FB2020_06, released Dec 22, 2020

Allele: Dmel\SCARk13811

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General Information
Symbol
Dmel\SCARk13811
Species
D. melanogaster
Name
FlyBase ID
FBal0328160
Feature type
allele
Associated gene
Dmel\SCAR
Associated Insertion(s)
P{lacW}SCARk13811
Carried in Construct
Also Known As
l(2)k13811
Genomic Maps
Allele class

hypomorphic allele - genetic evidence

Mutagen
Nature of the Allele
Allele class

hypomorphic allele - genetic evidence

(Schenck et al., 2004, Zallen et al., 2002)
Mutagen
P-element activity
(Bogdan and Klambt, 2003, Zallen et al., 2002, BDGP Project Members, 1994-1999)
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
transposable element insertion site
2L:10,976,824..10,976,824 [-]2L:10,976,824..10,976,824 [-]
(Hamp et al., 2016, Berger et al., 2008, Richardson et al., 2007, Bogdan and Klambt, 2003, Zallen et al., 2002, Mesilaty-Gross et al., 1999, Spradling et al., 1999, BDGP Project Members, 1994-1999)
Associated Sequence Data
DDBJ / EMBL / GenBank
DNA sequence
Protein sequence
 
UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
       
      Progenitor genotype
      Cytology
      Nature of the lesion
      Statement
      Reference

      P{lacW} insertion in the 5' UTR of SCAR.

      (Zallen et al., 2002)
      Insertion components
      P{lacW}SCARk13811
      Product class / Tool use(s)
      Encoded product / tool
      lacZ
      Tagged with
      Tag:NLS(P)
      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

      SCARk13811 mutant cells in mosaic follicular epithelia exhibit a non-cell-autonomous defect in trailing edge retraction, as wild type cells directly ahead of SCARk13811 mutant cells exhibit significantly elongated basal surfaces.

      (Barlan et al., 2017)

      SCARk13811 mutant embryos that lack both the zygotic and maternal SCAR gene products (derived from females containing homozygous germline clones mated to homozygous males) display a duplication of the RP2 neuron in one hemisegment and have one missing in the contralateral segment. Embryos are also seen in which RP2 neurons fail to migrate from their location of formation.

      (Zhu and Bhat, 2011)

      SCARk13811 mutant embryos show a partial loss of myoblast fusion at stage 14 and, unlike in wild type, enlarged actin foci persist at stage 15. The percentage of F-actin foci that are invasive and the depth of invasion are both comparable to wild type. These phenotypes are seen when just the zygotic contribution is removed, or when both the maternal and zygotic gene products are absent.

      (Sens et al., 2010)

      Homozygous SCARk13811 embryos exhibit a weak myoblast fusion defect. Unfused myoblasts are visible. Dorsal closure seems incomplete in these embryos.

      (Berger et al., 2008)

      SCARk13811 germline clone embryos, with reduced maternal and zygotic SCAR contributions exhibit a severe myoblast fusion defect, with increased numbers of free myoblasts and thinner muscles. SCARk13811 mutants show a dramatic increase in the size and number of actin foci.

      (Richardson et al., 2007)

      The spacing and morphology of nuclei is abnormal in cycle 12-13 blastoderm SCARK13811 germ-line clone embryos. By cycle 14, these embryos show dramatic abnormal accumulation of nuclei internally. The actin cytoskeletons of SCARK13811 germ-line clone embryos are also abnormal at these stages. This is particularly clear during metaphase when, in the majority of embryos, actin accumulates in aberrant structures positioned above individual spindles, rather than forming a network of metaphase furrows between adjacent spindles, as in wild-type. These defects are accompanied by a general decrease in filamentous actin levels, although cell cycle-dependent fluctuations in filamentous actin levels persist. CNS axon morphology in SCARK13811 homozygous embryos is normal. However, in SCARK13811 homozygous embryos from SCARK13811 germ-line clone mothers, gaps appear in both longitudinal and commissural bundles (93% of segments, n = 242). In extreme cases, a severe depletion of all axon bundles occurs (46% of segments). At a lower frequency, these embryos exhibit defects in commissure fasciculation and separation (18% of segments), and medial (13%) or lateral (9%) displacement of axons.

      (Zallen et al., 2002)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Phenotype Manifest In
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      Embryos that are maternally and zygotically mutant for SCARk13811 and zygotically mutant for Vrp1S1946 show a near complete block of myoblast fusion and a dramatic reduction in the size of the actin foci.

      Embryos that are zygotically mutant for both SCARk13811 and Vrp1S1946 show a near complete block of myoblast fusion and a dramatic reduction in the size of the actin foci. 76% of muscle cell adhesion sites are not associated with any F-actin enrichment.

      (Sens et al., 2010)

      A WASp3/+ background intensifies the appearance of unfused myoblasts in SCARk13811 mutants.

      (Berger et al., 2008)

      In the ventral nerve cord of SCARK13811/SCARK13811; WASp1/+ embryos, there is an severe depletion of axons in both longitudinal and commissural bundles, often leading to gaps. In the ventral nerve cord of SCARK13811/+; WASp1/Df(3R)3450 embryos, breaks occur in both longitudinal and commissural axon bundles, and axons are medially displaced.

      (Zallen et al., 2002)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Images (0)
      Mutant
      Wild-type
      Stocks (1)
      Notes on Origin
      Discoverer

      I. Kiss.

      (BDGP Project Members, 1994-1999)
      Comments
      Comments

      Complements: Nup15401501. Complements: l(2)0622506225. Complements: l(2)k05812k05812. Complements: l(2)k09104k09104. Complements: RfC38k13807. Complements: l(2)k15817k15817.

      (BDGP Project Members, 1994-1999)

      Lethality can be rescued by precise excision of P{lacW}SCARK13811.

      (Zallen et al., 2002)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (7)
      Reported As
      Symbol Synonym
      SCARK13811
      (Schenck et al., 2004)
      SCARk13811
      (Barlan et al., 2017)
      SCARK13811
      (Zhu and Bhat, 2011)
      l(2)k03107k13811
      l(2)k13811
      (Zallen et al., 2002, Mesilaty-Gross et al., 1999, Spradling et al., 1999)
      l(2)k13811k13811
      (BDGP Project Members, 1994-1999)
      scark13811
      (Hamp et al., 2016, Sens et al., 2010, Bogdan and Klambt, 2003)
      Name Synonyms
      Secondary FlyBase IDs
      • FBal0064116
      • FBal0150644
      References (14)