FB2025_01 , released February 20, 2025
Allele: Dmel\scrib673
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General Information
Symbol
Dmel\scrib673
Species
D. melanogaster
Name
FlyBase ID
FBal0103576
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
scrib2, l(3)673
Key Links
Nature of the Allele
Progenitor genotype
Cytology
Description
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 1 )
Modifiers Based on Experimental Evidence ( 1 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

scrib673 mutant eye disc clones are neoplastically transformed.

Homozygous clones in the eye-antennal disc results in defects in disc morphology and differentiation. Most of these animals die as pupae, and the few adult escapers are eyeless.

Stage 11 embryos lacking both maternal and zygotic scrib673 exhibit lost or severely disrupted tubule cell polarity.

Mutant eye discs (generated using the eyFLP-cell lethal system) show disorganised cellular architecture and reduced differentiation compared to wild type.

Animals containing mutant eye discs generated using the eyFLP-cell lethal system die as pharate adults without heads. Larvae containing these discs are increased in size compared to control larvae when examined as pupariation commences.

Cells from scrib673 wing discs are round (rather than elongated as in wild type) and have a multilayered organisation (rather than monolayered as in wild type), forming a solid spherical mass rather than the flat disc seen in wild type animals.

scrib673 wing discs show a dramatic increase in both the surface area and volume compared to wild type.

Animals with eyes homozygous for scrib673 never eclose, instead dying as headless pharate adults. The eye discs of these animals show disorganised ommatidial preclusters.

Adherens junctions are mislocalized and septate junctions are absent in scrib673 wing discs.

Cells from scribird15/scrib673 transheterozygous wing discs are round (rather than elongated as in wild type) and have a multilayered organisation (rather than monolayered as in wild type), forming a solid spherical mass rather than the flat disc seen in wild type animals.

scribird15/scrib673 transheterozygous wing discs show a dramatic increase in both the surface area and volume compared to wild type and contain approximately 500% more cells than wild type.

Like wild type, cells from scrib882/scrib673 transheterozygous wing discs are arranged in epithelial monolayers and maintain the folded structure of the tissue.

scrib882/scrib673 transheterozygous wing discs show a very slight increase in both the surface area and volume compared to wild type.

Like wild type, cells from scribdt6/scrib673 transheterozygous wing discs are arranged in epithelial monolayers and maintain the folded structure of the tissue. However, these mutant scrib cells show cuboidal rather than columnar morphology.

scribdt6/scrib673 transheterozygous wing discs show an intermediate increase in both the surface area and volume compared to wild type and contain approximately 300% more cells than wild type.

Like wild type, cells from scribdt12/scrib673 transheterozygous wing discs are arranged in epithelial monolayers and maintain the folded structure of the tissue. However, these scribdt12 mutant cells display altered shapes.

scribdt12/scrib673 transheterozygous wing discs show an intermediate increase in both the surface area and volume compared to wild type.

Like wild type, cells from scribdt14/scrib673 transheterozygous wing discs are arranged in epithelial monolayers and maintain the folded structure of the tissue.

scribdt14/scrib673 transheterozygous wing discs show a very slight increase in both the surface area and volume compared to wild type.

scrib1/scrib673 transheterozygous wing discs show a dramatic increase in both the surface area and volume compared to wild type.

Adherens junction formation is normal but septate junctions are severely disrupted in scribdt6/scrib673 transheterozygous wing discs.

Adherens junctions are mislocalized and septate junctions are absent in scrib1/scrib673 transheterozygous wing discs.

When somatic clones are made in the eye disc, ectopic DNA replication and mitoses are seen.

scribsmi97B/scrib673 adults show a significantly lower avoidance response to benzaldehyde compared to controls.

Embryos derived from scrib673 homozygous germline clones and lacking both maternal and zygotic scrib function have a poorly differentiated and convoluted cuticle.

scrib673 and scrib673/Df(3R)Tl-X third instar larvae exhibit a decrease in synaptic bouton size and a statistically significant increase in both vesicle density and basal lamina thickness. They also exhibit a decrease in the number of active zones per cross-sectional area, although this is statistically significant only in scrib673 homozygous boutons. The distribution and density of reserve vesicles (RP) appears to be specifically affected in scrib673/Df(3R)Tl-X mutants, as the number of vesicles up to 200nm around the active zone, which is assumed to encompass the readily-releasable vesicle pool (RRP). scrib673/Df(3R)Tl-X third instar larvae exhibit a significant decrease in the frequency of miniature synaptic events. In addition these larvae exhibit a slight but significant decrease in the amplitude of miniature synaptic events. High frequency stimulation causes scrib673/Df(3R)Tl-X synapses to exhibit both a lack of facilitation at low Ca2+ concentrations and faster synaptic depression at higher Ca2+ concentrations. scrib673/Df(3R)Tl-X mutants exhibit a modest potentiation after a train of high-frequency stimulation (post-tetanic potentiation), in contrast to the amplitude of wild-type excitatory junctional currents, which is potentiated more than twofold after post-tetanic potentiation.

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

scrib[+]/scrib673 is an enhancer of abnormal planar polarity phenotype of Vangstbm-153

scrib[+]/scrib673 is an enhancer of visible phenotype of Scer\GAL4GMR.PF, crbintra.UAS

NOT Enhancer of
Statement
Reference

scrib673 is a non-enhancer of visible phenotype of RetMEN2B.GMR

Suppressor of
Statement
Reference

scrib673 is a suppressor of visible phenotype of RetMEN2A.GMR

scrib[+]/scrib673 is a suppressor of visible phenotype of CycEJP

NOT Suppressor of
Statement
Reference

scrib673 is a non-suppressor of visible phenotype of RetMEN2B.GMR

Other
Statement
Reference
Phenotype Manifest In
Suppressed by
Statement
Reference
NOT suppressed by
Statement
Reference
Enhancer of
Statement
Reference

scrib[+]/scrib673 is an enhancer of egg chamber phenotype of RhoGAP19Dunspecified

scrib[+]/scrib673 is an enhancer of ommatidium phenotype of Vangstbm-153

scrib[+]/scrib673 is an enhancer of eye phenotype of Scer\GAL4GMR.PF, crbintra.UAS

NOT Enhancer of
Statement
Reference

scrib673 is a non-enhancer of eye phenotype of RetMEN2B.GMR

Suppressor of
NOT Suppressor of
Statement
Reference

scrib673 is a non-suppressor of eye phenotype of RetMEN2B.GMR

Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

EyFLP-induced clones that both express Egfr2.A887T.UAS under the control of Scer\GAL4Act.PU and are scrib673/scrib673 form cephalic and gonadal tumors. The gonadal tumors are highly proliferative compared to neighboring control tissue.

Clones homozygous for scrib673 and expressing Ras85DV12.Scer\UAS under the control of Scer\GAL4Act.PU in third instar larval eye-antennal imaginal discs form invasive tumors, which display increased proportions of clone cells entering the cell cycle (but not undergoing mitosis), undergoing apoptosis and presenting mitochondrial defects - i.e., significant increases in the average mass and number of mitochondria per cell, a strong increase in the proportion of burst mitochondria, and a significant increase in the levels of reactive oxygen species, as compared to controls; the presence of these tumor clones also leads to a cell non-autonomous increase in autophagosomes (assessed by a Atg8a fluorescence reporter) in both neighboring disc tissue and distant tissues - i.e. somatic muscles, midgut and fat body - and in significant decreases in the respiratory capacity in both tumor and neighboring disc tissue, as compared to controls.

scrib673-homozygous, Ras85DV12.Scer\UAS-expressing eye-antennal imaginal disc clone tumors are significantly suppressed by Atg13Δ81 homozygosity in clone cells (leading to reductions in the proportions of clone cells entering the cell cycle, but not undergoing mitosis or apoptosis, and leading to a reduction in the tumor size, but not invasiveness), in neighboring disc cells (leading to reductions in the tumor size and in the proportion of cell entering the cell cycle, but not undergoing mitosis or apoptosis), in the full organism except the clone cells (leading to reductions in the tumor size and invasiveness), or in the full organism (leading to reductions in the proportions of cells entering the cell cycle and undergoing mitosis, but not undergoing apoptosis, and leading to reductions in the tumor size and invasiveness); these tumors are also significantly suppressed by Atg14Δ5.2 homozygosity in the neighboring disc cells (leading to a reduction in the tumor size) or by the combination of Atg13Δ81 homozygosity in the tumor cells and Atg14Δ5.2 homozygosity in the neighboring disc cells. One copy of Atg13+tCH322-168O18 in the full organism suppresses the decrease in tumor size, but not invasiveness, resulting from Atg13Δ81 homozygosity in the full organism or in the full organism apart from the clone cells; one copy of Atg13ey.3.5 in the full organism also partially suppresses the decrease in tumor size resulting from Atg13Δ81 homozygosity. These tumors grow to significantly smaller sizes when grafted into the abdomen of either Atg14Δ5.2/Atg14EY14568 transheterozygous adult hosts (but not if the hosts possess one copy of Atg14+tCH322-175F03) or Atg8ad4 homozygous adult hosts, as compared to control hosts.

The cell non-autonomous increase in autophagosomes resulting from the presence of clones homozygous for scrib673 and expressing Ras85DV12.Scer\UAS under the control of Scer\GAL4Act.PU in third instar larval eye-antennal imaginal discs is suppressed by Atg13Δ81 homozygosity in either the full organism (suppression in distant tissues - somatic muscles, midgut and fat body) or in the full organism apart from the clone cells (suppression in neighboring disc tissue), or by the clonal co-expression of either domeΔCYT.Scer\UAS (suppression in neighboring disc tissue) or bskDN.Scer\UAS.cUa (suppression in the midgut, but not in the somatic muscles or the fat body), but not by Stat92E85C9 homozygosity in the full organism apart from the clone cells.

Clones homozygous for scrib673 and expressing Ras85DV12.Scer\UAS under the control of Scer\GAL4tub.PU in third instar larval wing imaginal discs lead to a cell non-autonomous increase in autophagosomes (assessed by a Atg8a fluorescence reporter) in neighboring disc tissue, as compared to controls.

Expression of hthHMS01112 under the control of Scer\GAL4tub.PU suppresses the neoplastic transformation seen in scrib673 mutant eye disc clones.

Expression of Ras85DV12.Scer\UAS under the control of Scer\GAL4Act.PU in clones in the eye-antennal disc (where the clones are also homozygous for scrib673) results in strong tumour growth at 7 days AEL. These animals grow as larvae until 13 days AEL and die before pupation. Co-expression of sds22Scer\UAS.cJa in these clones strongly suppresses the tumour growth phenotype in all clones observed at 7 days AEL and most of these animals can pupate, but die as early pupae.

The eye-antennal disc defects seen in larvae carrying homozygous scrib673 clones and the eye defects seen in adult escapers carrying homozygous scrib673 clones are suppressed by expression of sds22Scer\UAS.cJa under the control of Scer\GAL4Act.PU in the clones.

The cuticle defects observed when bazS980A.Scer\UAS.T:Avic\GFP is expressed under the control of Scer\GAL4arm.PS are strongly suppressed in a scrib673 mutant background.

Heterozygosity for scrib673 enhances the frequency of ommatidia that show planar cell polarity defects in Vangstbm-153 homozygotes.

Expression of hepAct.Scer\UAS in scrib673 mutant clones under the control of Scer\GAL4Act5C.PI suppressed the scrib673 phenotype to revert to an essentially wild-type appearance, without the marked lesions resulting from scrib-deficient tissue. Significantly, these phenotypically rescued eyes do not contain any clonal cells, suggesting that JNK activity (increased by expression of hep) counteracts the outgrowth of scrib1 tissue or causes the removal of the mutant cells. These eyes are the same size as wild-type.

The epithelial defects of crb11A2 embryos are markedly suppressed if the embryos are also mutant for scrib673; continuous patches of cuticle are formed in the double mutant embryos and the xonula adherens resembles that of wild-type embryos.

Embryos lacking both crb and scrib maternal and zygotic function (derived from scrib673 crb2 homozygous germline clones) have a phenotype similar to that of embryos derived from scrib673 homozygous germline clones (lacking scrib maternal and zygotic function). Formation of the zonula adherens is largely rescued in crb2 scrib673 double mutant embryos.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Expression of scribScer\UAS.cBa under the control of Scer\GAL469B fully rescues the cell polarization and disc overgrowth phenotypes of scrib673/scribird15 transheterozygotes.

Expression of scribScer\UAS.P\T.T:Avic\GFP under the control of Scer\GAL469B fully rescues the cell polarization and disc overgrowth phenotypes of scrib673/scribird15 transheterozygotes.

Expression of scribΔLRR.Scer\UAS.P\T.T:Avic\GFP under the control of Scer\GAL469B fails to rescue the cell polarization and disc overgrowth phenotypes of scrib673/scribird15 transheterozygotes.

Expression of scribL223Q.Scer\UAS.P\T.T:Avic\GFP under the control of Scer\GAL469B fails to rescue the cell polarization and disc overgrowth phenotypes of scrib673/scribird15 transheterozygotes.

Expression of scribΔLRR.Scer\UAS.P\T.T:Myr6,T:Avic\GFP under the control of Scer\GAL469B fails to rescue the cell polarization and disc overgrowth phenotypes of scrib673/scribird15 transheterozygotes.

Expression of scrib4.Scer\UAS.P\T.T:Avic\GFP under the control of Scer\GAL469B fully rescues the cell polarization phenotype but only partially rescues the disc overgrowth phenotype of scrib673/scribird15 transheterozygotes.

Expression of scribΔPDZs.Scer\UAS.P\T.T:Avic\GFP under the control of Scer\GAL469B fully rescues the cell polarization phenotype but only partially rescues the disc overgrowth phenotype of scrib673/scribird15 transheterozygotes.

Expression of scribΔPDZ3.4.Scer\UAS.P\T.T:Avic\GFP under the control of Scer\GAL469B fully rescues the cell polarization and disc overgrowth phenotypes of scrib673/scribird15 transheterozygotes.

Expression of scribΔLRR.Scer\UAS.P\T.T:Avic\GFP under the control of Scer\GAL469B fails to rescue the cell polarization and disc overgrowth phenotypes of scrib673/scribdt6 transheterozygotes.

Expression of scribΔLRR.Scer\UAS.P\T.T:Avic\GFP under the control of Scer\GAL469B fails to rescue the cell polarization and disc overgrowth phenotypes of scrib673/scribj7B3 transheterozygotes.

Expression of scribΔLRR.Scer\UAS.P\T.T:Myr6,T:Avic\GFP under the control of Scer\GAL469B fails to rescue the cell polarization and disc overgrowth phenotypes of scrib673/scribdt6 transheterozygotes.

Expression of scribΔLRR.Scer\UAS.P\T.T:Myr6,T:Avic\GFP under the control of Scer\GAL469B fails to rescue the cell polarization and disc overgrowth phenotypes of scrib673/scribj7B3 transheterozygotes.

Co-expression of scribΔLRR.Scer\UAS.P\T.T:Myr6,T:Avic\GFP and scrib<up>ΔPDZs.Scer\UAS.P\T. T:Avic \GFP</up> under the control of Scer\GAL469B fails to rescue the cell polarization and disc overgrowth phenotypes of scrib673/scribird15 transheterozygotes, even when expression levels are increased via raising larvae at 29 oC.

Expression of scrib4.Scer\UAS.P\T.T:Avic\GFP or scribΔPDZs.Scer\UAS.P\T.T:Avic\GFP under the control of Scer\GAL469B provides a more complete rescue of the size phenotype of scrib673/scribdt6 and scrib673/scribj7B3 transheterozygous discs compared to scrib null discs. Increasing the level of transgene expression via raising larvae at 29 oC further increases this rescue. Moreover, the apicolateral enhancement of septate junction markers is restored and cell shape is columnar rather than cuboidal in rescued scrib673/scribdt6 discs.

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Wild-type
Stocks (1)
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External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (8)
References (49)