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General Information
Symbol
Dmel\fra3
Species
D. melanogaster
Name
FlyBase ID
FBal0057434
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Nucleotide change:

G12560784A

Reported nucleotide change:

G?A

Amino acid change:

W1028term | fra-PA; W877term | fra-PB; W1019term | fra-PC

Reported amino acid change:

W1028term

Comment:

G to A nucleotide change at the second or third position of the Trp codon leads to a nonsense mutation. (exact site of mutation unspecified).

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Nucleotide substitution: G?A.

Amino acid replacement: W1028term.

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 ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

commissure & embryo & axon

Detailed Description
Statement
Reference

In 33 out of 72 abdominal segments examined in fra3/fra4 third instar larvae, the LCh1 cap cell migrates ventrally instead of dorsally; in 14 of 33 segments the cap cell travels along the ventral midline (along the VChA and VChB organs) and morphology of cap cells is largely normal, while in the remaining 19 segments the LCh1 cap cell often migrates towards the LCh5 LA cell and then turns ventrally after contact with the LA cell and cap cell morphology is abnormal. Similar phenotypes are seen with the migrating VChB cap cell, where in 18 out of 72 mutant segments it does not reach or attach to the LA cell.

fra3 homozygous embryonic heart cardioblasts show significant decreases in migration velocity, as well as in filopodial and lamellopodial extensions and activities, as compared to controls; these are associated with gaps in the leading edge (and lost adhesions with ipsilateral partners), cell clumping, improper linear alignment of the cardioblasts, and embryonic heart lumen formation defects, as compared to controls. fra3 heterozygous cardioblasts also show a significant decrease in migration velocity and filopodial activity, but not in lamellopodial activity, as compared to controls.

fra3/fra4 embryos show thinning of commissures in the central nervous system, with the EW axons failing to cross the midline in 30% of abdominal segments.

fra3/fra6 stage 15 embryos exhibit defects in EW midline axon crossing.

fra3/Df(2R)BSC3 mutants exhibit EW axon midline crossing defects in over 30% of segments.

fra3 mutants exhibit defects in axon guidance. Posterior commissures are thin or absent and occasional breaks in longitudinal connectives occur.

fra3/Df(2R)vg135 embryos exhibit defects in midline crossing in eg-positive axons (EW neurons).

fra3/fra4 mutants exhibit defects in Fas2-positive axons, including occasional breaks in longitudinal pathways, although the fascicles always remain ipsilateral.

EW axons in fra3/fra6 hypomorphic mutants fail to cross in ~20% of segments.

Approximately 88.7% of the R8 axons in fra3 mutant eye clones exhibit strong projection defects: 56.2% stall at the medulla neuropil border, while 32.5% terminate prematurely at the more distal layers M1 and M2. In contrast, ganglion-specific targeting of R1-R6 axons to the lamina and layer-specific targeting of R7 axons to the M6 layer appear unaffected.

In Scer\GAL80ey.3.5 fra3 eye mosaics, a small proportion of fra mutant R8 axons at 24 hours (12%) and 42 hours (6.2%) proceed prematurely into the neuropil located between R8 and R7 growth cones. At 55 hours, the majority of mutant R8 axons stall at the medulla neuropil border (91%).

fra3/fra4 mutants exhibit virtually complete loss of C4da neuron commissural fascicles. Furthermore the terminal processes of C4da axons in fra3/fra4 mutants appear to lose the asymmetric orientation towards the midline.

fra3/fra4 embryos display display commissure loss. One of the predominant defects in fra3/fra4 mutants is thinning and missing posterior commissures, with nearly a quarter of segments showing this defect.

Fas2-positive fascicles tend to fuse together or form small gaps in fra3/fra4 embryos.

Some hemisegments in fra3/fra4 embryos have ectopic glial cell clusters in the dorsal periphery. These ectopic clusters correspond to misplaced interface glia.

Single cell robo1 leg motoneuron clones induced 48 hr after hatching have the following phenotypes: the posterior dendritic branch fails to approach and cross the midline; there is an increase in dendritic arborization in the lateral regions of the neuropil; the mean centre of mass is shifted away from the midline compared to controls; the mean 33rd percentile of arborization is shifted away from the midline.

Single cell robo1 leg motoneuron clones induced 96 hr after hatching do not show a major change in position of their dendrites.

In fra3/fra4 mutant embryos, dendritic targeting to the midline is abolished in MN-VO4-6 and MN-VO4/5 projecting-neurons.

In fra3/fra4 mutant embryos, 63% of MN-LL1 dendritic arbors lack the normally pronounced intermediate dendritic arborisation, while targeting of MN-DA3 dendrites is not significantly affected. MN-LL1 has a clearly reduced innervation of the intermediate neuropile in 63-64% of cases.

26% of fra3/fra4 embryos show defects in axon guidance in the Bolwig's nerve.

fra3/fra4 embryos show defects in the commissures of the central nervous system; 2% of anterior commissures are absent, 4% of anterior commissures are thin, 3% of posterior commissures are absent and 8% of posterior commissures are thin. 8% of segments fail to separate the anterior and posterior commissures correctly.

EW axons frequently fail to cross the midline in fra3/fra4 mutant embryos. The trajectories of the EG axons are unaffected in these mutants.

fra3/fra4 transheterozygote embryos show salivary gland guidance defects. Most mutants have salivary glands that lie parallel to the CNS midline as in wild type. However, in 4% of mutants, the glands curve laterally away from the midline and in 2% of mutants, the glands curve medially toward the midline.

fra3/fra4 embryos exhibit breaks in Con-positive commissural axons and longitudinal tracts.

dMP2 axons make pathfinding errors in fra3/fra4 mutant embryos, often extending laterally, turning anteriorly or stalling. Expression of fraΔC.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4605 in fra3/fra4 embryos results in abnormal spreading of the dMP2 growth cone over the region of induced ectopic NetB accumulation.

The RP3 axon extends dorsally past and just adjacent to muscles 7 and 6 and then reached back to innervate them. RP3 neuron may extend into its normal muscle domain but fail to innervate muscles 7 and 6. The ISNb fails to innervate muscles 7 and 6.

Commissural axons are absent or reduced in number and gaps appear in the longitudinal axon tracts. In fra3/fra4 embryos 12% of anterior commissures and 43% of posterior commissures in abdominal segments A1-A7 are thin or absent. Commissures that appear to have normal thickness are often less well organised than normal. Occasional breaks are also observed in the longitudinal tracts. A subset of motor axons exit the ventral CNS in the intersegmental nerve and extend dorsally, in fra3/fra4 embryos the axons often extend a colateral branch into an adjacent segment or make inappropriate contacts with dorsal muscles when they reach the dorsal muscle region.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
NOT Enhanced by
Statement
Reference
Suppressed by
NOT suppressed by
Enhancer of
Statement
Reference

fra3, Df(1)NP5, fra[+], + is an enhancer of abnormal neuroanatomy phenotype of Trim946

NOT Enhancer of
Suppressor of
NOT Suppressor of
Other
Phenotype Manifest In
Enhanced by
Statement
Reference

fra3 has embryonic heart cardioblast phenotype, enhanceable by robo11/robo1[+]

fra3 has filopodium | embryonic stage phenotype, enhanceable by robo11/robo1[+]

fra3 has lamellipodium | embryonic stage phenotype, enhanceable by robo11/robo1[+]

fra3 has embryonic heart cardioblast phenotype, enhanceable by Dscam1[+]/Dscam11

fra3 has filopodium | embryonic stage phenotype, enhanceable by Dscam1[+]/Dscam11

fra3/fra4 has EW neuron phenotype, enhanceable by robo2X123/robo2x135

fra6/fra3 has EW neuron phenotype, enhanceable by Abl1/Abl[+]

fra6/fra3 has symmetrical commissure phenotype, enhanceable by Abl1/Abl[+]

fra6/fra3 has EW neuron phenotype, enhanceable by Abl2/Abl[+]

fra6/fra3 has symmetrical commissure phenotype, enhanceable by Abl2/Abl[+]

fra6/fra3 has EW neuron phenotype, enhanceable by Abl4/Abl[+]

fra6/fra3 has symmetrical commissure phenotype, enhanceable by Abl4/Abl[+]

fra3 has EW neuron phenotype, enhanceable by drl[+]/drlR343

NOT Enhanced by
Statement
Reference

Df(2R)BSC3/fra3 has EW neuron phenotype, non-enhanceable by Abl1/Abl[+]

Df(2R)BSC3/fra3 has symmetrical commissure phenotype, non-enhanceable by Abl1/Abl[+]

fra6/fra3 has EW neuron phenotype, non-enhanceable by unc-5[+]/unc-52

fra6/fra3 has larval posterior commissure phenotype, non-enhanceable by unc-5[+]/unc-52

fra6/fra3 has larval longitudinal connective phenotype, non-enhanceable by unc-5[+]/unc-52

fra6/fra3 has EW neuron phenotype, non-enhanceable by drlR343

fra6/fra3 has EW neuron phenotype, non-enhanceable by drl[+]/drlR343

fra6/fra3 has larval posterior commissure phenotype, non-enhanceable by drl[+]/drlR343

Suppressed by
Statement
Reference

fra3 has embryonic heart cardioblast phenotype, suppressible by robo11/robo1[+]

fra6/fra3 has EW neuron phenotype, suppressible by Src64B[+]/Src64Bko

fra6/fra3 has larval posterior commissure phenotype, suppressible by Src64B[+]/Src64Bko

NOT suppressed by
Statement
Reference

Df(2R)BSC3/fra3 has EW neuron phenotype, non-suppressible by Abl1/Abl[+]

Df(2R)BSC3/fra3 has symmetrical commissure phenotype, non-suppressible by Abl1/Abl[+]

fra6/fra3 has EW neuron phenotype, non-suppressible by unc-5[+]/unc-52

fra6/fra3 has larval posterior commissure phenotype, non-suppressible by unc-5[+]/unc-52

fra6/fra3 has larval longitudinal connective phenotype, non-suppressible by unc-5[+]/unc-52

fra6/fra3 has EW neuron phenotype, non-suppressible by drlR343

fra6/fra3 has EW neuron phenotype, non-suppressible by drl[+]/drlR343

fra6/fra3 has larval posterior commissure phenotype, non-suppressible by drl[+]/drlR343

Enhancer of
Statement
Reference

fra3/fra[+] is an enhancer of filopodium | embryonic stage phenotype of robo11

fra3/fra[+] is an enhancer of lamellipodium | embryonic stage phenotype of robo11

fra3/fra[+] is an enhancer of filopodium | embryonic stage phenotype of Dscam11

fra3/fra[+] is an enhancer of filopodium | embryonic stage phenotype of Dscam105518/Dscam11

fra3, Df(1)NP5, fra[+], + is an enhancer of dopaminergic neuron phenotype of Trim946

robo[+], fra3, robo11, fra[+] is an enhancer of commissure phenotype of Trim946

NOT Enhancer of
Suppressor of
NOT Suppressor of
Other
Additional Comments
Genetic Interactions
Statement
Reference

The decreased filopodial and lamellopodial activities, but not the slow migration, displayed by fra3 homozygous embryonic heart cardioblasts are partially suppressed by the expression of robo1Scer\UAS.cKa under the control of Scer\GAL4Mef2.247; the associated embryonic heart lumen formation defects observed in fra3 homozygotes are also partially suppressed by the expression of robo1Scer\UAS.cKa.

fra3, robo11 double heterozygotes show a more severe decrease in filopodial activity compared to either single heterozygote conditions and a more severe decrease in lamellopodial activity compared to robo11 heterozygotes, but do not show significant changes in migration velocity compared to wild-type controls. Dscam11, fra3 double heterozygotes show a severe decrease in lamellopodial activity compared to wild-type controls and a more severe decrease in filopodial activity compared to either single heterozygote conditions, but do not show significant changes in migration velocity compared to wild-type controls.

The decreased filopodial and lamellopodial activities, but not the decreased migration velocity, observed in Dscam11/Dscam105518 transheterozygous embryonic heart cardioblasts are enhanced by fra3 heterozygosity.

robo2X123/robo2x135 strongly enhances the midline crossing defects seen in fra3/fra4 embryos: approximately 70% of EW neurons fail to cross the midline in the double mutant embryos.

An Abl1/+ heterozygous background enhances the EW axon midline crossing defects seen in fra3/fra6 stage 15 embryos.

An Abl2/+ heterozygous background enhances the EW axon midline crossing defects seen in fra3/fra6 stage 15 embryos. However, the addition of AblK417N.Scer\UAS or AblK417N.Scer\UAS.T:Avic\GFP (under the control of Scer\GAL4eg-Mz360) to these embryos reduces the percentage of segments affected with EW midline crossing defects.

An Abl4/+ heterozygous background enhances the EW axon midline crossing defects seen in fra3/fra6 stage 15 embryos. However, the addition of AblK417N.Scer\UAS or AblK417N.Scer\UAS.T:Avic\GFP (under the control of Scer\GAL4eg-Mz360) to these embryos significantly reduces the percentage of segments affected with EW midline crossing defects.

An Abl1/+ heterozygous background fails to significantly affect the level of EW axon midline crossing defects seen in fra3/Df(2R)BSC3 stage 15 embryos.

A Src64Bko heterozygous background suppresses the EW axon midline crossing defects found in fra3/fra6 hypomorphic mutants.

Co-expression of Src64BYF.Scer\UAS under the control of Scer\GAL4eg-Mz360 enhances the EW axon midline crossing defects found in fra3/fra6 hypomorphic mutants.

An unc-52 heterozygous background does not affect the level EW axon midline crossing defects found in fra3/fra6 hypomorphic mutants.

A drlR343 homo or heterozygous background does not affect the level EW axon midline crossing defects found in fra3/fra6 hypomorphic mutants.

A drlR343 heterozygous background enhances the percentage of fra3 mutant embryonic segments containing EW axon crossing defects.

Expression of Trim9Scer\UAS.cSa under the control of Scer\GAL4ppk.1.9 fails to suppress the fra3 mutant phenotype.

The Trim946 axon midline crossing phenotype is significantly enhanced in a Df(1)NP5 and fra3 heterozygous background.

Over-expression of AblScer\UAS.cHa using Scer\GAL4insc-Mz1407 enhances the degree of thinning and missing posterior commissures in fra3/fra4 embryos, and many anterior commissures disappear. Large bundles of axons are observed ectopically exiting the central nervous system (CNS), often extending beyond the CNS/PNS boundary.

A rare commissure may be malformed in heterozygous fra3 embryos expressing Scer\GAL4insc-Mz1407>AblScer\UAS.cHa.

Pan-neural expression of AblKN.Scer\UAS under the control of Scer\GAL4insc-Mz1407 in fra3 heterozygotes has no embryonic commissural phenotype.

Pan-neural expression of AblKN.Scer\UAS under the control of Scer\GAL4insc-Mz1407 in fra3/fra4 embryos significantly increases the frequency of thin and missing posterior commissure defects.

Commissure formation is restored in fra3/fra4 mutants expressing both fraΔP1.Scer\UAS and AblScer\UAS.cHa under the control of Scer\GAL4insc-Mz1407.

Commissure formation is restored in fra3/fra4 mutants expressing both fraΔP2.Scer\UAS and AblScer\UAS.cHa under the control of Scer\GAL4insc-Mz1407.

Commissure formation is restored in fra3/fra4 mutants expressing both fraΔP3.Scer\UAS and AblScer\UAS.cHa under the control of Scer\GAL4insc-Mz1407.

Nearly a third of hemi-segments in fra3/fra4 embryos expressing Scer\GAL4insc-Mz1407>AblScer\UAS.cHa exhibit defects characterised by Fas2-positive axons ectopically exiting the central nervous system (CNS).

Less than 10% of fra3/fra4 embryos expressing Scer\GAL4insc-Mz1407>AblKN.Scer\UAS exhibit defects characterised by Fas2-positive axons ectopically exiting the central nervous system (CNS).

fra3/fra4 Dscam3c02826 embryos show defects in the commissures of the central nervous system; 2% of anterior commissures are absent, 3% of anterior commissures are thin, 1% of posterior commissures are absent and 9% of posterior commissures are thin. 48% of segments fail to separate the anterior and posterior commissures correctly.

Expression of fra::roboScer\UAS.FΔC.T:Hsap\MYCunder the control of Scer\GAL4elav.PLu fails to rescue the fra3/fra4 axon guidance phenotypes.

Approximately 58% of fra3/Df(2R)en-SFX31 double mutants exhibit defects in axonal pathfinding. Stage 15 embryos display dramatic defects in ventral nerve cord architecture, with the posterior commissures missing or fused with the anterior commissures, and longitudinal tracts thinner. Nearly all the segments are affected in these embryos.

Approximately 42.1% of fra3/Df(2R)en-SFX31 double mutants are adult lethal.

fra3 strongly suppresses the dMP2 axon misprojection phenotype seen in homozygous robo1 embryos, reducing the penetrance of the contralateral misprojection along the anterior commissure of the next segment from 99% to 24%. Expression of fraΔC.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4insc-Mz1407, but not under the control of Scer\GAL415J2, restores the aberrant midline-crossing phenotype in these animals.

The pCC and vMP2 midline-crossing phenotypes seen in homozygous robo1 embryos are partially and strongly suppressed by fra3 respectively. Expression of fraΔC.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4605 restores the aberrant midline-crossing phenotype in these animals.

In mewM6/Y; fra3/fra4 double mutant embryos, the misguided salivary gland phenotype is modified, compared to that of each single mutant. Like fra3/fra4 mutants, the majority (75%) of misguided glands curve laterally, but levels of penetrance are high, similar to mewM6/Y single mutants. In sli2; fra3/fra4 double mutants, the penetrance of the salivary gland guidance defects is by 40% compared to sli2 single mutants.

A reduction in midline crossing is observed upon removal of two copies of the fra gene in Scer\GAL4elav-C155/Gα49BQ203L.Scer\UAS;fra3/fra4, from 48.10% of abdominal segments exhibiting midline crossover in Scer\GAL4elav-C155/Gα49BQ203L.Scer\UAS embryos to 5.3% in Scer\GAL4elav-C155/Gα49BQ203L.Scer\UAS;fra3/fra4 mutant embryos. Embryos of the genotype Scer\GAL4elav-C155/Gα49BQ203L.Scer\UAS and fra3/fra4 exhibit breaks in Con-positive commissural axons and longitudinal tracts, similar to Scer\GAL4elav-C155/Gα49BQ203L.Scer\UAS; fra3/fra4 embryos, indicating that Gα49B does not have an effect on the fra mutant phenotype.

Expression of NetBScer\UAS.cHa under the control of Scer\GAL4605 in fra3/fra4 embryos results in abnormal spreading of the dMP2 growth cone over the region of ectopic NetB expression.

Scer\GAL4how-24B-mediated expression of NetAScer\UAS.cHa or NetBScer\UAS.cHa allows the axons of the transverse nerve to ectopically innervate muscles 7 and 6, loss of fra function suppresses this phenotype.

Xenogenetic Interactions
Statement
Reference

Expression of Rnor\DccScer\UAS.T:Hsap\MYC under the control of Scer\GAL4eg-Mz360 rescues the EW commissural axon defects seen in fra3/Df(2R)vg135 embryos.

Expression of Rnor\DccScer\UAS.T:Hsap\MYC under the control of Scer\GAL4eg-Mz360 rescues the midline crossing defects found in EW neurons in fra3/fra4 mutants.

Expression of Rnor\DccY1418F.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4eg-Mz360 rescues the midline crossing defects found in EW neurons in fra3/fra4 mutants.

Expression of Rnor\DccY1418F.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4eg-Mz360 rescues the EW commissural axon defects seen in fra3/Df(2R)vg135 embryos.

Pan-neuronal expression of Rnor\DccScer\UAS.T:Hsap\MYC (under the control of Scer\GAL4elav.PLu) does not rescue the motor guidance defects or longitudinal connective defects found in fra3 mutants and only mildly rescues the commissural guidance phenotype.

Over-expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS using Scer\GAL4insc-Mz1407 enhances the degree of thinning and missing posterior commissures in fra3/fra4 embryos, and many anterior commissures disappear. Large bundles of axons are observed ectopically exiting the central nervous system (CNS), often extending beyond the CNS/PNS boundary. The anterior commissures, which are virtually unaffected in fra3/fra4 embryos, are thin or missing in 41% of segments.

Fuzzy commissures remain evident in heterozygous fra3 embryos expressing Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS under the control of Scer\GAL4insc-Mz1407.

Re-expression of fraScer\UAS.cKa in fra3/fra4 mutants reverts the phenotype back to that seen when Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS is expressed alone under the control of Scer\GAL4insc-Mz1407 : fuzzy commissures.

Re-expression of fraScer\UAS.cKa in fra3/fra4 mutants reverts the phenotype back to that seen when AblScer\UAS.cHa is expressed alone under the control of Scer\GAL4insc-Mz1407 : normal anterior and posterior commissure formation.

In fra3/fra4 mutants expressing Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS, expression of fraΔP1.Scer\UAS is able tor revert the commissure loss seen in fra3/fra4 mutants. These mutants display fuzzy commissures.

In fra3/fra4 mutants expressing Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS, expression of fraΔP2.Scer\UAS is able tor revert the commissure loss seen in fra3/fra4 mutants. These mutants display fuzzy commissures.

In fra3/fra4 mutants expressing Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS, expression of fraΔP3.Scer\UAS restores commissure formation in fra3/fra4 mutants. The frequency of fuzzy commissures is also significantly reduced.

fra3/fra4 significantly reduces the frequency of ectopic axonal midline-crossovers resulting from the expression of Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS.

fra3/fra4 fails to reduce the frequency of ectopic axonal midline-crossovers resulting from the expression of Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS when fraScer\UAS.cKa is co-expressed.

fra3/fra4 fails to reduce the frequency of ectopic axonal midline-crossovers resulting from the expression of Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS when fraΔP1.Scer\UAS is co-expressed.

fra3/fra4 fails to reduce the frequency of ectopic axonal midline-crossovers resulting from the expression of Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS when fraΔP2.Scer\UAS is co-expressed.

fra3/fra4 significantly reduces the frequency of ectopic axonal midline-crossovers resulting from the expression of Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS when fraΔP3.Scer\UAS is co-expressed.

Nearly a third of hemi-segments in fra3/fra4 embryos expressing Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS exhibit defects characterised by Fas2-positive axons ectopically exiting the central nervous system (CNS).

The midline crossover phenotype caused expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng is completely suppressed by fra3/+.

Complementation and Rescue Data
Partially rescued by
Comments

The fra3 homozygous embryonic heart cardioblast defects (i.e. migration velocity and in filopodial and lamellopodial extensions and activities) and embryonic heart lumen formation defects are rescued by the expression of fraScer\UAS.cKa under the control of Scer\GAL4Mef2.247.

Expression of fraScer\UAS.cOa.T:Hsap\MYC under the control of Scer\GAL4eg-Mz360 rescues the EW commissural axon defects seen in fra3/Df(2R)vg135 embryos.

Expression of fraScer\UAS.cOa.T:Hsap\MYC in all neurons, through expression under the control of Scer\GAL4elav.PLu, rescues EW midline crossing defects in fra3/fra4 mutants.

Pan-neuronal expression of fraScer\UAS.cOa.T:Hsap\MYC (under the control of Scer\GAL4elav.PLu) rescues both the commissural and longitudinal axon defects found in fra3 mutants.

Pan-neuronal expression of fra9YF.Scer\UAS.T:Hsap\MYC (under the control of Scer\GAL4elav.PLu) rescues both the commissural and longitudinal axon defects found in fra3 mutants.

Expression of fraScer\UAS.cOa.T:Hsap\MYC in all neurons, through expression under the control of Scer\GAL4elav.PLu, fully rescues fra3 commissural axon defects.

Expression of fra9YF.Scer\UAS.T:Hsap\MYC in all neurons, through expression under the control of Scer\GAL4elav.PLu, fully rescues fra3 commissural axon defects.

Expression of fra9YF.Scer\UAS.T:Hsap\MYC in all neurons, through expression under the control of Scer\GAL4elav.PLu, rescues EW midline crossing defects in fra3/fra4 mutants.

Expression of fraScer\UAS.cKa in C4da neurons under the control of Scer\GAL4ppk.PG partially rescues the axonal defects seen in fra3/fra4 mutants.

Expression of fraScer\UAS.cKa under the control of Scer\GAL4gcm.PU rescues the defects in interface glial cell migration seen in fra3/fra4 embryos.

Expression of fraScer\UAS.cKa under the control of Scer\GAL4MZ1580 weakly rescues the defects in interface glial cell migration seen in fra3/fra4 embryos.

The defects in interface glial cell migration seen in fra3/fra4 embryos are not rescued by expression of fraScer\UAS.cKa under the control of any one of Scer\GAL4repo, Scer\GAL4pros.PMG, Scer\GAL4elav.PU or Scer\GAL4Mz605.

Expression of fraScer\UAS.cKa under the control of Scer\GAL4eve.CQ2 rescues dendritic targeting to the midline in fra3/fra4 mutant MN-VO4-6 and MN-VO4/5 neurons.

Expression of fraScer\UAS.cKa under the control of Scer\GAL4eve.CQ2 selectively in MN-LL1 neurons in fra3/fra4 mutant embryos efficiently rescues dendritic targeting to the intermediate neuropile. Moreover, this manipulation leads to a greater proportion of dendritic branches innervating the intermediate neuropile.

Expression of fraScer\UAS.T:Hsap\MYC under the control of Scer\GAL4eg-Mz360 cell-autonomously rescues the EW guidance defects of fra3/fra4 embryos.

Expression of fraScer\UAS.T:Ivir\HA under the control of Scer\GAL4eg-Mz360 cell-autonomously rescues the EW guidance defects of fra3/fra4 embryos.

Expression of fraScer\UAS.cKa under the control of Scer\GAL415J2 does not rescue the dMP2 axonal phenotype of fra3/fra4 embryos. Expression of fraScer\UAS.cKa under the control of Scer\GAL4605 does rescue the dMP2 axonal phenotype of fra3/fra4 embryos.

Scer\GAL41407 induced expression of fraScer\UAS.cKa in fra3/fra4 embryos rescues the commissure phenotype, commissures form normally in abdominal segments A1-A7. ISN motor axons also innervate their targets at near wild type levels. Scer\GAL4how-24B induced expression of fraScer\UAS.cKa in fra3/fra4 embryos fails to rescue the ISN motor axon defects.

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References (34)