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General Information
Symbol
Dmel\spi2
Species
D. melanogaster
Name
FlyBase ID
FBal0016006
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
spiIIT25, spiT25
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
spi2 homozygous embryos exhibit a mild invagination phenotype (approximately 35% of the placodes show an abnormal invagination).
In spi2 stage 15 embryos, the genital disc precursor cells are completely missing.
spi2 mutant embryos have about 23 cells in each Malpighian tubule cell (as opposed to about 125 in wild-type).
The stomatogastric nervous system (SNS) anlage forms normally in mutant embryos. However, the stomodeal invaginations that are seen in wild-type stage 11 embryos are not seen in mutant embryos at this stage. Stage 17 mutant embryos lack SNS ganglia and nerves.
Mutant somatic clones have no effect on the lamina. Clones in the eye disc contain only isolated R8 neurons, which project to appropriate retinotopic positions in the lamina, and trigger early LPC maturation but not their neuronal differentiation.
Homozygous embryos have a reduced number of cells in the anterior Malpighian tubules compared to wild-type embryos.
Germline clones fail to rescue the female sterile phenotype of Fs(2)Ugr.
No effect on the faf eye phenotype.
Epidermal defects and fusion of the anterior and posterior commissures. In the PNS some sensory organs are missing, there is a ventral-dorsal gradient of severity. Several muscle fibres are always missing in the dorsolateral region and there are variable abnormalities in the number, shape and attachment sites of the eight ventral oblique muscle fibres.
embryonic lethal
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Enhanced by
Statement
Reference
spi2 has tracheal primordium phenotype, enhanceable by cv-c[+]/cv-c7
Suppressor of
Statement
Reference
spi2 is a suppressor of phenotype of rhohs.sev
Additional Comments
Genetic Interactions
Statement
Reference
The mild invagination observed in spi2 homozygous embryos is significantly enhanced by the presence of a single copy of cv-c7, with approximately 67% of placodes exhibiting an abnormal invagination, compared to approximately 35% in spi2 mutants.
Reduction in dose of spi rescues the rhohs.sev eye to a near wild-type phenotype; regular array of ommatidia, regular arrangement of photoreceptors and unbroken lattice of pigment cells. Rescue is not always complete.
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Comments
Animals heterozygous for spiSCP2 and spi2 which have been rescued by spiScer\UAS.cSa with Scer\GAL4hs.PB to the third instar stage show relatively normal ommatidial development at the posterior of the eye imaginal disc. More anterior columns of ommatidia have reduced photoreceptors. In the lamina, retinal projections appeared normal but LPCs show no neuronal differentiation. This phenotype is rescued by the introduction of Scer\GAL4GMR.PF or in clones induced to produce Scer\GAL4αTub84B.PP.
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
References (16)