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General Information
Symbol
Dmel\Fmr13
Species
D. melanogaster
Name
FlyBase ID
FBal0137500
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
dfmr13, dfmr3
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
Excision of P{EP}Fmr1EP3517 and deletion of proximal and distal flanking DNA including sequences into the eighth coding exon of the Fmr1 ORF.
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 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
gamma-lobe & neuron | somatic clone
germ cell & egg chamber
mushroom body & neuron & dendrite | somatic clone
mushroom body & neuron | somatic clone
neuron & beta-lobe, with Fmr1I244N
neuron & beta-lobe, with Fmr1I307N
neuron & beta-lobe (with Fmr1I244N)
neuron & beta-lobe (with Fmr1I307N)
synapse & larval neuromuscular junction
Detailed Description
Statement
Reference
Fmr1Δ50M/Fmr13 mutant females display a strong reduction in fertility. Ovaries from a subset of Fmr1Δ50M/Fmr13 female mutants display developmental defects, including fused egg chambers, aberrant nurse cell numbers, and occasional oocyte misspecification or multiple oocytes per egg chamber.
Fmr13 adult flies show impaired immediate olfactory conditioning memory (learning) in an aversive olfactory memory assay.
Homozygous Fmr13 mutant flies exhibit normal short-term habituation (STH) when flies are exposed to either ethyl butyrate (EB) or CO[[2]]] for 30 minutes. In contrast, Fmr13 mutant flies exhibit a complete block of the long-term habituation (LTH) that is normally seen when flies are exposed to either ethyl butyrate (EB) or CO[[2]]] for 4 days.
Fmr13/+ flies exhibit significant learning and long term memory deficits in a negatively reinforced olfactory learning paradigm. Learning and deficits in Fmr13 heterozygotes are completely rescued upon feeding flies with the pyrrolidinone Rolipram or with 2-Methyl-6-(phenylethynyl)pyridine. Long term memory deficits in Fmr13 heterozygotes are completely rescued upon feeding flies with the pyrrolidinone Rolipram or with 2-Methyl-6-(phenylethynyl)pyridine, but only if the drug is administered both before and after conditioning until testing. Fmr13/+ flies show increased learning performance with 2 or 4 CS-US pairings, worse performance with 6 or 8 pairings, and similar performance with 12 pairings, compared to controls. Fmr13/Fmr13 flies have highly penetrant mushroom body defects. Fmr13/+ flies do not exhibit macroscopic mushroom body defects. Fmr13/Fmr13 flies exhibit reduced adult longevity and severly suppressed locomotor activity, while Fmr13/+ flies exhibit increased locomotor activity.
Mutant larvae have a significantly increased average number of boutons at the neuromuscular junction compared to controls. The mushroom bodies of mutant pharate adult brains show a high frequency of β-lobe crossover.
Fmr13 mutant larvae exhibit an increase in type Ib and 1s synaptic boutons and branching compared to wild-type controls. Fmr13 mutant larvae exhibit an increase in the length of the primary nerve branch when compared with controls.
Fmr13/Fmr1Δ83M flies have significant locomotor defects (climbing ability) and display excessive grooming behavior compared to rescued controls at 5 days old, getting progressively worse with aging (day 15, 25 and 35). Fmr13/Fmr1Δ83M males show significantly decreased courtship behavior compared to rescued controls.
Homozygous larvae have an increased number of boutons at the neuromuscular junction compared to wild type. Mushroom body β-lobe axons frequently cross the midline homozygous flies. Approximately 80% of homozygous adults do not maintain rhythmic locomotion activity under constant darkness conditions. Mutant males show a reduction in naive courtship activity compared to wild-type males. After training (the males are paired with unreceptive females for an hour), the mutant males do not show a reduction in courtship index at 0-2 or 60 minutes after training when placed with a receptive female, indicating a defect in immediate recall and short-term memory.
Fmr13/Fmr13 mutant flies exhibit a greater frequency of stopping for long lengths of time than wild type. Fmr13/Fmr13 mutant flies tend to spend less time in close physical proximity to other flies, and this is not significantly affected by whether the other flies are also Fmr13/Fmr13 mutants or wild type.
5-day old males heterozygous for Fmr13 do not show any defects in their courtship behavior.
25% of embryos derived from Fmr13/Df(3R)Exel6265 females show a delay in furrow formation compared to controls.
Fmr13/Fmr1Δ50M and homozygous Fmr13 ovaries contain aberrant egg chambers. Some of the abnormal egg chambers display an increased number of germ cells, while others show fewer germ cells per chamber than the normal number of 16. Fmr13 and Fmr13/Fmr1Δ50M mutant germaria contain significantly more mitotic cells than controls. Nurse cells in Fmr13 mutants display increased DNA synthesis throughout oogenesis and exhibit endocycle defects. Fmr13 follicle cells appear normal.
Fmr13 mutants show a tendency towards elevated response amplification compared to controls. However, there are no statistically significant differences in EJC amplitude between Fmr13 and controls. Fmr13 mutants show comparable levels of short-term facilitation as wild-type controls. During prolonged 10-Hz stimulation, Fmr13 mutants maintain a relatively constant 2- to 4-fold increase in EJC response amplitude compared with basal transmission (as in controls). In response to a HFS, Fmr13 mutants rarely manifest early onset LTF but maintain a low level of augmentation for the duration of the HFS train, as in controls. During prolonged 20Hz HFS, aproximately 56% Fmr13 mutants manifest periodic cycling of EJC response amplitudes, which begin with enhanced EJC amplitudes, followed by cycling between abnormally low and abnormally high values. During the lulls in EJC response to the HFS, complete loss of EJC response amplitude is not manifested but rather is greatly depressed, but persistent EJCs are recorded: there is no increased incidence of synaptic transmission failure. Additionally, a ramping-up of response amplitude can often be seen during the larger response amplitude phases of the cycling rather than an immediate stepwise increase in response amplitude compared with the LTF threshold. Fmr13 mutants routinely display the aberrant profile of multiple, enlarged EJC events in response to a single stimulus during a prolonged HFS train. During 20Hz stimulation trains, 88% of Fmr13 mutants manifest this multi-response profile, starting early during the HFS train. During the post-HFS period, Fmr13 mutants present a hyperexcitable state characterised by multiple, enlarged synaptic responses to a single nerve stimulus.
Fmr13 mutants respond normally to odors and foot shock. Homozygous Fmr13 or Fmr13/Fmr1B155 transheterozygous mutants show significant defects in 1-d memory after spaced training, but not after massed training. Homozygous Fmr13 or Fmr13/Fmr1B155 transheterozygous mutants exhibit significant defects in olfactory learning and a β-lobe midline crossing defect. Heterozygous Fmr13 flies show normal 1-d memory after spaced or massed training. At relatively low concentrations of cycloheximide or puromycin, 1-d memory after spaced training is significantly ameliorated in Fmr13 mutants (and unaffected in wild-type), while there are no effects on 1-d memory after massed training. There is also a significant improvement in Long-Term Memory with the addition of metabotropic glutamate receptor antagonist MPEP to Fmr13 mutants.
Fmr13 mutants do not display defects in coordinated behavior (such as in a roll-over assay).
Homozygosity for Fmr13 results in a defasciculation phenotype of the termini of the LNv neuron's dorsal projections.
Flies carrying one copy of Fmr1I244N or Fmr1I307N in a homozygous Fmr13 background show no significant increase in the number of type I boutons at the larval neuromuscular junction compared to wild type (muscles 6/7, 12 and 4 from segment A3 have been studied). Flies carrying Fmr1I244N or Fmr1I307N in a homozygous Fmr13 background show an increased frequency of midline crossing of mushroom body β-lobe neurons compared to controls. Animals carrying Fmr1I244N or Fmr1I307N in a homozygous Fmr13 background show a significant increase in the percentage of flies that are arrhythmic for locomotor activity under constant darkness conditions compared to controls. Animals carrying Fmr1I244N or Fmr1I307N in a homozygous Fmr13 background show a reduced courtship index towards virgin females than that seen in wild-type males.
Fmr1- embryos derived from crossing homozygous females and males (the embryos lack maternal and zygotic Fmr1 function) show abnormal pole cell formation. Abnormalities are first seen in nuclear cycle 9-10 embryos, when the polar buds begin to protrude from the posterior end of the embryo; in the Fmr1- embryos the newly formed pole cells are not fully extruded from the surface of the embryo, in contrast to wild type. In nuclear cycle 12-13 Fmr1- embryos the pole cells are not tightly clustered and several of them are separated from the main group. In addition, somatic cells are intermingled with the pole cells in these Fmr1- embryos, in contrast to wild-type embryos. Stage 12-13 Fmr1- embryos derived from crossing homozygous females and males have an average of 14.5 pole cells per embryo (compared to an average of 22.8 pole cells per embryo in wild type) and there is considerable variation in pole cell number between different Fmr1- embryos (some have no pole cells). The number of germ cells in the coalesced gonad of stage 14-15 Fmr1- embryos is also reduced compared to wild-type embryos., although there is no difference in the number of somatic gonadal precursor cells. Somatic nuclei of nuclear cycle 13 Fmr1- embryos (derived from crossing homozygous females and males) show a number of abnormalities; they are not always elongated along the apical-basal axis (in contrast to wild-type embryos), often have an irregular shape and are often displaced from the surface of the embryo. The nuclear division cycles are asynchronous in 25-30% of Fmr1- embryos (derived from crossing homozygous females and males). Abnormal mitotic figures are seen, with defects including lagging chromosomes, chromosome bridges and chromosomal breaks. Centrosome duplication and migration can occur in these embryos, but they can occur even in the apparent absence of a nucleus or DNA and many "free" centrosomes that are not associated with nucleus or DNA are seen. Mitotic nuclei in which all the chromosomes appear to be moving towards one of the centrosomes are also seen.
68% of embryos produced by females with Fmr13 germline clones are devoid of pole cells and the remaining 32% contain ~22 pole cells. 597% of these embryos are arrested at embryonic cycle 1 or are unfertilized, and 9% are arrested before cycle 8. In addition, these embryos show severe defects in chromosomal segregation, nuclear distribution and supernumerary mitoses. Among mitotically normal embryos from Fmr13 mothers at cycle 9-14, only 3% of them had no pole cells and 20% of them contained fewer than ten pole cells, yet 77% displayed approximately normal numbers of pole cells.
Fmr13/Df(3R)Exel6265 females produce morphologically normal eggs at similar rates to wild-type females when crossed to wild-type males. However, fewer of the embryos from Fmr13/Df(3R)Exel6265 females hatch. The viability of these embryos is determined by the maternal genotype. Embryos produced from Fmr13/Df(3R)Exel6265 females and wild-type males exhibit a subtle defect in the duration of nuclear cycles 12 and 13, and a fully penetrant cellularisation phenotype. Approximately 75% of the embryos display a significant reduction in the rate of furrow ingression, whereas the remaining 25% display dramatic cellularisation defect characterised by uneven furrow ingression.
A significant number of Fmr13/Fmr13 egg chambers have either reduced or increased numbers of germline cells. In addition, almost 10% of these egg chambers contain presumptive oocytes with polyploid oocyte nuclei or two oocytes located at opposite poles.
The learning ability of Fmr13 mutant males during the training phase of conditioned courtship is not impaired compared to wild-type but they display immediate recall (0-2min) memory defects.
Fmr13 homozygous larvae exhibit hyperplasia of neuromuscular junctions: The number of boutons per neuromuscular juntion is significantly increased.
Slightly over 65% of homozygous Fmr13 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. Slightly over 70% of transheterozygote Fmr13/Fmr1Δ113M mutants exhibit severe midline crossing in the β-lobe of the mushroom body. Just under 10% of these mutants exhibit 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). Slightly over 85% of transheterozygous Fmr1Δ83M/Fmr13 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). Approximately 5% exhibit 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), with another 5% exhibiting mild midline crossing (defined as when a thin band of fibers cross the midline). No sexual dimorphism in penetrance or expressivity is found. In fewer than 10% of cases, transheterozygous Fmr1Δ83M/Fmr13 mutants exhibit misdirected or missing α-lobes.
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.
Fmr13/Fmr14.L wandering larvae have defects in crawling behaviour; they spend significantly less time on linear locomotion than wild-type control larvae and the average duration of linear locomotion is reduced compared to controls. The average direction change (direction change is defined as the difference in direction from one frame to the next in the analysis) is increased compared to controls.
Flies show no visible phenotypic abnormalities. Phototactic and chemotactic abilities are normal. Mutant flies are arrhythmic with respect to locomotor behavior as measured in an actogram and periodogram and show disrupted eclosion periodicity. General motor functions and locomotor abilities appear normal. Mutants can be driven to display activity rhythms in the presence of light:dark cycles. Mutant males spend significantly less time than wild type engaged in courtship, and fail to engage in advanced courtship behavior - progressing no further than following/tapping. Adult brains have wild type numbers of small and large ventral lateral neurons, and projection to the optic lobes via posterior optic tract and to the ipsilateral dorsal protocerebrum are present, but a high frequency of collateral branches emanate from these axons in mutant brains. Termini are unusually arborized. Mushroom bodies of mutant brains do not appear to be morphologically different from those of wild type.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
Suppressed by
Statement
Reference
Fmr1Δ50M/Fmr13 has cell number defective | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8SM206
Fmr1Δ50M/Fmr13 has female semi-sterile phenotype, suppressible | partially by Zfrp8[+]/Zfrp8SM206
Atx2X1/Atx2[+], Fmr13 has learning defective | dominant phenotype, suppressible by Atx2+t10.4
Atx2X1/Atx2[+], Fmr13 has learning defective | dominant phenotype, suppressible by Fmr1+t14
Fmr13, me31B[+]/me31BΔ2 has learning defective | dominant phenotype, suppressible by Fmr1+t14
AGO1k08121/AGO1[+], Fmr13 has learning defective | dominant phenotype, suppressible by Fmr1+t14
Fmr13 has learning defective | dominant | adult stage phenotype, suppressible by dnc1/dnc[+]
Fmr13 has memory defective | dominant | adult stage phenotype, suppressible by dnc1/dnc[+]
Fmr13, PsnB3/Psn[+] has courtship behavior defective phenotype, suppressible by Fmr1+t14
NOT suppressed by
Statement
Reference
Enhancer of
Statement
Reference
Fmr13/Fmr1[+] is an enhancer of memory defective phenotype of AGO1k08121
Fmr13/Fmr1[+] is an enhancer of memory defective phenotype of stau2
NOT Enhancer of
Statement
Reference
Suppressor of
Other
Phenotype Manifest In
Suppressed by
Statement
Reference
Fmr1Δ50M/Fmr13 has ovary | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8SM206
Fmr1Δ50M/Fmr13 has egg chamber | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8SM206
Fmr1Δ50M/Fmr13 has nurse cell | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8SM206
Fmr1Δ50M/Fmr13 has germarium | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8SM206
Fmr13 has type I bouton phenotype, suppressible by Adar5G1
Fmr13 has nurse cell phenotype, suppressible by CblF165/Cbl[+]
Fmr13 has nurse cell | supernumerary phenotype, suppressible | partially by CblF165/Cbl[+]
Fmr1Δ50M/Fmr13 has nurse cell phenotype, suppressible | partially by CblF165/Cbl[+]
Fmr13 has NMJ bouton | larval stage phenotype, suppressible by aPKCk06403/aPKC[+]
Fmr13 has synapse & larval neuromuscular junction phenotype, suppressible by aPKCk06403/aPKC[+]
NOT suppressed by
Statement
Reference
Fmr13 has synapse phenotype, non-suppressible by Adar5G1
Fmr13 has neuromuscular junction phenotype, non-suppressible by Adar5G1
Fmr1Δ50M/Fmr13 has nurse cell | supernumerary phenotype, non-suppressible by CblF165/Cbl[+]
Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference
Fmr13 is a non-enhancer of neuromuscular junction phenotype of Adar5G1
Fmr13 is a non-enhancer of type I bouton phenotype of Adar5G1
Fmr13 is a non-enhancer of synapse phenotype of Adar5G1
Suppressor of
NOT Suppressor of
Statement
Reference
Fmr13 is a non-suppressor of type I bouton phenotype of Adar5G1
Fmr13 is a non-suppressor of synapse phenotype of Adar5G1
Fmr13 is a non-suppressor of neuromuscular junction phenotype of Adar5G1
Other
Statement
Reference
Fmr13, l(2)gl[+]/l(2)gl4 has synapse & larval neuromuscular junction phenotype
Fmr13/Fmr1[+], l(2)gl4 has synapse & larval neuromuscular junction phenotype
Additional Comments
Genetic Interactions
Statement
Reference
Zfrp8SM206/+ partially restores fertility and restores ovary morphology to normal in Fmr1Δ50M/Fmr13 mutants.
Fmr13, Atx2X1 double heterozygotes exhibit a complete block of the long-term habituation (LTH) normally seen when flies are exposed to either ethyl butyrate (EB) or CO[[2]]] for 4 days. LTH appears normal in either heterozygote alone. This loss of EB-evoked LTH is restored by expression of either Atx2+t10.4 or Fmr1+t14. Short term habituation following one hour exposure to EB appears normal. Fmr1Δ50M, me31BΔ2 double heterozygotes exhibit a complete block of the long-term habituation (LTH) normally seen when flies are exposed to either ethyl butyrate (EB) or CO[[2]]] for 4 days. LTH appears normal in either heterozygote alone. This loss of EB-evoked LTH is restored by expression of Fmr1+t14. Short term habituation following one hour exposure to EB appears normal. Fmr1Δ50M, AGO1k08121 double heterozygotes exhibit a complete block of the long-term habituation (LTH) normally seen when flies are exposed to either ethyl butyrate (EB) or CO[[2]]] for 4 days. LTH appears normal in either heterozygote alone. This loss of EB-evoked LTH is restored by expression of Fmr1+t14. Short term habituation following one hour exposure to EB appears normal.
The memory and learning deficit of Fmr13 heterozygotes is enhanced when in trans with either the TM3-Sb or TM6C balancers. Expression of mGluRGD707 under the control of Scer\GAL4elav.PU or under the control of Scer\GAL4c747 (in combination with GAL80ts to limit expression to adult stage) rescues the learning and long term memory phenotypes of Fmr13 mutants. Trans-heterozygotes of Fmr13 and dnc1 do not exhibit learning or long term memory deficits. Trans-heterozygotes of Fmr13 and dncML do not exhibit learning deficits.
Adar5G1; Fmr13 double mutant larvae exhibit an Adar5G1 single mutant-like phenotype with respect to the subclasses of type 1 synaptic boutons and primary branch length. An Adar5G1 heterozygous background suppresses the Fmr13 neuromuscular junction phenotype to wild-type with respect to the number of type 1 synaptic boutons.
The courtship behavior of 5-day-old Fmr13/+;PsnB3/+ double heterozygous males is severely impaired compared to either of the single heterozygotes that display normal courtship. This defect in naive courtship behavior can be rescued by combination with Fmr1+t14 allele.
The proportion of embryos displaying a delay in furrow formation increases from 25% observed for embryos derived from Fmr13/Df(3R)Exel6265 females to 75% observed for embryos from females that are also heterozygous for CCT6G0057. The proportion of embryos displaying a delay in furrow formation increases from 25% observed for embryos derived from Fmr13/Df(3R)Exel6265 females to 50% observed for embryos from females that are also heterozygous for Df(2L)Exel6034, remains at 25% for embryos laid by Df(2R)Exel6052/+;Fmr13/Df(3R)Exel6265 females and is below 25% for embryos from RpS131/+;Fmr13/Df(3R)Exel6265 females.
Capr2/Df(3L)Cat, Fmr13/+ flies are viable, but 50% of embryos laid by these females display a dramatic disruption in the timing of the mid-blastula transition: they initiate cleavage furrow formation normally, but enter mitosis 14 prematurely rather than undergoing a prolonged interphase. During the premature mitosis, the nascent cleavage furrows regress, only to reform during interphase of cycle 15, when the embryos attempt to complete cellularization. (No significant difference in nuclear cycle duration is seen until cycle 14, there are no signs of aberrant mitosis, and spindle morphology and nuclear spacing appears normal during mitosis 13 and 14.) Reduction of maternal CycB by one half (using the CycB2 allele) in the Capr2/Df(3L)Cat, Fmr13/+ background partially rescues the premature mitosis 14 phenotype seen in embryos of this genotype. (Reduction of the zygotic contribution of CycB has no effect.)
CblF165 is a dominant suppressor of the germ cell proliferation defects in Fmr13 and Fmr13/Fmr1Δ50M mutant ovaries. The fewer germ cell phenotype in homozygous Fmr13 mutants is completely suppressed by CblF165/+, while the supernumerary germ cell phenotype is only partially. The fewer germ cell phenotype in Fmr13/Fmr1Δ50M ovaries is largely suppressed by CblF165/+, while the supernumerary germ cell phenotype is not suppressed at all.
The Fmr13; mGluRA112b double mutant displays a cyclic response amplitude defect during 20Hz HFS (as in Fmr13 single mutants). However, almost half as many double mutant animals display the phenotype compared with Fmr13 single mutants. When the cycling is manifest, there is not significant difference in the average time from HFS onset to initiation of the cycling phenotype. The number of EJC events in a complete cycle seems greater in the double mutant, but the increase is not significant. The level of modulation from peak EJC to depressed EJC is greater in the Fmr13 single mutant compared with the Fmr13; mGluRA112b double mutant. The multiple discrete EJC events characteristic of Fmr13 mutants are very much reduced by co-removal of mGluRA112b.
Double heterozygous stau2/+; Fmr13/+ mutant flies show defective 1-d memory after spaced training, but not after massed training. At relatively low concentrations of cycloheximide or puromycin, 1-d memory after spaced training is significantly ameliorated in AGO1k08121/+; Fmr13/+ mutants (and unaffected in wild-type).
A Fmr13 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.
Ectopic expression of mir-124Scer\UAS.cXa in ddaC neurons (under the control of Scer\GAL4477) in a homozygous Fmr13 or Fmr13/Fmr14.L background results in a significantly attenuated phenotype, where the number of dendritic ends is partially rescued (although not to the wild-type level). Interestingly, the dendritic fields of ddaC neurons are similar in size to those of wild-type neurons.
A Fmr13/+ background mildly enhances the cellularisation phenotype observed in embryos derived from trale03082/+ females crossed with wild-type males.
Fmr13/+; l(2)gl4/+ larvae exhibit hyperplasia of neuromuscular junctions: The number of boutons per neuromuscular juntion is significantly increased. This phenotype is not seen in either heterozygote. The hyperplasia of larval neuromuscular junctions and the concomitant increase in boutons at these junctions seen in Fmr13 homozygous larvae is suppressed by aPKCk06403/+
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Fmr13 is partially rescued by Fmr1WTR
Fmr13 is partially rescued by Fmr1WTR-SN
Fmr13 is partially rescued by Fmr1WTR-LN
Fmr13 is partially rescued by Fmr1ΔQN
Fmr13 is partially rescued by Fmr1L
Comments
Expression of Fmr1+t14 rescues the long term habituation (LTH) defects seen in Fmr13 mutant flies following exposure to either ethyl butyrate (EB) or CO[[2]]] for 4 days.
Fmr1+t14 (but not Fmr1FS) or expression of Fmr1Scer\UAS.cWa driven by Scer\GAL4c747 or Scer\GAL4Mef2.247 (but not Scer\GAL4Alp4-c507 or Scer\GAL4NP1131) rescues learning and memory defects in Fmr13/+ heterozygotes.
The increased number of boutons at the neuromuscular junction that is seen in Fmr13 larvae is rescued by Fmr1WTR, Fmr1WTR-SN, Fmr1WTR-LN and Fmr1WTRLN-ATG. The high frequency of β-lobe crossover seen in the mushroom bodies of Fmr13 pharate adult brains is partially suppressed by Fmr1WTR, Fmr1WTR-SN, Fmr1WTR-LN and Fmr1WTRLN-ATG.
Fmr1+t14 (but not Fmr1FS) rescues locomotor defects and excessive grooming behavior at all ages (day 5, 15, 25, 35) in Fmr13/Fmr1Δ83M flies; courtship behavior defects at day 15 are also rescued by Fmr1+t14 but not Fmr1FS.
Fmr1ΔQN partially rescues the maternal effect embryonic lethality of Fmr13. Fmr1ΔQN and Fmr1+t14 each rescue the midline crossing phenotype of mushroom body β-lobe axons that is seen in Fmr13 adults. Fmr1+t14 rescues the increased number of boutons at the neuromuscular junction that is seen in homozygous Fmr13 larvae. Fmr1ΔQN does not rescue the increased number of boutons at the neuromuscular junction that is seen in homozygous Fmr13 larvae. Fmr1+t14 almost completely rescues the loss of rhythmic locomotion activity which is seen in Fmr13 flies under constant darkness conditions. Fmr1ΔQN partially rescues the loss of rhythmic locomotion activity which is seen in Fmr13 flies under constant darkness conditions. Fmr1+t14 rescues the reduction in naive courtship activity seen in Fmr13 males and also rescues the defects in immediate recall and short-term memory after training, so that the rescued males show a reduction in courtship index at 0-2 and 60 minutes after training when placed with a receptive female. Fmr1ΔQN does not rescue the reduction in naive courtship activity seen in Fmr13 males. The defects in immediate recall after training are partially rescued, while the short-term memory defects seen after training are not rescued; the rescued males show some reduction in courtship index at 0-2 minutes after training but no reduction in courtship index at 60 minutes after training when placed with a receptive female. Fmr1L rescues the reduction in naive courtship activity seen in Fmr13 males, and the rescued males show normal short-term memory after training (showing a reduction in courtship index 60 minutes after training when placed with a receptive female). However, the rescued males show a deficit in long-term memory after training; they do not show a significant reduction in courtship index 4 days after training when placed with a receptive female.
The presence of Fmr1+t14 rescues the long-term memory defect associated with Fmr13 or Fmr1B155 homozygotes and Fmr13/Fmr1B155 transheterozygotes.
The cellularisation phenotypes observed in embryos derived from mating Fmr13/Df(3R)Exel6265 females with wild-type males can be rescued through expression of Fmr1+tJa.
The defective immediate recall as well and short-term memory characteristic for Fmr13 mutant males is restored by combination with a single copy of the Fmr1+t14 but not the Fmr1FS transgene.
The presence of a single copy of Fmr1+t14 to Fmr13/Fmr1Δ83M or Fmr13/Fmr1Δ113M transheterozygotes greatly reduces the penetrance and expressivity of the β-lobe midline-crossing phenotype.
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Synonyms and Secondary IDs (8)
References (38)