FB2024_03 , released June 25, 2024
Allele: Dmel\Shark1
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General Information
Symbol
Dmel\Shark1
Species
D. melanogaster
Name
FlyBase ID
FBal0101317
Feature type
allele
Associated gene
Dmel\Shark
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Allele class

amorphic allele - genetic evidence

Mutagen
Nature of the Allele
Allele class

amorphic allele - genetic evidence

(Fernandez et al., 2000)
Mutagen
ethyl methanesulfonate
(Fernandez et al., 2000, Liu et al., 1999)
Progenitor genotype
Cytology
Description

Amino acid replacement: Q210term.

(Fernandez et al., 2000)

Nucleotide substitution: C685T.

(Fernandez et al., 2000)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
point_mutation
2R:16,202,030..16,202,030 [-]
Nucleotide change:

C16202030T

Reported nucleotide change:

C685T

Amino acid change:

Q210term | Shark-PA

Reported amino acid change:

Q210term

(Fernandez et al., 2000)
Variant Molecular Consequences
Associated Sequence Data
DDBJ / EMBL / GenBank
DNA sequence
Protein sequence
 
UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
      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 )
       
      Disease-implicated variant(s)
       
      Phenotypic Data
      Phenotypic Class
      Phenotype Manifest In
      Detailed Description
      Statement
      Reference

      Mutants show defects in glial phagocytic function; significant amounts of axonal debris remain within Or85e-innervated glomeruli and in the maxillary nerve 5 days after ablation of maxillary palps in heterozygous animals, in contrast to control animals.

      Homozygous stage 14-15 embryos show a marked increase in the number of central nervous system cell corpses (43.3 cell corpses per hemisegment) compared to control embryos (24.4 cell corpses per hemisegment).

      shark1/Df(2R)Exel6063 stage 14-15 embryos show a marked increase in the number of central nervous system cell corpses (46.5 cell corpses per hemisegment) compared to control embryos (24.4 cell corpses per hemisegment).

      (Ziegenfuss et al., 2008)

      Homozygous follicle cell clones affect the morphology of the dorsal appendages and the structure of the dorsal appendage chorion. In some eggs, the dorsal appendage material appears vacuolated, with gaps interposed with a skeletal network. This chorion defect is seen when a significant fraction of the dorsal appendage cells are clonal. Homozygous follicle cells clones in the main body of the egg show no obvious structural defects in the chorion. Other eggs have shortened dorsal appendages with a normal chorion. The shortened dorsal appendage phenotype is seen when large clones encompass the stretch cells.

      (Tran and Berg, 2003)

      shark1/Df(2R)Jp4 flies that have been rescued by sharkhs.PF without heat shock (suboptimal rescue conditions) often have a split thorax or hep-like defects such as the failure of a wing to outgrow (with variable penetrance ranging from 40% to 80%). In addition, if these females are fertilised with shark1 sperm, they give rise to embryos that show a defective dorsal closure phenotype. Homozygous or shark1/Df(2R)Jp7 embryos derived from homozygous female germline clones (lacking both maternal and zygotic shark function) have a strong defective dorsal closure phenotype. These cuticle defects are rescued by a paternal shark+ allele, resulting in viable, fertile adults. Leading edge and lateral epidermal cells maintain their polygonal shape and fail to elongate towards the dorsal midline during dorsal closure in the anterior three-quarters of homozygous embryos derived from homozygous female germline clones.

      (Fernandez et al., 2000)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Suppressed by
      Phenotype Manifest In
      Suppressed by
      Statement
      Reference

      Shark1 has embryo | germline clone | dorsal closure stage phenotype, suppressible by JraAsp.hs.sev

      (Fernandez et al., 2000)
      NOT suppressed by
      Enhancer of
      Statement
      Reference

      shark[+]/Shark1 is an enhancer of dorsal appendage phenotype of bwkunspecified

      (Tran and Berg, 2003)
      NOT Suppressor of
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      Larval hemocytes prepared from shark1/+ drprΔ5/+ flies show the same the level of phagocytosis of S. aureus as either single heterozygote.

      (Hashimoto et al., 2009)

      drprΔ5/+ ; shark1/+ double heterozygotes show a striking suppression of clearance of severed axons in Or85e-innervated glomeruli and in the maxillary nerve compared to controls 5 days after ablation of maxillary palps.

      (Ziegenfuss et al., 2008)

      JraAsp.hs.sev completely rescues the dorsal closure defects of shark1 embryos derived from shark1 female germline clones when expressed using heat shock between 5 and 10 hours after egg laying. Embryos expressing tkvQ253D.Scer\UAS.cLa under the control of Scer\GAL469B show partial dorsalisation of their cuticles. This phenotype is not altered if the embryos are derived from homozygous shark1 female germ-line clones (and fertilised by a shark+ sperm). The dorsal closure defects of homozygous shark1 embryos derived from shark1 female germline clones are not rescued by expression of tkvQ253D.Scer\UAS.cLa under the control of Scer\GAL469B. Embryos expressing tkvQ253D.Scer\UAS.cNb under the control of Scer\GAL469B show partial dorsalisation of their cuticles. This phenotype is not altered if the embryos are derived from homozygous shark1 female germ-line clones (and fertilised by a shark+ sperm). The dorsal closure defects of homozygous shark1 embryos derived from shark1 female germline clones are not rescued by expression of tkvQ253D.Scer\UAS.cNb under the control of Scer\GAL469B.

      (Fernandez et al., 2000)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Rescued by

      Shark1/Df(2R)Jp4 is rescued by Sharkhs.PF

      (Fernandez et al., 2000)

      Shark1 is rescued by SharkUAS.cFa/Scer\GAL469B

      (Fernandez et al., 2000)
      Not rescued by

      Shark1 is not rescued by SharkK698R.hs

      (Fernandez et al., 2000)

      Shark1 is not rescued by Scer\GAL4pnr-MD237/SharkUAS.cFa

      (Fernandez et al., 2000)
      Comments

      Expression of sharkhs.PF using heat shock can rescue the lethality of shark1/Df(2R)Jp4 flies. sharkScer\UAS.cFa rescues the dorsal closure defect of shark1 embryos derived from shark1 female germline clones when expressed under the control of Scer\GAL469B. sharkScer\UAS.cFa fails to rescue the dorsal closure defect of shark1 embryos derived from shark1 female germline clones when expressed under the control of Scer\GAL4pnr-MD237.

      (Fernandez et al., 2000)
      Images (0)
      Mutant
      Wild-type
      Stocks (2)
      Notes on Origin
      Discoverer
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (5)
      Reported As
      Symbol Synonym
      Shark1
      W-4
      (Fernandez et al., 2000)
      l(2)W4G
      (Steward, 2000.8.14)
      l(2)W4unspecified
      shark1
      (Chakrabarti and Visweswariah, 2020, Hashimoto et al., 2009, Ziegenfuss et al., 2008)
      Name Synonyms
      Secondary FlyBase IDs
        References (8)