A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Dmel\FB{}Cskj1D8 Insertion

General Information
Symbol Dmel\FB{}Cskj1D8 Species D. melanogaster
Name FlyBase ID FBti0064511
Feature type transposable_element_insertion_site
Description
Inserted element FB Expression data
Affected gene(s) Csk Viability / fertility
Causes allele(s) Cskj1D8 Stock availability none publicly available
LINE ID l(3)j1D8
Genomic Location
Chromosomal location 3R ( 86E13 ) Sequence location
Member of Large Scale Dataset(s)
Dataset
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Description
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FB2013_03
FB2013_02
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hide Detailed Mapping Data
Chromosome (arm)
Sequence Location
Orientation
Cytological location
(computed by FlyBase)
86E13 ( near gene of known cytology )
Cytological location
(reported)
Comments concerning
location
hide Sequence Data
Flanking sequence
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Construct FB
Location-dependent
role
Size
Associated alleles
Molecular map
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Insertion may
affect gene
hide Alleles and Phenotypes
Causes alleles
Lethality
References
lethal | pupal stage
lethal | pupal stage | recessive
Sterility
References
hide Phenotype Manifest In
eye | somatic clone
eye-antennal disc | somatic clone
ommatidium | somatic clone | supernumerary
wing disc
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Statement
Reference
A Csk[j1D8]/+ background enhances the visual system degeneration seen in Scer\GAL4[GMR.PF], Ppt1[Scer\UAS.cKa] flies.
68% of ASPP[d] ; Csk[j1D8]/+ flies have notched wings.
Csk[j1D8] dominantly suppresses the rough eye phenotype caused by expression of Zzzz\CTG[i480.Scer\UAS.cGa] under the control of Scer\GAL4[sev.PU].
Wing discs of homozygous third instar larvae show considerable apoptosis.
ASPP[8]/ASPP[8] Csk[j1D8]/+ adults show a notched wing phenotype. Wing discs of ASPP[8]/ASPP[8] Csk[j1D8]/+ third instar larvae show considerable apoptosis. Neither phenotype is seen in ASPP[8]/ASPP[8] or Csk[j1D8]/+ single mutants. Btk29A[k00206]/+ largely suppresses the ectopic apoptosis in wing discs and notched wing phenotype seen in ASPP[8]/ASPP[8] Csk[j1D8]/+ animals. puc[E69]/+ Csk[j1D8]/+ double heterozygotes have a notched wing phenotype, and third larval instar wing discs show ectopic apoptosis within the wing pouch. The ectopic apoptosis seen in the wing discs of puc[E69]/+ Csk[j1D8]/+ double heterozygotes is enhanced if they are also heterozygous for ASPP[8], resulting in adults with a severely reduced wing size. These adults also have leg deformities.
Cskj1D8, Stat92Ej6C8 mutant eyes are smaller than eyes mutant for Cskj1D8 or Stat92Ej6C8 alone. In addition, adult eyes are frequently fragmented, with scars and/or patches of eye tissue separated by patches of cuticle. Stat92E06346. Cskj1D8 mutant larval eye-antennal discs frequently show reduced sizes relative to the single mutants. Mutants also frequently show a reduction or absence of developing antennal tissues. Mutant larval eye tissue also contains many apoptotic cells.
Mutant larvae die within 6-8 hours after pupariation. The larval body mass of mutants increases up to 180% of the wild-type mass during the wandering stage. The brain ventral ganglion and salivary glands of mutants are enlarged. Pupariation is delayed. The body length of mutant pupae are about 121% the size of wild-type. Imaginal discs of mutant larvae are also larger than wild-type. The larval body mass of Cskj1D8/CskS030003 mutants increases up to 150% of the wild-type mass during the wandering stage. In the rare cases mutants survived to pharate adult stage, the head and eyes are enlarged. The posterior ommatidia are sometimes misaligned, though individual ommatidia are morphologically normal. Mutant eyes contain more ommatidia than wild-type. Rarely the eyes are replaced with duplicated antennae. In addition the wings and legs are severely malformed, the notum is sometimes split, and the head, legs and notum often contain cuticle overgrowths. In Cskj1D8/CskS030003 and homozygous Cskj1D8 mutant developing eye discs, an increase is seen in the number of mitotic cells in the morphogenetic furrow. Mutant pupal retinas contain excess mitotic cells in the interommatidial lattice. Cskj1D8/CskS030003 eye antennal disc cells exhibit a decrease in the proportion of cells in G0-G1 phase, and a consequent increase in cells in G2-M phase when compared to wild-type controls. Homozygous mutant clones in the eye produced severely overgrown eyes. Eyes have more than 1200 ommatidia, compared to about 687 in wild-type. Eyes can become malformed as a result. The extra ommatidia are occasionally inverted in their planar polarity but are otherwise normal in size and morphology. Occasionally mutant clones result in antennal duplication and cuticle overgrowth.
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Reporter Expression
Additional Information
Statement
Reference
Marker for
Reflects
expression of
Reporter construct
used in assay
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Line ID
Origin as a multiple insertion line
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Aberration
Balancer
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Reported As
Symbol Synonym
Secondary FlyBase IDs
hide References ( 11 )
Research paper
Saja et al., 2010, Neurobiol. Disease 40(1): 135--145
Identifying cellular pathways modulated by Drosophila palmitoyl-protein thioesterase 1 function. [FBrf0211567]
Langton et al., 2009, Curr. Biol. 19(23): 1969--1978
The dASPP-dRASSF8 complex regulates cell-cell adhesion during drosophila retinal morphogenesis. [FBrf0209661]
Garcia-Lopez et al., 2008, PLoS ONE 3(2): e1595
Genetic and chemical modifiers of a CUG toxicity model in Drosophila. [FBrf0210239]
Langton et al., 2007, Dev. Cell 13(6): 773--782
Drosophila ASPP regulates C-terminal Src kinase activity. [FBrf0202129]
Bellen et al., 2004, Genetics 167(2): 761--781
The BDGP gene disruption project: single transposon insertions associated with 40% of Drosophila genes. [FBrf0179132]
Read et al., 2004, Mol. Cell. Biol. 24(15): 6676--6689
Drosophila C-terminal Src kinase negatively regulates organ growth and cell proliferation through inhibition of the Src, Jun N-terminal kinase, and STAT pathways. [FBrf0179404]
Stewart et al., 2003, Oncogene 22(41): 6436--6444
A genetic screen for modifiers of the lats tumor suppressor gene identifies C-terminal Src kinase as a regulator of cell proliferation in Drosophila. [FBrf0162272]
Spradling et al., 1999, Genetics 153(1): 135--177
The Berkeley Drosophila genome project gene disruption project. Single P-element insertions mutating 25% of vital Drosophila genes. [FBrf0111489]
Personal communication to FlyBase
Gene Disruption Project members, 2001-, (Computer file)
(Computer file) [FBrf0132177]
BDGP Project Members, 1994-1999, BDGP Project Members, 1994-1999, Berkeley Drosophila Genome Project. (Computer file)
BDGP Project Members, 1994-1999, Berkeley Drosophila Genome Project. (Computer file) [FBrf0067338]
FlyBase analysis
FlyBase, 1992-, FlyBase curation.
FlyBase curation. [FBrf0105495]