A Database of Drosophila Genes & Genomes

FB2008_06, released July 3, 2008
 

Allele Dmel\S1

General Information
SymbolDmel\S1SpeciesD. melanogaster
NameFlyBase IDFBal0015108
Feature typealleleCreated / Updated2006-08-22/2006-08-22
Associated geneDmel\S
Allele class
Mutagenspontaneous
hide Nature of the Allele
Allele class
Mutagen
Mapped Features and Mutations
Type
Symbol & Location
Additional Notes
References
 
 
 
 
Associated Sequence Data
DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
      Progenitor genotype
      Nature of the lesion
      Statement
      Reference
      Mutation is not visible cytologically. Southern blots reveal a breakpoint between coordinates -12.0 and -12.5.
      Assay mode
      Cytology
      Polytene chromosomes normal.
      hide Phenotypic Data
      hide Phenotypic Class
      hide Phenotype Manifest In
      hide Detailed Description
      Statement
      Reference
      Heterozygotes have slightly reduced eyes with irregularly shaped facets and disarranged facet hairs.
      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.
      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.
      Projection patterns of retinal axons in heterozygous larvae are indistinguishable from wild type.
      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.
      Homozygous female germline clones do not develop beyond stage 1 of oogenesis.
      Heterozygotes do not have defects in the ovary.
      hide Interactions
      hide Phenotypic Class
      hideEnhanced by
      Statement
      Reference
      S1 has visible | dominant phenotype, enhanceable by astrv3
      S1 has visible phenotype, enhanceable by astK6/ast[+]
      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
      hideEnhancer of
      Statement
      Reference
      S1 is an enhancer of visible phenotype of rux3
      hideOther
      Statement
      Reference
      hide Phenotype Manifest In
      hideEnhanced by
      Statement
      Reference
      S1 has phenotype, enhanceable by ast4
       
      S1 has eye phenotype, enhanceable by ast4
      S1 has eye phenotype, enhanceable by Egfr[+]/EgfrE1
      S1 has eye phenotype, enhanceable by Egfr[+]/Egfrf6
      S1 has phenotype, enhanceable by astrv3
       
      S1 has eye phenotype, enhanceable by astrv3
      S1 has eye phenotype, enhanceable by astK6/ast[+]
      S1 has phenotype, enhanceable by ast5
       
      S1 has phenotype, enhanceable by astX
       
      S1 has phenotype, enhanceable by e(S)1
       
      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
      hideNOT Enhanced by
      Statement
      Reference
      S1 has eye phenotype, non-enhanceable by Snr1E1
      hideNOT suppressed by
      Statement
      Reference
      S1 has eye phenotype, non-suppressible by Snr1E1
      S1 has phenotype, non-suppressible by su(Hw)2
      hideEnhancer of
      Statement
      Reference
      S1 is an enhancer of phenotype of cswlf
      S1 is an enhancer of eye phenotype of rux3
      S[+]/S1 is an enhancer of ovary phenotype of Df(2L)esc-P2-0/aretPD
      S[+]/S1 is an enhancer of ovary phenotype of aretPA/aretPD
      S[+]/S1 is an enhancer of ovary phenotype of aretQB/aretPD
      S[+]/S1 is an enhancer of eye phenotype of EgfrE1
      hideSuppressor of
      Statement
      Reference
      ast1/S1 is a suppressor of phenotype of pxunspecified
      S1 is a suppressor of phenotype of pxunspecified
      S[+]/S1 is a suppressor of wing vein | ectopic phenotype of Snr1E1
      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
      hideOther
      Statement
      Reference
      S1, ast4 has eye phenotype
      S1, ast3 has eye phenotype
      S1, astrv3 has eye phenotype
      hide Additional Comments
      hide Genetic Interactions
      Statement
      Reference
      ml1 enhances the irregular distribution of the ommatidia seen in S1 flies.
      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.
      In S1/ast1 transheterozygotes the eyes are reduced in size and many ommatidia are missing.
      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/+.
      hide Xenogenetic Interactions
      Statement
      Reference
      hide Complementation & Rescue Data
      Fails to complement
      Rescued by
      Comments
      hide Stocks ( 63 )
      Bloomington
      Kyoto
      hide Notes on Origin
      Discoverer
      Bridges, 21st Feb. 1915.
      hide Comments
      Dominantly enhances the mutant eye phenotype of rux3.
      hide Synonyms & Secondary IDs ( 2 )
      Reported As
      Symbol Synonym
      S1
       
      Name Synonym
      Secondary FlyBase IDs
      • FBal0030529
      hide References ( 25 )
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      hide Recent research papers (0)
      All research papers listed in FlyBase were published before 2006