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General Information
Symbol
Dmel\S1
Species
D. melanogaster
Name
FlyBase ID
FBal0015108
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
S
Allele class
Mutagen
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology

Polytene chromosomes normal.

Nature of the lesion
Statement
Reference

Mutation is not visible cytologically. Southern blots reveal a breakpoint between coordinates -12.0 and -12.5.

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

The increase in lamellocyte number and melanotic capsule formation that are seen following wasp infestation in wild type are not seen in heterozygous S1 larvae.

Heterozygotes have a rough eye phenotype.

Heterozygotes do not have defects in the ovary.

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

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.

Projection patterns of retinal axons in heterozygous larvae are indistinguishable from wild type.

S1/+ shows a slight rough eye phenotype. A few ommatidia are missing R cells. Mosaic analysis suggests that neuronal development does not take place when S function is missing.

In stage 12/3 homozygous embryos the commissures are thicker and narrower than wild type and by stage 14 they remain incompletely separated. In stage 12/5 embryos the wild type number of midline glia are present but appear tightly clustered and displayed dorsally. Reduction in cell number from stage 13 until 14. Reduction in the VUM cell number at stage 11, during stage 13 half the wild type number of neurons migrate ventrally, these are still present at stage 14. MP1 neurons appear wild-type at stage 13 but there is a reduction in number. In stage 14 embryos there is a reduced number of en+ neurons present at the midline.

Anterior and posterior commissure fuse. Initial development of the axon commissures appears normal but the axon tracts fail to separate at the time of midline glia migration. Midline glial cells appear and then die.

Heterozygotes have slightly reduced eyes with irregularly shaped facets and disarranged facet hairs.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference

DCTN1-p1501, S[+]/S1 has visible | dominant phenotype, enhanceable by Dhc64C[+]/Dhc64C1-1

S1 has visible | dominant phenotype, enhanceable by Dhc64C[+]/Dhc64C1-1

S1 has visible phenotype, enhanceable by astK6/ast[+]

S1 has visible | dominant phenotype, enhanceable by astrv3

S1 has visible | dominant phenotype, enhanceable by ast1

S1 has visible | dominant phenotype, enhanceable by E(S)1

S1 has visible phenotype, enhanceable by ml1

NOT suppressed by
Statement
Reference

DCTN1-p1501, S[+]/S1 has visible | dominant phenotype, non-suppressible by Dhc64C[+]/Dhc64C8-1

DCTN1-p1501, S[+]/S1 has visible | dominant phenotype, non-suppressible by Dhc64C8-1/Dhc64C77

DCTN1-p1501, S[+]/S1 has visible | dominant phenotype, non-suppressible by Dhc64C77/Su(Gl)77[+]

Enhancer of
Statement
Reference

S[+]/S1 is an enhancer of visible | dominant phenotype of DCTN1-p1501

S1 is an enhancer of visible phenotype of rux3

Other
Statement
Reference

S1, ast4 has visible | dominant phenotype

S1, ast2 has lethal | dominant phenotype

S1, ast3 has viable phenotype

S1, ast3 has visible | dominant phenotype

Phenotype Manifest In
Enhanced by
Statement
Reference

DCTN1-p1501, S[+]/S1 has eye phenotype, enhanceable by Dhc64C[+]/Dhc64C1-1

S1 has eye phenotype, enhanceable by Dhc64C[+]/Dhc64C1-1

S1 has eye phenotype, enhanceable by astK6/ast[+]

S1 has eye phenotype, enhanceable by Egfr[+]/EgfrE1

S1 has eye phenotype, enhanceable by Egfr[+]/Egfrf6

S1 has eye phenotype, enhanceable by astrv3

S1 has eye phenotype, enhanceable by ast4

S1 has eye phenotype, enhanceable by ast1

S1 has ommatidium phenotype, enhanceable by ast1

S1 has eye phenotype, enhanceable by E(S)1

S1 has eye phenotype, enhanceable by ml1

S1 has ommatidium phenotype, enhanceable by ml1

S1 has phenotype, enhanceable by ast4

S1 has phenotype, enhanceable by astrv3

S1 has phenotype, enhanceable by ast5

S1 has phenotype, enhanceable by astX

S1 has phenotype, enhanceable by e(S)r1

NOT Enhanced by
Statement
Reference

S1 has eye phenotype, non-enhanceable by Snr1E1

NOT suppressed by
Statement
Reference

DCTN1-p1501, S[+]/S1 has eye phenotype, non-suppressible by Dhc64C[+]/Dhc64C8-1

DCTN1-p1501, S[+]/S1 has eye phenotype, non-suppressible by Dhc64C8-1/Dhc64C77

DCTN1-p1501, S[+]/S1 has eye phenotype, non-suppressible by Dhc64C77/Su(Gl)77[+]

S1 has eye phenotype, non-suppressible by Snr1E1

S1 has phenotype, non-suppressible by su(Hw)2

Enhancer of
Statement
Reference

S[+]/S1 is an enhancer of eye phenotype of DCTN1-p1501

S[+]/S1 is an enhancer of ovary phenotype of bru1QB/bru1PD

S[+]/S1 is an enhancer of ovary phenotype of Df(2L)esc-P2-0/bru1PD

S[+]/S1 is an enhancer of ovary phenotype of bru1PA/bru1PD

S1 is an enhancer of phenotype of cswlf

S[+]/S1 is an enhancer of eye phenotype of EgfrE1

S1 is an enhancer of eye phenotype of rux3

Suppressor of
Statement
Reference

S[+]/S1 is a suppressor of wing vein | ectopic phenotype of Snr1E1

ast1/S1 is a suppressor of phenotype of pxunspecified

S1 is a suppressor of phenotype of pxunspecified

ast1/S1 is a suppressor of phenotype of netunspecified

S1 is a suppressor of phenotype of netunspecified

S1 is a suppressor of phenotype of Dl3

Other
Statement
Reference

S1, ast4 has eye phenotype

S1, astrv3 has eye phenotype

S1, ast4 has wing vein phenotype

S1, ast3 has eye phenotype

Additional Comments
Genetic Interactions
Statement
Reference

Gll1 shows little or no dominant interaction with S1 in the eye.

Dhc64C1-1/+ enhances the rough eye phenotype of S1/+ flies, resulting in more disruption of the hexagonal packing of the ommatidia. and in a smaller eye.

The S1 mutation overcomes the suppression of the Gl1 rough eye phenotype by Dhc64C8-1 or Dhc64C77, so that triple heterozygotes have an enhanced rough eye phenotype compared to Gl1 single heterozygotes.

The enhanced rough eye phenotype of Gl1/+ S1/+ flies is not suppressed by Dhc64C77/Dhc64C8-1.

The dominant rough eye phenotype caused by S1 is not affected if Snr1E1 is also present.

Oogenesis arrests at the germarial stage in S1 aretPD/Df(2L)esc-P2-0 females. The ovarioles fail to bud off into individual egg chambers and instead, multiple undifferentiated germ cells appear in the severely truncated ovarioles. Oogenesis arrests at stage 6/7 in S1 aretPA/aretPD females. Oogenesis arrests at about stage 3 in S1 aretPD/aretQB females and no oocyte is specified. The oogenesis defects of S1 aretPD/Df(2L)esc-P2-0 females are partially suppressed by one copy of Df(3R)M-Kx1; egg chambers bud off from the germarium, although they are abnormal - each egg chamber has more than the normal number of 16 germ cells and no oocyte is specified. Df(3R)Dl-BX12 dominantly alters the ovary phenotype of S1 aretPD/Df(2L)esc-P2-0 females; the germarium is greatly expanded to produce a large volume of germ cells surrounded by a layer of follicle cells. The oogenesis arrest phenotype of S1 aretPD/Df(2L)esc-P2-0 females is suppressed by Df(3R)mbc-R1/+.

In S1/ast1 transheterozygotes the eyes are reduced in size and many ommatidia are missing.

The phenotype is dominantly enhanced by ast1 : double heterozygotes have extremely small, diamond-shaped eyes in which many of the facets are fused and the remainder are irregular in size and distribution. The phenotype is dominantly enhanced by E(S)1. Lethal in double heterozygous combination with ast2. S1 ast3 flies are late hatching, those flies which emerge have good viability and fertility, normal wing venation and extremely small eyes. S1/ast4 flies have smaller eyes than S1/+ flies and they also occasionally have gaps at the tips of the longitudinal wing veins. Partially suppresses the phenotype of netunspecified or pxunspecified homozygotes. S1/ast1 tends to completely suppress the phenotype of netunspecified or pxunspecified homozygotes. astrv3 produces a slightly rougher eye than that characteristic of S1/+ in combination with S1.

ml1 enhances the irregular distribution of the ommatidia seen in S1 flies.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Rescued by
Comments
Images (1)
Stocks (71)
Notes on Origin
Discoverer

Bridges, 21st Feb. 1915.

Comments
Comments

Dominantly enhances the mutant eye phenotype of rux3.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
Reported As
Name Synonyms
Secondary FlyBase IDs
  • FBal0030529
References (29)