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General Information
Symbol
Dmel\SIIN
Species
D. melanogaster
Name
FlyBase ID
FBal0015112
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
SIIN23, StarIIN, S11N23
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 ( 1 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

SIIN heterozygotes display a very mild loss of photoreceptor differentiation phenotype.

Mutant embryos show a decrease in the number of dorsolateral and lateral adult muscle precursor cells compared to wild type.

Homozygous SIIN mutant third instar larva eye discs show misrotated ommatidia and missing photoreceptors. Photoreceptor axons are correctly targeted to the lamina, but defects in lamina cartridge neuron differentiation are seen. Only a small number of cells in the posterior lamina appear to have differentiated correctly.

In SIIN stage 15 embryos, the genital disc precursor cells are completely missing.

Homozygous embryos have a reduced number of midline glia per ventral nerve cord segment compared to wild type. The embryos have breaks in the dorsal trunk of the tracheal system at stage 15.

No increase is seen in cardioblast numbers in the developing embryo.

SIIN embryos have an average of 3.04 +/- 0.2 neurons per lch5 organ.

Homozygous female germline clones do not develop beyond stage 1 of oogenesis.

Homozygous embryos lack many myofibres.

Homozygous embryos have a reduced number of cells in both the anterior and posterior Malpighian tubules compared to wild-type embryos. The number of cells in the anterior Malpighian tubules is severely reduced in rho7M43 SIIN double mutant embryos.

Early CNS development is essentially normal in mutant embryos.

The central nervous system (CNS) is narrower than normal and the commissures are thicker than normal and incompletely separated in SIIN embryos.

S1/SIIN embryos exhibit deletion of the ventral denticles and Keilin's organs are missing or defective. Wing, leg, haltere and eye/antenna S1/SIIN mutant discs can be in vivo cultured.

Mutant embryos exhibit tracheal phenotype.

Nondefective in gonad assembly.

All or nearly all of the ventral epidermal cells are absent in mutant embryos.

No changes in phenotype of tor13D embryos.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressor of
Statement
Reference

S[+]/SIIN is a suppressor of visible phenotype of Scer\GAL4Tub.PU, cswN308D.UASp

SIIN is a suppressor of visible phenotype of RetMEN2B.GMR

SIIN is a suppressor of visible phenotype of RetMEN2A.GMR

S[+]/SIIN is a suppressor of planar polarity defective | recessive phenotype of sl9

Other
Phenotype Manifest In
Enhanced by
Statement
Reference

SIIN has photoreceptor cell phenotype, enhanceable by step[+]/stepk08110

NOT Enhanced by
Statement
Reference

SIIN has photoreceptor cell phenotype, non-enhanceable by InR[+]/InR05545

SIIN has phenotype, non-enhanceable by rhohs.PSt

Suppressed by
Statement
Reference
NOT suppressed by
Statement
Reference

SIIN has photoreceptor cell phenotype, non-suppressible by InR[+]/InR05545

SIIN has phenotype, non-suppressible by rhohs.PSt

Enhancer of
Statement
Reference

SIIN is an enhancer of eye phenotype of DCTN1-p1501

S[+]/SIIN is an enhancer of eye phenotype of HScer\UAS.cMa/HUAS.cMa, Scer\GAL4GMR.PU

SIIN is an enhancer of somatic muscle | embryonic stage phenotype of Egfrf1

S[+]/SIIN is an enhancer of somatic muscle | embryonic stage phenotype of Egfrf1, spi1

NOT Enhancer of
Statement
Reference

SIIN is a non-enhancer of wing phenotype of KrnUAS.cRa, Scer\GAL4Bx-MS1096

SIIN is a non-enhancer of eye phenotype of Nspl-1

Suppressor of
Statement
Reference

S[+]/SIIN is a suppressor of wing vein | ectopic phenotype of Scer\GAL4Tub.PU, cswN308D.UASp

SIIN is a suppressor of eye phenotype of RetMEN2B.GMR

SIIN is a suppressor of eye phenotype of RetMEN2A.GMR

S[+]/SIIN is a suppressor | partially of ommatidium phenotype of sl9

S[+]/SIIN is a suppressor of interommatidial bristle phenotype of sl9

S[+]/SIIN is a suppressor of phenotype of Src42ASu(Raf)1-1

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

SIIN/stepk08110 trans-heterozygotes exhibit a photoreceptor differentiation phenotype, increased in severity from SIIN heterozygotes.

SIIN/+;InR05545/+ flies do not exhibit an enhanced photoreceptor differentiation phenotype compared to SIIN heterozygotes.

The presence of a SIIN background significantly suppresses ectopic wing vein formation found in cswY279C.Scer\UAS (Scer\GAL4tub) mutants.

A SIIN background suppresses the cswY279C.Scer\UAS (Scer\GAL4tub) rough eye phenotype, normalizing the numbers of R7 and ommatidial rotation.

The small-eye phenotype observed in animals expressing HScer\UAS.cMa in the eye under the control of Scer\GAL4GMR.PU is enhanced in a SIIN/+ background.

The increase in the number of midline glia per ventral nerve cord segment seen in embryos expressing jingScer\UAS.cSa under the control of Scer\GAL4sli.PS is not suppressed by SIIN, but expression of jingScer\UAS.cSa under the control of Scer\GAL4sli.PS in a homozygous SIIN background does not induce extra midline glia and the number of midline glia per ventral nerve cord segment in these double mutant embryos is reduced compared to wild type and is similar to that seen in homozygous SIIN single mutants. SIIN/Df(2R)ST1 double heterozygous embryos have a reduced number of midline glia per segment compared to wild type. SIIN/jing3 and SIIN/jing01094 double heterozygous embryos have breaks in the dorsal trunk of the tracheal system at stage 15.

salm3 SIIN double mutant embryos have an average of 3.05 +/- 0.20 neurons per lch5 organ, similar to SIIN single mutant embryos. The embryos show misplacement of the lch5 organ along the dorsoventral axis comparable to the phenotype seen in salm single mutants.

The ubiquitous expression of rhohs.PSt under heatshock has no effect on SIIN embryos.

Has no effect on the eye phenotype of Nspl-1.

Flies doubly mutant for SIIN and either phl12 or Ras85DN17.sev have no R7 photoreceptor cells.

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

Embryos expressing EgfrDN.Scer\UAS.cBa under the control of both Scer\GAL4twi.PG and Scer\GAL4how-24B show a partial reduction in the development of muscles DA1 and VA2. This phenotype is dominantly enhanced by SIIN. Dominantly enhances the mild muscle phenotype of Egfrf1 embryos raised at 18oC. Further enhancement of the phenotype is also seen if the flies are also heterozygous for spi1.

Germline clones fail to rescue the female sterile phenotype of Fs(2)Ugr.

The width of the CNS is closer to wild-type if SIIN embryos are also mutant for Df(3L)H99, although commissure separation remains incomplete.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Fails to complement
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments

Less than 10% of wild type number of ventral epidermal cells expressing P{lacZ}BP28 are evident in mutant embryos. oc expression is greatly reduced along the midline.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
References (42)