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General Information
Symbol
Dmel\SCARΔ37
Species
D. melanogaster
Name
FlyBase ID
FBal0150645
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
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
Caused by aberration
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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Bouton numbers are unaffected at the NMJ of SCARΔ37/+ third instar larvae.

SCARΔ37 heterozygous embryos display stalling of the ISNb motor nerve at the junction of muscles 6 and 13, with failure to innervate muscle 12 (observed in 16% of examined hemisegments).

SCARΔ37 mutant clones in the follicular epithelium completely lack actin-rich cellular protrusions, in contrast to wild type controls, but show no defects in the formation or alignment of basal actin bundles.

Gut constriction formation and gut morphology in SCARΔ37 mutant embryos show no defects compared to wild-type.

Homozygous embryos show weak defects in myoblast fusion.

SCARΔ37/+ mutant embryos show no defects in development or survival.

SCARΔ37 mutant follicle cell clones are apically constricted, and adherens junctions appear jagged between mutant cells and between mutant and wild type cells. The phenotypes vary between cells but are most pronounced in stage 11 or older egg chambers.

Eyes homozygous mutant for SCARΔ37 appear rough and display misaligned and fused ommatidia, crater-like intrusions and bent interommatidial bristles. Rhabdomeres appear short and bulky, photoreceptors have fallen through the underlying fenestrated membrane, retina depth is decreased and actin-based cytoskeletal architecture is disturbed.

SCARΔ37 mutant embryos display a duplication of the RP2 neuron in one hemisegment and have one missing in the contralateral segment. A maximum of 15% of the hemisegments are affected.

Homozygous SCARΔ37 embryos exhibit a weak myoblast fusion defect. Unfused myoblasts are visible and muscles appear to be reduced in size in SCARΔ37 mutants. Dorsal closure seems incomplete in these embryos.

Homozygous clones that encompass the morphogenetic furrow do not result in a defect in cell constriction in the morphogenetic furrow.

Homozygous SCARΔ37 mutant embryos exhibit a moderate, but completely penetrant, myoblast fusion defect. Analysis of F-actin foci in zygotic SCARΔ37 mutants reveals a range in foci size from wild-type to enlarged, with an average size of 2.3υm[2]. SCARΔ37 mutants show a dramatic increase in the size and number of actin foci.

Single cell γ neuron mutant clones in the mushroom body do not show axon growth defects.

Mutant embryos show axon defects, including ectopic crossing of the midline by axons and ectopic branching of the intersegmental nerve. Heterozygous larvae have significantly shorter synapses at the neuromuscular junction (96.5 +/- 4.6 μm) compared to wild type (111.1 μm). These synapses do not show abnormal budding.

SCARΔ37 germ-line clones produce multinucleate nurse cells, connected by abnormally small ring canals, that are often occluded. These germ-line clones do produce in fertilisable eggs. The sensory organ pattern in adult heads carrying somatic clones of SCARΔ37 appears wild type, whereas the eye facet arrangement is abnormal, and there is some loss of interommatidial bristles.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Statement
Reference
Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference

SCARΔ37/SCAR[+] is a non-suppressor of neuroanatomy defective | larval stage phenotype of Abl4/Abl1

Other
Phenotype Manifest In
Enhanced by
Enhancer of
Suppressor of
Statement
Reference

SCARΔ37/SCAR[+] is a suppressor of neuromuscular junction & synapse phenotype of Fmr1unspecified

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

SCARΔ37/+;trio123.4/+ or SCARΔ37/+;AbiKO/+ double heterozygous embryos show stalling of the ISNb motor nerve at the junction of muscles 6 and 13 with failure to innervate muscle 12 in 51% and 79% of examined hemisegments, respectively - a strongly increased penetrance compared to any of the single heterozygotes.

SCARΔ37/+ partially suppresses the embryonic lethality and dorsal closure defects seen in embryos expressing crbY10A in a crbGX24w-/crbGX24w- background, resulting in some adults surviving, although these adults show defects in abdominal development.

SCARΔ37/+ does not lead to any dorsal closure defects in embryos expressing crb+tfos in a crbGX24w-/crb11A22 background.

SCARΔ37;Vrp1f06715 double homozygous mutant embryos show normal gut constriction but aberrant morphology. Longitudinal visceral muscle founder cells show aberrant migration and severe muscle fusion defects are observed: mostly mononucleated and binucleated muscle cells are seen at late embryonic stages. These defects are weaker in SCARΔ37/SCARΔ37;Vrp1f06715/+ embryos (founder cell migration mostly normal though fusion defects are still observed) and not much improved in SCARΔ37/+;Vrp1f06715/Vrp1f06715 embryos (both founder cell migration and muscle fusion defects observed).

A SCARΔ37 heterozygous mutant background enhances the actin remodelling and subsequent basolateral invasion of epithelial cells seen in flies expressing CskGD9345 in a stripe of cells at the anterior/posterior boundary of the larval wing disc under the control of Scer\GAL4ptc-559.1.

Pak3del SCARΔ37 double mutant embryos have a more severe myoblast fusion defect than either single mutant.

Heterozygosity for SCARΔ37 suppresses the split microchaete phenotype caused by expression of Abp1Scer\UAS.T:Myr-Src64B,T:Avic\GFP under the control of Scer\GAL4sca.PU.

One copy of SCARΔ37 partially suppresses the cuticle defects seen in α-Cat1 mutant embryos. Embryos show less severe defects on average and a fraction of embryos have normal heads. The phenotype is more severe when SCARΔ37 is introduced maternally rather than paternally.

One copy of SCARΔ37 partially suppresses the cuticle defects seen in arm043A01 mutant embryos.

SCARΔ37/+ increases the fraction of wing cells that have multiple wing hairs in Cip4Δ32/Df(3L)Exel8098 adults.

The increased bouton number per muscle area that is seen at the neuromuscular junction of Abl1/Abl4 larvae is suppressed by SCARΔ37/+.

SCARΔ37 Vrp1f06715 double mutants exhibit a dramatically increased myoblast-fusion defect compared to the single mutants.

A SCARΔ37 heterozygous background enhances the patterning defects found in Scer\GAL4GMR.PF>cindrdsRNA.PC.PD.Scer\UAS mutants. The mean interommatidial precursor cell number and the number of cone and/or 1[o] cell errors is increased in these double mutants.

The extra notopleural bristles induced by expression of AbiScer\UAS.T:Myr1 under the control of Scer\GAL4sca-537.4 are not suppressed by SCARΔ37.

The overgrown synapse phenotype seen at the neuromuscular junction of Fmr1unspecified/+ larvae is suppressed by one copy of SCARΔ37. The reduced synaptic length seen at the neuromuscular junction of Hem03335/+ larvae is not modified by SCARΔ37/+.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
References (33)