non-enhanceable by Scer\GAL4^elav-C155/Hsap\FXR2^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M has s-LNv Pdf neuron phenotype, non-enhanceable by Scer\GAL4^elav-C155/Hsap\FXR1^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M has bouton phenotype, non-enhanceable by Scer\GAL4^elav-C155/Hsap\FXR1^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M has protocerebrum phenotype, non-enhanceable by Scer\GAL4^elav-C155/Hsap\FXR1^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M has s-LNv Pdf neuron phenotype, non-enhanceable by Scer\GAL4^elav-C155/Hsap\FXR2^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M has bouton phenotype, non-enhanceable by Scer\GAL4^elav-C155/Hsap\FXR2^UAS.Tag:MYC

(Coffee et al., 2010)

Suppressed by

Statement

Reference

Fmr1^Δ50M/Fmr1³ has axon terminus | adult stage phenotype, suppressible | partially by Scer\GAL4^elav-C155/CRMP^TH02545.N

(Zhao et al., 2021)

Fmr1^Δ50M/Fmr1³ has adult s-LNv neuron phenotype, suppressible | partially by Scer\GAL4^elav-C155/CRMP^TH02545.N

(Zhao et al., 2021)

Fmr1^Δ50M/Fmr1³ has l-LNv neuron phenotype, suppressible | partially by Scer\GAL4^elav-C155/CRMP^TH02545.N

(Zhao et al., 2021)

Fmr1^Δ50M/Fmr1³ has axon terminus | adult stage phenotype, suppressible | partially by Scer\GAL4^elav-C155/CRMP^KK108924

(Zhao et al., 2021)

Fmr1^Δ50M/Fmr1³ has adult s-LNv neuron phenotype, suppressible | partially by Scer\GAL4^elav-C155/CRMP^KK108924

(Zhao et al., 2021)

Fmr1^Δ50M/Fmr1³ has l-LNv neuron phenotype, suppressible | partially by Scer\GAL4^elav-C155/CRMP^KK108924

(Zhao et al., 2021)

Fmr1^Δ50M has NMJ bouton | increased number | third instar larval stage phenotype, suppressible by wnd³

(Russo and DiAntonio, 2019)

Fmr1^Δ50M has NMJ bouton | increased number | third instar larval stage phenotype, suppressible by Scer\GAL4^elav.PU/bsk^HMS04479

(Russo and DiAntonio, 2019)

Fmr1^Δ50M has NMJ bouton | increased number | third instar larval stage phenotype, suppressible by Scer\GAL4^elav.PU/kay^Fbz.UAS

(Russo and DiAntonio, 2019)

Fmr1^Δ50M has NMJ bouton | increased number | third instar larval stage phenotype, suppressible by wnd^GL00282/Scer\GAL4^elav.PU

(Russo and DiAntonio, 2019)

Fmr1^Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible by wnd³

(Russo and DiAntonio, 2019)

Fmr1^Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible by wnd^GL00282/Scer\GAL4^elav.PU

(Russo and DiAntonio, 2019)

Fmr1^Δ50M/Df(3R)Exel6265 has NMJ bouton | increased number | third instar larval stage phenotype, suppressible by wnd³/wnd¹

(Russo and DiAntonio, 2019)

Fmr1^Δ50M/Df(3R)Exel6265 has adult mushroom body alpha-lobe phenotype, suppressible by wnd³/wnd¹

(Russo and DiAntonio, 2019)

Fmr1^Δ50M has adult mushroom body alpha-lobe | adult stage phenotype, suppressible by Nab2^ex3/Nab2[+]

(Bienkowski et al., 2017)

Fmr1^Δ50M/Df(3R)Exel6265 has ovary | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8^SM206

(Tan et al., 2016)

Fmr1^Δ50M/Df(3R)Exel6265 has egg chamber | adult stage phenotype, suppressible | partially by Zfrp8[+]/Zfrp8^SM206

(Tan et al., 2016)

Fmr1^Δ50M/Df(3R)Exel6265 has nurse cell | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8^SM206

(Tan et al., 2016)

Fmr1^Δ50M/Df(3R)Exel6265 has germarium | adult stage phenotype, suppressible | partially by Zfrp8[+]/Zfrp8^SM206

(Tan et al., 2016)

Fmr1^Δ50M/Fmr1³ has ovary | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8^SM206

(Tan et al., 2016)

Fmr1^Δ50M/Fmr1³ has egg chamber | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8^SM206

(Tan et al., 2016)

Fmr1^Δ50M/Fmr1³ has nurse cell | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8^SM206

(Tan et al., 2016)

Fmr1^Δ50M/Fmr1³ has germarium | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8^SM206

(Tan et al., 2016)

Fmr1^Δ50M has spermatocyte | spermatogenesis phenotype, suppressible by aub^sting-1/aub[+]

(Bozzetti et al., 2015)

Fmr1^Δ50M has adult mushroom body beta-lobe phenotype, suppressible by CenG1A[+]/CenG1A^EY01217

(Gross et al., 2015)

Fmr1^Δ50M has larval multidendritic class IV neuron | somatic clone | third instar larval stage phenotype, suppressible by Abl¹/Abl[+]

(Sterne et al., 2015)

Fmr1^Δ50M has type I bouton | third instar larval stage phenotype, suppressible by dlp[+]/dlp^A187

(Friedman et al., 2013)

Fmr1^Δ50M has type I bouton | third instar larval stage phenotype, suppressible by dlp[+]/Sdc[+]/dlp^A187/Sdc²³

(Friedman et al., 2013)

Fmr1^Δ50M has larval dorsal multidendritic neuron ddaC phenotype, suppressible by Dscam1¹⁸

(Kim et al., 2013)

Fmr1^Δ50M has synapse phenotype, suppressible by Dscam1¹⁸

(Kim et al., 2013)

Fmr1^Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible by Top3β²⁶

(Xu et al., 2013)

Fmr1^Δ50M has NMJ bouton | third instar larval stage phenotype, suppressible by Top3β²⁶

(Xu et al., 2013)

Fmr1^Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible by Scer\GAL4^elav.PU/Hsap\FMR1^UAS.Tag:MYC

(Coffee et al., 2012)

Fmr1^Δ50M has NMJ bouton | increased number | third instar larval stage phenotype, suppressible by Scer\GAL4^elav.PU/Hsap\FMR1^UAS.Tag:MYC

(Coffee et al., 2012)

Fmr1^Δ50M has s-LNv Pdf neuron | increased number | third instar larval stage phenotype, suppressible by Scer\GAL4^elav.PU/Hsap\FMR1^UAS.Tag:MYC

(Coffee et al., 2012)

Fmr1^Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible by Scer\GAL4^elav.PU/Hsap\FMR1^{S500D.UAS.Tag:MYC}

(Coffee et al., 2012)

Fmr1^Δ50M has NMJ bouton | increased number | third instar larval stage phenotype, suppressible by Scer\GAL4^elav.PU/Hsap\FMR1^{S500D.UAS.Tag:MYC}

(Coffee et al., 2012)

Fmr1^Δ50M has s-LNv Pdf neuron | increased number | third instar larval stage phenotype, suppressible by Scer\GAL4^elav.PU/Hsap\FMR1^{S500D.UAS.Tag:MYC}

(Coffee et al., 2012)

Fmr1^Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible by Scer\GAL4^da.G32/Timp^UAS.cPa

(Siller and Broadie, 2011)

Fmr1^Δ50M has NMJ bouton | increased number | third instar larval stage phenotype, suppressible by Scer\GAL4^da.G32/Timp^UAS.cPa

(Siller and Broadie, 2011)

Fmr1^Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible by Mmp1^Q112stop

(Siller and Broadie, 2011)

Fmr1^Δ50M has NMJ bouton | increased number | third instar larval stage phenotype, suppressible by Mmp1^Q112stop

(Siller and Broadie, 2011)

Fmr1^Δ50M has spermatid axoneme phenotype, suppressible by Scer\GAL4^{VP16.nanos.UTR}/Hsap\FXR1^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M has axonemal microtubule phenotype, suppressible by Scer\GAL4^{VP16.nanos.UTR}/Hsap\FXR1^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M has spermatid axoneme phenotype, suppressible by Hsap\FXR2^UAS.Tag:MYC/Scer\GAL4^{VP16.nanos.UTR}

(Coffee et al., 2010)

Fmr1^Δ50M has axonemal microtubule phenotype, suppressible by Hsap\FXR2^UAS.Tag:MYC/Scer\GAL4^{VP16.nanos.UTR}

(Coffee et al., 2010)

Fmr1^Δ50M has s-LNv Pdf neuron phenotype, suppressible by Scer\GAL4^elav-C155/Hsap\FMR1^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M has bouton phenotype, suppressible by Scer\GAL4^elav-C155/Hsap\FMR1^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M has protocerebrum phenotype, suppressible by Scer\GAL4^elav-C155/Hsap\FMR1^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M has embryonic/larval neuromuscular junction phenotype, suppressible by Scer\GAL4^elav-C155/Hsap\FMR1^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M has spermatid axoneme phenotype, suppressible by Scer\GAL4^{VP16.nanos.UTR}/Hsap\FMR1^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M has axonemal microtubule phenotype, suppressible by Scer\GAL4^{VP16.nanos.UTR}/Hsap\FMR1^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M has embryonic/larval neuromuscular junction phenotype, suppressible by RanBPM^k05201/l(2)k05201[+]

(Scantlebury et al., 2010)

Fmr1^Δ50M has NMJ bouton phenotype, suppressible by RanBPM^k05201/l(2)k05201[+]

(Scantlebury et al., 2010)

Fmr1^Δ50M/Fmr1³ has nurse cell phenotype, suppressible | partially by Cbl^F165/Cbl[+]

(Epstein et al., 2009)

Fmr1^Δ50M has neuromuscular junction phenotype, suppressible by mGluR^112b

(Pan et al., 2008)

Fmr1^Δ50M has synaptic vesicle phenotype, suppressible by mGluR^112b

(Pan et al., 2008)

Fmr1^Δ50M has bouton phenotype, suppressible by futsch^N94

(Zhang et al., 2001)

Fmr1^Δ50M has neuromuscular junction phenotype, suppressible by futsch^N94

(Zhang et al., 2001)

Fmr1^Δ50M has synapse phenotype, suppressible by futsch^N94

(Zhang et al., 2001)

NOT suppressed by

Statement

Reference

Fmr1^Δ50M has adult mushroom body beta-lobe | adult stage phenotype, non-suppressible by Nab2^ex3/Nab2[+]

(Bienkowski et al., 2017)

Fmr1^Δ50M has s-LNv Pdf neuron | increased number | third instar larval stage phenotype, non-suppressible by Scer\GAL4^elav.PU/Hsap\FMR1^{S500A.UAS.Tag:MYC}

(Coffee et al., 2012)

Fmr1^Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype, non-suppressible by Scer\GAL4^elav.PU/Hsap\FMR1^{S500A.UAS.Tag:MYC}

(Coffee et al., 2012)

Fmr1^Δ50M has NMJ bouton | increased number | third instar larval stage phenotype, non-suppressible by Scer\GAL4^elav.PU/Hsap\FMR1^{S500A.UAS.Tag:MYC}

(Coffee et al., 2012)

Fmr1^Δ50M has s-LNv Pdf neuron phenotype, non-suppressible by Scer\GAL4^elav-C155/Hsap\FXR1^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M has bouton phenotype, non-suppressible by Scer\GAL4^elav-C155/Hsap\FXR1^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M has protocerebrum phenotype, non-suppressible by Scer\GAL4^elav-C155/Hsap\FXR1^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M has s-LNv Pdf neuron phenotype, non-suppressible by Scer\GAL4^elav-C155/Hsap\FXR2^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M has bouton phenotype, non-suppressible by Scer\GAL4^elav-C155/Hsap\FXR2^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M has protocerebrum phenotype, non-suppressible by Scer\GAL4^elav-C155/Hsap\FXR2^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M has embryonic/larval neuromuscular junction phenotype, non-suppressible by Scer\GAL4^elav-C155/Hsap\FXR1^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M has embryonic/larval neuromuscular junction phenotype, non-suppressible by Scer\GAL4^elav-C155/Hsap\FXR2^UAS.Tag:MYC

(Coffee et al., 2010)

Fmr1^Δ50M/Fmr1³ has nurse cell | increased number phenotype, non-suppressible by Cbl^F165/Cbl[+]

(Epstein et al., 2009)

Fmr1^Δ50M has synapse phenotype, non-suppressible by mGluR^112b

(Pan et al., 2008)

Fmr1^Δ50M has presynaptic active zone phenotype, non-suppressible by mGluR^112b

(Pan et al., 2008)

Enhancer of

Statement

Reference

Fmr1^Δ50M/Fmr1[+] is an enhancer of adult mushroom body alpha-lobe | adult stage phenotype of Nab2^ex3

(Bienkowski et al., 2017)

Fmr1^Δ50M/Fmr1[+] is an enhancer of eye | adult stage phenotype of Hsap\TARDBP^UAS.YFP.cEa, Scer\GAL4^GMR.PU

(Coyne et al., 2015)

Fmr1^Δ50M/Fmr1[+] is an enhancer of eye | adult stage phenotype of Hsap\TARDBP^{G298S.UAS.YFP}, Scer\GAL4^GMR.PU

(Coyne et al., 2015)

NOT Enhancer of

Statement

Reference

Fmr1^Δ50M/Fmr1[+] is a non-enhancer of adult mushroom body beta-lobe | adult stage phenotype of Nab2^ex3

(Bienkowski et al., 2017)

Fmr1^Δ50M is a non-enhancer of eye phenotype of Hsap\MAPT^V337M.UAS, Scer\GAL4^GMR.PF

(Shulman and Feany, 2003)

Fmr1^Δ50M is a non-enhancer of ommatidium phenotype of Hsap\MAPT^V337M.UAS, Scer\GAL4^GMR.PF

(Shulman and Feany, 2003)

Suppressor of

Statement

Reference

Fmr1^Δ50M/Fmr1[+] is a suppressor of eye phenotype of Nab2^EP3716, Scer\GAL4^GMR.PU

(Bienkowski et al., 2017)

Fmr1^Δ50M/Fmr1[+] is a suppressor of ommatidium | adult stage phenotype of Nab2^EP3716, Scer\GAL4^GMR.PU

(Bienkowski et al., 2017)

Fmr1^Δ50M is a suppressor | partially of embryonic/larval neuromuscular junction | third instar larval stage phenotype of Top3β²⁶

(Xu et al., 2013)

Fmr1^Δ50M is a suppressor | partially of NMJ bouton | third instar larval stage phenotype of Top3β²⁶

(Xu et al., 2013)

Fmr1^Δ50M is a suppressor of tracheal section phenotype of Mmp1^Q112stop

(Siller and Broadie, 2011)

Fmr1^Δ50M is a suppressor of tracheal section phenotype of Scer\GAL4^da.G32, Timp^UAS.cPa

(Siller and Broadie, 2011)

Fmr1^Δ50M is a suppressor of bouton phenotype of futsch^N94

(Zhang et al., 2001)

Fmr1^Δ50M is a suppressor of neuromuscular junction phenotype of futsch^N94

(Zhang et al., 2001)

Fmr1^Δ50M is a suppressor of synapse phenotype of futsch^N94

(Zhang et al., 2001)

NOT Suppressor of

Statement

Reference

Fmr1^Δ50M is a non-suppressor of eye phenotype of Hsap\MAPT^V337M.UAS, Scer\GAL4^GMR.PF

(Shulman and Feany, 2003)

Fmr1^Δ50M is a non-suppressor of ommatidium phenotype of Hsap\MAPT^V337M.UAS, Scer\GAL4^GMR.PF

(Shulman and Feany, 2003)

Other

Statement

Reference

Fmr1^Δ50M/Fmr1[+], stau¹ has embryonic/larval neuromuscular junction | third instar larval stage phenotype

(Song et al., 2022)

Fmr1^Δ50M/Fmr1[+], stau¹ has NMJ bouton | increased number | third instar larval stage phenotype

(Song et al., 2022)

Abl⁴, Fmr1^Δ50M has NMJ bouton | third instar larval stage phenotype

(Kim et al., 2019)

Fmr1^Δ50M, Rac1^J11 has NMJ bouton | third instar larval stage phenotype

(Kim et al., 2019)

Fmr1^Δ50M, Rac1^J11 has embryonic/larval neuromuscular junction | third instar larval stage phenotype

(Kim et al., 2019)

Abl⁴, Fmr1^Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype

(Kim et al., 2019)

Abi⁵, Fmr1^Δ50M has NMJ bouton | third instar larval stage phenotype

(Kim et al., 2019)

Abi⁵, Fmr1^Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype

(Kim et al., 2019)

Fmr1^Δ50M, dlp[+]/dlp^A187 has embryonic/larval neuromuscular junction | third instar larval stage phenotype

(Friedman et al., 2013)

Fmr1^Δ50M, Sdc[+]/Sdc²³, dlp[+]/dlp^A187 has embryonic/larval neuromuscular junction | third instar larval stage phenotype

(Friedman et al., 2013)

Fmr1^Δ50M, spartin[+]/spartin¹ has NMJ bouton | increased number | third instar larval stage phenotype

(Nahm et al., 2013)

Dad^j1E4/Dad[+], Fmr1^Δ50M has NMJ bouton | increased number | third instar larval stage phenotype

(Nahm et al., 2013)

Fmr1^Δ50M, ban[+]/mir-ban¹² has female germline stem cell phenotype

(Yang et al., 2009)

Additional Comments

Genetic Interactions

Statement

Reference

Fmr1^Δ50M, stau¹ double heterozygotes show supernumerary boutons in the third instar larval neuromuscular junction.

(Song et al., 2022)

The mushroom body α-lobe morphological defects characteristic for Fmr1^Δ50M homozygous adults are ameliorated by combination with a single copy of Nab2^ex3, whereas the reverse is true for Nab2^ex3 homozygotes in which the combination with one copy of Fmr1^Δ50M 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 Fmr1^Δ50M heterozygotes in an aversive olfactory conditioning assay are enhanced by Nab2^ex3 heterozygosity.

The eye defects (reduced size, partial depigmentation and disorganization of the ommatidial lattice) observed in adult flies expressing Nab2^EP3716 under the control of Scer\GAL4^GMR.PU can be suppressed by combination with a single copy of Fmr1^Δ50M.

(Bienkowski et al., 2017)

Expression of Torsin^{dsRNA.Scer\UAS.WIZ} driven by Scer\GAL4^αTub84B.PL does not enhance increased numbers of type I NMJ boutons seen in Fmr1^Δ50M/Fmr1^Δ50M larvae.

(Nguyen et al., 2016)

Zfrp8^SM206/+ partially restores fertility and suppresses the majority of ovary defects in Fmr1^Δ50M/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.

Zfrp8^SM206/+ partially restores fertility and restores ovary morphology to normal in Fmr1^Δ50M/Fmr1³ mutants.

(Tan et al., 2016)

The male sterility of Fmr1^Δ50M/Fmr1^Δ113M transheterozygotes and the crystalline aggregates observed in the spermatocytes of Fmr1^Δ50M homozygotes are suppressed by aub^sting-1/+ heterozygosity.

(Bozzetti et al., 2015)

Heterozygous CenG1A^EY01217 increases the viability of flies homozygous for Fmr1^Δ50M.

Heterozygosity for CenG1A^EY01217 suppresses the mushroom body phenotype of beta-lobe fusion and the impaired short-term memory defect in homozygous Fmr1^Δ50M flies.

(Gross et al., 2015)

The increased presynaptic terminal length of class IV dendritic arborizing neurons in Fmr1^Δ50M/Fmr1^Δ50M MARCM somatic clones in third instar larvae is completely suppressed by combination with Abl¹ in heterozygous state.

(Sterne et al., 2015)

rin^NP3248/rin², Fmr1^Δ113M/Fmr1^Δ50M animals reach a late pupal stage - pupae are long and slender.

rin^NP5420/rin², Fmr1^Δ113M/Fmr1^Δ50M animals develop into adult flies that die soon after eclosion - pupae are long and slender.

rin^{T:Disc\RFP-mCherry} rescues the slender pupae phenotype and lethality associated with rin^NP3248/rin², Fmr1^Δ113M/Fmr1^Δ50M animals.

rin^{T:Disc\RFP-mCherry} rescues the slender pupae phenotype and lethality associated with rin^NP5420/rin², Fmr1^Δ113M/Fmr1^Δ50M animals.

(Baumgartner et al., 2013)

dlp^A187/+, or both dlp^A187/+ and Sdc²³/+, suppresses the increase in NMJ branching and synaptic bouton number; and both Sdc²³/+ and dlp^A187/+ (but not dlp^A187/+ alone) suppresses the increased amplitude of evoked junctional currents seen in Fmr1^Δ50M/Fmr1^Δ50M mutant larvae.

(Friedman et al., 2013)

The mild overgrowth of presynaptic terminals in Fmr1^Δ50M mutant C4 ddaC neuron clones is completely abolished by a Dscam1¹⁸ mutant background.

(Kim et al., 2013)

Fmr1^Δ50M spartin¹ and Fmr1^Δ50M Dad^j1E4 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 Fmr1^Δ50M double mutant third instar larvae than in either mutant alone.

(Xu et al., 2013)

Expression of Timp^Scer\UAS.cPa under the control of Scer\GAL4^da.G32 suppresses the NMJ defects seen in Fmr1^Δ50M 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 Timp^Scer\UAS.cPa under the control of Scer\GAL4^da.G32 in a Fmr1^Δ50M mutant background are robust, healthy and fully viable.

Homozygous Fmr1^Δ50M fully suppresses the tracheal defects seen when Timp^Scer\UAS.cPa is expressed under the control of Scer\GAL4^da.G32.

Homozygous Fmr1^Δ50M fully suppresses the tracheal defects seen in Mmp1^Q112stop mutant flies.

Homozygous Mmp1^Q112stop partially suppresses the NMJ defects seen in Fmr1^Δ50M 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 Fmr1^Δ50M larvae is significantly suppressed by RanBPM^k05201/+.

(Scantlebury et al., 2010)

Cbl^F165 is a dominant suppressor of the germ cell proliferation defects in Fmr1³/Fmr1^Δ50M mutant ovaries. The fewer germ cell phenotype is largely suppressed by Cbl^F165/+, while the supernumerary germ cell phenotype is not suppressed at all.

(Epstein et al., 2009)

7.7% of ban¹²/Fmr1^Δ50M transheterozygous adult females are fertile. Double heterozygous adult females of ban¹²/Fmr1^Δ50M 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 Fmr1^Δ50M mutant background suppresses the behavioral/movement impairment seen in mGluR^112b mutant larva. In these double mutants the roll-over behavioral response is smooth and efficient, with a significantly shorter 'struggle' time compared to mGluR^112b single mutants. Quantitatively, the double mutant shows comparable behavior to the wild-type control.

Fmr1^Δ50M;mGluR^112b double mutants display some suppression of the Fmr1^Δ50M single mutant synaptic overbranching phenotype but the level of overbranching is still significant compared to wild-type controls.

Fmr1^Δ50M;mGluR^112b double mutants do not show any suppression of the increased neuromuscular junction synaptic area characteristic of Fmr1^Δ50M single mutants.

Fmr1^Δ50M;mGluR^112b double mutants display a synergistic increase in synaptic bouton number compared to Fmr1^Δ50M single mutants.

Fmr1^Δ50M;mGluR^112b double mutants show a significant rescue of the elevated vesicle density phenotype seen in Fmr1^Δ50M 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\TARDBP^{Scer\UAS.T:Avic\GFP-YFP.cEa} under the control of Scer\GAL4^GMR.PU or Scer\GAL4^Toll-6-D42 respectively, are exacerbated further by combination with Fmr1^Δ50M 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\TARDBP^{G298S.Scer\UAS.T:Avic\GFP-YFP} under the control of Scer\GAL4^GMR.PU or Scer\GAL4^Toll-6-D42 respectively, are exacerbated further by combination with Fmr1^Δ50M in heterozygous state.

(Coyne et al., 2015)

Expression of Hsap\FMR1^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^elav.PU rescues the neuromuscular junction synapse architecture defects seen in Fmr1^Δ50M mutant third instar larvae. The increase in Futsch-positive loops is also fully rescued.

Expression of Hsap\FMR1^{S500D.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^elav.PU rescues the neuromuscular junction synapse architecture defects seen in Fmr1^Δ50M mutant third instar larvae. The increase in Futsch-positive loops is also fully rescued.

Expression of Hsap\FMR1^{S500A.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^elav.PU is unable to rescue the neuromuscular junction synapse architecture defects seen in Fmr1^Δ50M mutant third instar larvae. The increase in Futsch-positive loops is also not rescued.

Expressing Hsap\FMR1^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^elav.PU rescues the expanded terminals and supernumerary synaptic boutons seen in the small ventrolateral neurons of Fmr1^Δ50M mutant adults.

Expressing Hsap\FMR1^{S500D.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^elav.PU rescues the expanded terminals and supernumerary synaptic boutons seen in the small ventrolateral neurons of Fmr1^Δ50M mutant adults.

Expressing Hsap\FMR1^{S500A.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^elav.PU fails to rescue the expanded terminals and supernumerary synaptic boutons seen in the small ventrolateral neurons of Fmr1^Δ50M mutant adults.

Expression of Hsap\FMR1^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^ey-OK107 rescues the decreases in olfactory learning seen in Fmr1^Δ50M mutants.

Expression of Hsap\FMR1^{S500D.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^ey-OK107 rescues the decreases in olfactory learning seen in Fmr1^Δ50M mutants.

Expression of Hsap\FMR1^{S500A.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^ey-OK107 fails to rescue the decreases in olfactory learning seen in Fmr1^Δ50M mutants.

(Coffee et al., 2012)

Expression of Hsap\FMR1^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^elav-C155 completely suppresses the synaptic overgrowth defects characterising Fmr1^Δ50M mutants.

Expression of Hsap\FXR1^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^elav-C155 fails to suppress the synaptic overgrowth defects characterising Fmr1^Δ50M mutants.

Expression of Hsap\FXR2^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^elav-C155 fails to suppress the synaptic overgrowth defects characterising Fmr1^Δ50M mutants.

Expression of Hsap\FMR1^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^elav-C155 fully rescues both the enlarged neuromuscular junctional area and increased synaptic branching that characterise Fmr1^Δ50M mutants.

Expression of Hsap\FXR1^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^elav-C155 fails to suppress the enlarged neuromuscular junctional area and increased synaptic branching that characterise Fmr1^Δ50M mutants.

Expression of Hsap\FXR2^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^elav-C155 fails to suppress the enlarged neuromuscular junctional area and increased synaptic branching that characterise Fmr1^Δ50M mutants.

Pre-synaptic expression of Hsap\FMR1^{Scer\UAS.T:Hsap\MYC} using Scer\GAL4^elav-C155 completely restores bouton number to control levels in Fmr1^Δ50M mutants.

Pre-synaptic expression of Hsap\FXR1^{Scer\UAS.T:Hsap\MYC} using Scer\GAL4^elav-C155 is totally incapable of restoring bouton number to control levels in Fmr1^Δ50M mutants.

Pre-synaptic expression of Hsap\FXR2^{Scer\UAS.T:Hsap\MYC} using Scer\GAL4^elav-C155 is totally incapable of restoring bouton number to control levels in Fmr1^Δ50M mutants.

Scer\GAL4^elav-C155>Hsap\FMR1^{Scer\UAS.T:Hsap\MYC} can strongly rescue the mini-bouton number in Fmr1^Δ50M mutants back to wild-type levels.

Scer\GAL4^elav-C155>Hsap\FXR1^{Scer\UAS.T:Hsap\MYC} is totally incapable of restoring the elevated mini-bouton number in Fmr1^Δ50M mutants.

Scer\GAL4^elav-C155>Hsap\FXR2^{Scer\UAS.T:Hsap\MYC} is totally incapable of restoring the elevated mini-bouton number in Fmr1^Δ50M mutants.

Expression of Hsap\FMR1^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^{nos.UTR.T:Hsim\VP16} completely suppresses the male fecundity phenotype that characterises Fmr1^Δ50M mutants.

Expression of Hsap\FXR1^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^{nos.UTR.T:Hsim\VP16} completely suppresses the male fecundity phenotype that characterises Fmr1^Δ50M mutants.

Expression of Hsap\FXR2^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^{nos.UTR.T:Hsim\VP16} completely suppresses the male fecundity phenotype that characterises Fmr1^Δ50M mutants.

Expression of Hsap\FMR1^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^{nos.UTR.T:Hsim\VP16} can fully restore the spermatid axoneme architecture in Fmr1^Δ50M mutants.

Expression of Hsap\FXR1^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^{nos.UTR.T:Hsim\VP16} can fully restore the spermatid axoneme architecture in Fmr1^Δ50M mutants.

Expression of Hsap\FXR2^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^{nos.UTR.T:Hsim\VP16} can fully restore the spermatid axoneme architecture in Fmr1^Δ50M mutants.

(Coffee et al., 2010)

The rough eye phenotype caused by expression of Hsap\MAPT^{V337M.Scer\UAS} under the control of Scer\GAL4^GMR.PF is not modified if the flies are also carrying Fmr1^Δ50M.

(Shulman and Feany, 2003)

Complementation and Rescue Data

Rescued by

Fmr1^Δ50M/Fmr1^Δ113M is rescued by Fmr1^UAS.cZa/Scer\GAL4^T76

(Bozzetti et al., 2015)

Fmr1^Δ50M is rescued by Fmr1^UAS.cZa/Scer\GAL4^T76

(Bozzetti et al., 2015)

Fmr1^Δ50M/Fmr1[+] is rescued by Fmr1^UAS.cZa/Scer\GAL4^T76

(Bozzetti et al., 2015)

Fmr1^Δ50M is rescued by Fmr1^UAS.cZa/Scer\GAL4^GMR12G04

(Doll and Broadie, 2015)

Fmr1^Δ50M is rescued by Fmr1^UAS.cZa/Scer\GAL4^GMR65G01

(Doll and Broadie, 2015)

Fmr1^Δ50M is rescued by Fmr1^+t14

(Gatto and Broadie, 2011)

Fmr1^Δ50M is rescued by Fmr1^{UAS.Tag:MYC,Tag:HA}

(Coffee et al., 2010)

Fmr1^Δ50M/Fmr1³ is rescued by Fmr1^+t14

(Epstein et al., 2009)

Fmr1^Δ50M is rescued by Fmr1^+t14

(Epstein et al., 2009)

Not rescued by

Fmr1^Δ50M is not rescued by Scer\GAL4^{elav.Switch.PO}/Fmr1^UAS.cZa

(Gatto and Broadie, 2009)

Comments

The expression of Fmr1^Scer\UAS.cZa under the control of Scer\GAL4^T76 partially rescues the male sterility of Fmr1^Δ50M homozygotes and of Fmr1^Δ50M/Fmr1^Δ113M transheterozygotes, and partially rescues the decreased fertilities of Fmr1^Δ50M heterozygous males, of Fmr1^Δ50M homozygous and heterozygous females, and of Fmr1^Δ50M/Fmr1^Δ113M transheterozygous females.

(Bozzetti et al., 2015)

Expression of Fmr1^Scer\UAS.cZa under the control of Scer\GAL4^GMR12G04 (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 Fmr1^Δ50M/Fmr1^Δ50M mutants.

Expression of Fmr1^Scer\UAS.cZa under the control of Scer\GAL4^GMR65G01 (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 Fmr1^Δ50M/Fmr1^Δ50M mutants.

(Doll and Broadie, 2015)

Expression of Fmr1^+t14 strongly diminishes PDF-TRI neuron retention in Fmr1^Δ50M mutants.

(Gatto and Broadie, 2011)

Expression of Fmr1^{Scer\UAS.T:Hsap\MYC,T:Ivir\HA1} under the control of Scer\GAL4^elav-C155 completely rescued the synaptic overgrowth characterising the Fmr1^Δ50M mutant, and the terminals become clearly more restricted in extent and refined in the number of synaptic boutons.

Expression of Fmr1^{Scer\UAS.T:Hsap\MYC,T:Ivir\HA1} under the control of Scer\GAL4^elav-C155 fully rescues both the enlarged neuromuscular junctional area and increased synaptic branching that characterise Fmr1^Δ50M mutants.

Pre-synaptic expression of Fmr1^{Scer\UAS.T:Hsap\MYC,T:Ivir\HA1} using Scer\GAL4^elav-C155 completely rescues bouton number back to control levels in Fmr1^Δ50M mutants.

Scer\GAL4^elav-C155>Fmr1^{Scer\UAS.T:Hsap\MYC,T:Ivir\HA1} can strongly rescue the mini-bouton number in Fmr1^Δ50M mutants back to wild-type levels.

Expression of Fmr1^{Scer\UAS.T:Hsap\MYC,T:Ivir\HA1} under the control of Scer\GAL4^{nos.UTR.T:Hsim\VP16} completely rescues the male fecundity defect that characterises Fmr1^Δ50M mutants.

Expression of Fmr1^{Scer\UAS.T:Hsap\MYC,T:Ivir\HA1} under the control of Scer\GAL4^{nos.UTR.T:Hsim\VP16} can strongly rescue the spermatid axoneme defects that characterise Fmr1^Δ50M mutants.

(Coffee et al., 2010)

Provision of Fmr1 transiently during the early stages of neural development, through expression of Fmr1^Scer\UAS.cZa under the RU486-induced control of Scer\GAL4^{elav.Switch.PO} in a Fmr1^Δ50M 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 Fmr1^Δ50M mutants.

(Gatto and Broadie, 2009)

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Mutant

Wild-type

Stocks (1)

Bloomington

6930

w¹¹¹⁸; Fmr1^Δ50M/TM6B, Tb¹

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (33)

Reported As

Symbol Synonym

FMR1^D50M

(Baumgartner et al., 2013)

FMR1^Δ50M

(Starke et al., 2022)

Fmr1-Δ50

(Li et al., 2023)

Fmr1^Delta50M

(De Donno et al., 2023)

Fmr1^null

(Cvetkovska et al., 2013)

Fmr1^Δ50

(Greenblatt and Spradling, 2018, Gross et al., 2015, Michel et al., 2004, Morales et al., 2002)

Fmr1^Δ50M

(Titus et al., 2021, Worpenberg et al., 2021, Fingerhut et al., 2019, Lee et al., 2018, Tan et al., 2016, Andlauer et al., 2014, van Alphen et al., 2013, Bushey et al., 2009)

d50

(van Alphen et al., 2013)

dFMR1^50M

(Cziko et al., 2009)

dFMR1^Δ50

(Kashima et al., 2017)

dFMR1^Δ50M

(Yuan et al., 2020, Kashima et al., 2017)

dFMRP^50M

(Kim et al., 2013)

dFMRP^Δ50M

(Sterne et al., 2015, Gareau et al., 2013)

dFmr1^50M

(Epstein et al., 2009)

dFmr1^Δ50

(Bozzetti et al., 2015)

dFmr1^Δ50M

(Kim et al., 2019, Russo and DiAntonio, 2019, Gross et al., 2015)

dfmr1⁵⁰

(Scantlebury et al., 2010)

dfmr1^delta50

(Zhang et al., 2014)

dfmr1^delta5

(Yang et al., 2009)

dfmr1^Δ50

(Bienkowski et al., 2017)

dfmr1^Δ50M

(Honda et al., 2024, Li and Gavis, 2022, Golovin et al., 2021, Zhao et al., 2021, Xu et al., 2013, Siller and Broadie, 2011)

dfmr^50M

(Pan et al., 2004)

dfmr^del50

(Mutsuddi et al., 2004)

dfmr^Δ50

(Yang et al., 2009)

dfmr^Δ50M

(Nahm et al., 2013)

dfxr null

(Zhang et al., 2001)

dxfr1^50M

(Zhang et al., 2004, Shulman and Feany, 2003)

fmr1^50M

(Dong et al., 2015)

fmr1^Delta50M

(Luhur et al., 2017)

fmr1^Δ50

(Zhang et al., 2022, Tadros et al., 2007)

fmr1^Δ50M

(Matsumoto et al., 2018, Mansilla et al., 2017, Nguyen et al., 2016, Wan et al., 2015, Scantlebury et al., 2010)

fmr1^Δ50m

(Luhur et al., 2017)

Name Synonyms

Secondary FlyBase IDs

References (79)

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