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General Information
Symbol
Dmel\spiSC1
Species
D. melanogaster
Name
FlyBase ID
FBal0056122
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
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

Photoreceptor differentiation is defective in somatic clones of spiSC1 homozygous cells in the eye disc. This phenotype is rescued if the clones are made in a spiScer\UAS.cSa; Scer\GAL4αTub84B.PL; Scer\GAL80αTub84B.PL background and lack Scer\GAL80αTub84B.PL. However, this rescue is not seen if spiCS.m.Scer\UAS is used in place of spiScer\UAS.cSa.

Homozygous clones in the eye disc undergo less than half as many mitoses as control clones. Dividing cells within the clone are usually next to the boundary with wild-type cells. BrdU incorporation is normal in mutant cells.

Heterozygotes have wild-type wings.

Germline clones reveal no requirement for spi in patterning the egg, or in the viability or patterning of the embryo.

In mutant eye clones the initial single neuron stage ommatidia appear normal, as do their spacing. However no further progression occurs, and the clusters appear to be arrested at the one neuron stage. The wave of DNA synthesis immediately following the furrow is unaffected in spi mutant clones. The early development of the preclusters is normal up until the 5-cell stage. Development proceeds normally anterior to and in the furrow (up to the specification and early differentiation of the founding R8 photoreceptor cells) but the specification of R2 and R5, and all subsequent steps, fail. Homozygous spi mutant clones are apparently equal in size to their homozygous wild-type twin-spots.

Retinal clones induced during first larval instar show defects in the formation of photoreceptor cells R8, R2, R5, R3 and R4.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Other
Statement
Reference
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

In spiSC1; Df(3L)γ3 double mutant somatic clones in the 3rd instar eye disc, photoreceptors R2-R5 undergo G1 arrest, but do not differentiate.

spiSC1 ; Df(3L)γ3; double mutant clones in the eye disc develop similarly to spiSC1 single mutant cells, but occasionally R8 spacing is affected so that twinned R8 cells are seen.

S104E Df(2R)CX1 double heterozygotes show notching of the wing margin.

Dominantly suppresses the ability of Src42ASu(phl)1-1 to suppress the lethality of phl1/Y flies.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Fails to complement
Not rescued by
Comments

Unlike spiScer\UAS.cSa; Scer\GAL4da.G32, spiCS.m.Scer\UAS; Scer\GAL4da.G32 completely fails to rescue lethality due to spi1/spiSC1.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (15)