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General Information
Symbol
Dmel\CblF165
Species
D. melanogaster
Name
FlyBase ID
FBal0118589
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
D-cblF165
Key Links
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Nucleotide change:

C8425654T

Reported nucleotide change:

C?T

Amino acid change:

Q116term | Cbl-PA; Q116term | Cbl-PB

Reported amino acid change:

Q116term

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

Amino acid replacement: Q116term.

Nucleotide substitution: C?T.

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
Detailed Description
Statement
Reference

CblF165 heterozygote adult females do not display any defects in the number of cytoophidia (CTPsyn filaments) in the egg chambers (when kept at 29[o]C) or in DNA replication (measured by BrdU incorporation) in stage 9 egg chambers compared to respective controls.

Majority of follicle cells in CblF165 homozygous somatic clones display significantly reduced number or complete absence of cytoophidia (CTPsyn filaments) in stage 9 and 10 egg chambers compared to controls. However, the cytoophidia are maintained as normal in CblF165 mutant clones in younger egg chambers - before stage 6 and still in the mitotic stages of their development and the macro-cytoophidia in germline clone cells are also not affected. Decrease in cytoophidia numbers is also observed CblF165/CblF165 somatic clones in salivary glands of third instar larvae.

Follicle cells in CblBB28 homozygous mutant somatic clones display endocycle defects in stage 9 and 10A (but not 10B) egg chambers: the number of cells in S-phase (BrdU positive) is significantly decreased compared to controls.

CblF165 homozygous third instar larvae are of a normal size but their salivary glands are smaller and display endocycle defects (measured by BrdU incorporation) compared to wild-type. However, average nuclear size of cells in CblF165 somatic clones (both in salivary glands in third instar larvae and follicle cells in adult females) is not significantly changed compared to twin clone controls.

CblF165 heterozyous ovaries do not exhibit any abnormalities.

CblF165 mutant cells are preferentially located at the front of the cluster during border cell posterior and dorsal migration in mosaic border cell clusters consisting of both wild-type and mutant cells.

Border follicle cells are correctly specified in somatic clones of CblF165 homozygous cells but their migration is severely defective and sometimes fails completely. However, around 50% of migrating clusters do eventually reach the oocyte.

Females containing somatic clones of CblF165 induced in the follicle cells produce dorsalised embryos and egg shells; in some cases egg shells with two dorsal appendages positioned further apart than normal are produced (characteristic of a weakly dorsalised phenotype), and partially or completely dorsalised embryos are produced as evidenced by the loss of ventrally derived structures. Only clones at ventral positions within the follicle cell epithelium result in a dorsalised embryo phenotype, such as a missing head skeleton, reduction of ventral structures (such as denticle belts) in the thoracic and anterior abdominal segments and a twisted embryo. Clones that are confined to the dorsal half of the follicle epithelium do not produce a visible embryonic mutant phenotype. When dorsolateral follicle cells are homozygous for CblF165, dorsal appendages are shifted to more lateral positions than normal. When more lateral cells (adjacent to the dorsal appendages) are homozygous for CblF165, extra or wider dorsal appendages are produced. Somatic clones of CblF165 induced in the wing result in an extra vein phenotype. Embryos lacking both maternal and zygotic Cbl function (derived from homozygous germline clones) have a distinct head defect. Zygotic Cbl function is able to rescue the maternal lack of Cbl function, resulting in normal embryos that hatch.

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

CblF165 is a non-suppressor of visible phenotype of CanBGMR.PS, Pp2B-14Dact.GMR

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

CblF165 is a non-enhancer of eye phenotype of CanBGMR.PS, Pp2B-14Dact.GMR

Suppressor of
Statement
Reference

CblF165 is a suppressor | somatic clone of eye disc phenotype of Rbf120a

CblF165/Cbl[+] is a suppressor of nurse cell phenotype of Fmr13

CblF165/Cbl[+] is a suppressor | partially of nurse cell | increased number phenotype of Fmr13

CblF165/Cbl[+] is a suppressor | partially of nurse cell phenotype of Fmr1Δ50M/Fmr13

NOT Suppressor of
Statement
Reference

CblF165/Cbl[+] is a non-suppressor of nurse cell | increased number phenotype of Fmr1Δ50M/Fmr13

CblF165 is a non-suppressor of eye phenotype of CanBGMR.PS, Pp2B-14Dact.GMR

Other
Additional Comments
Genetic Interactions
Statement
Reference

The number of cytoophidia (CTPsyn filaments) in the egg chambers of adult Prosβ61,CblF165 double heterozygote females is significantly reduced compared to either Prosβ61 or CblF165 single heterozygotes.

About a fifth of eggs laid by CblF165 heterozygous females expressing CTPsynGD4740 under the control of Scer\GAL4CY2 has a defective collapsed phenotype that is not observed in eggs laid by CblF165/+ flies.

The loss of cytoophidia (CTPsyn filaments) observed in somatic clones of CblF165 homozygous mutant follicle cells is not suppressed by expression of CTPsynScer\UAS.T:Zzzz\FLAG under the control of Scer\GAL4hs.PU in the clones, although the CTPsynScer\UAS.T:Zzzz\FLAG protein can be incorporated in the cytoophidia filament structure together with endogenous CTPsyn protein in wild-type cells.

The loss of cytoophidia observed in somatic clones of CblF165 homozygous mutant follicle cells is suppressed by expression of CTPsynC399G.Scer\UAS.T:Zzzz\FLAG under the control of Scer\GAL4hs.PU in the clones, although the CTPsynC399G.Scer\UAS.T:Zzzz\FLAG protein cannot be incorporated in the cytoophidia filament structure together with endogenous CTPsyn protein in wild-type cells.

The endocycle defects (decrease in DNA replication measured by BrdU incorporation) seen in somatic clones of CblF165 homozygous mutant follicle cells is partially suppressed by expression of CTPsynScer\UAS.T:Zzzz\FLAG but not suppressed by expression of CTPsynC399G.Scer\UAS.T:Zzzz\FLAG under the control of Scer\GAL4hs.PU in the clones.

The decrease in percentage of follicle cells undergoing DNA replication (measured by BrdU incorporation) observed in stage 9 egg chambers as well as the decreased follicle cell nuclear size in stage 10A egg chamber expressing CTPsynGD4740 under the control of Scer\GAL4CY2 is further decreased by combination with CblF165 in heterozygous state.

The generation of CblF165 mutant eye disc clones suppresses the amount of cell death seen in Rbf120a mutant eye discs.

CblF165/+ enhances the mis-patterning of interommatidial precursor cells, primary primary pigment cells and cone cells caused by co-expression of cindrdsRNA.Scer\UAS and cindrdsRNA.PC.PD.Scer\UAS under the control of Scer\GAL4GMR.PF.

CblF165 is a dominant suppressor of the germ cell proliferation defects in Fmr13 and Fmr13/Fmr1Δ50M mutant ovaries.

The fewer germ cell phenotype in Fmr13 mutant ovaries is completely suppressed by CblF165/+, while the supernumerary germ cell phenotype is suppressed 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 loss of photoreceptor cells seen in homozygous mopT612 clones in the eye disc is rescued if the clones are also homozygous for CblF165.

Defective migration of border follicle cells in CblF165 homozygous somatic clones is suppressed by grkunspecified/+ but enhanced by EgfrScer\UAS.cBa or PvrScer\UAS.cDa with Scer\GAL4slbo.2.6.

spri6G1/spri6G1 also enhances the migration defects seen in border follicle cells in CblF165 homozygous somatic clones. I these animals, border follicle cell clusters rarely reach the oocyte.

Expression of Socs36EScer\UAS.P\T.cCa under the control of Scer\GAL4en-e16E in a CblF165/+ background results in a partial rescue of the Socs36EScer\UAS.P\T.cCa anterior crossvein phenotype, with a reduction in penetrance from 95 to 48%. The penetrance of the outstretched wing phenotype of Scer\GAL4ap-md544>Socs36EScer\UAS.P\T.cCa flies is reduced from 82 to 54% when flies have a CblF165/+ background.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by

CblF165 is partially rescued by CblS.Hsp83

CblF165 is partially rescued by CblS.Hsp83

CblF165 is partially rescued by CblL.mPR.Hsp83

CblF165 is partially rescued by CblL.mPR.Hsp83

Comments

Expression of either CblL.mPR.Hsp83 or CblS.Hsp83 in the follicle cell somatic clones homozygous for CblF165 partially rescues the loss of cytoophidia in stage 9 egg chambers - the proportion of cells completely lacking cytoophidia is significantly decreased.

Expression of either CblS.Δ70Z.Hsp83 or CblL.Δ70Z.Hsp83 in the follicle cell somatic clones homozygous for CblF165 does not rescues the loss of cytoophidia (CTPsyn filaments) in stage 9 egg chambers.

Expression of CblL.mPR.Hsp83 rescues the lethality of CblF165, and 75-80% of animals develop to adults.

Expression of CblL.Δ70Z.Hsp83 fails to rescue CblF165.

Lethality due to CblF165/CblF165 is rescued by CblS.αTub84B.PJ or CblL.αTub84B.PJ as is the border cell migration defect seen in CblF165 homozygous somatic clones. In contrast, CblC369A.SαTub84B.PJ fails to rescue either of these phenotypes.

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Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
References (18)