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General Information
Symbol
Df(1)CHES-1-like1
Species
D. melanogaster
Name
FlyBase ID
FBab0047384
Feature type
Computed Breakpoints include
Sequence coordinates
X:7,679,892..7,679,892 (Df(1)CHES-1-like[1]:bk1)
X:7,709,922..7,709,922 (Df(1)CHES-1-like[1]:bk2)
Member of large scale dataset(s)
Nature of Aberration
Cytological Order
Mutagen
Class of aberration (relative to wild type)
Class of aberration (relative to progenitor)
Breakpoints
Causes alleles
Carries alleles
Transposon Insertions
Formalized genetic data
Genetic mapping information
Comments

Deletion of CHES-1-like resulting from FLP-catalyzed recombination using the FRT-containing transposons PBac{RB}e02377 and PBac{RB}e04245 that flank the gene.

Comments on Cytology
Sequence Crossreferences
DNA sequence
Protein sequence
Gene Deletion and Duplication Data
Genes Deleted / Disrupted
Complementation Data
Completely deleted / disrupted
Partially deleted / disrupted
Molecular Data
Partially deleted
Genes NOT Deleted / Disrupted
Complementation Data
 
Molecular Data
 
Genes Duplicated
Complementation Data
Completely duplicated
Partially duplicated
Molecular Data
Completely duplicated
Partially duplicated
Genes NOT Duplicated
Complementation Data
 
Molecular Data
 
Affected Genes Inferred by Location
Phenotypic Data
In combination with other aberrations

Df(1)CHES-1-like1 ; Df(3R)Exel6157 double mutant embryos show more severe defects in the arrangement of cardial cells compared to either single mutant.

Df(3L)DocA/+ ; Df(1)CHES-1-like1/+ double heterozygous embryos show defects in the symmetric cell divisions that give rise to the tin-expressing cardial cells that are significantly more severe than the additive effects of each of the two single heterozygotes. Asymmetric cell division defects in "svp" cardiac progenitor cells are not significantly different from the additive effects of each of the two single heterozygotes.

numb3/+ ; Df(1)CHES-1-like1/+ double heterozygous embryos show asymmetric cell division defects in "svp" cardiac progenitor cells that are significantly more severe than the additive effects of each of the two single heterozygotes. Defects in the symmetric cell divisions that give rise to the tin-expressing cardial cells in the double heterozygotes are not significantly different from the additive effects of each of the two single heterozygotes.

pnrVX6/+ ; Df(1)CHES-1-like1/+ double heterozygous embryos show asymmetric cell division defects in "svp" cardiac progenitor cells that are not significantly different from the additive effects of each of the two single heterozygotes. Defects in the symmetric cell divisions that give rise to the tin-expressing cardial cells in the double heterozygotes are not significantly different from the additive effects of each of the two single heterozygotes.

poloS025604/+ ; Df(1)CHES-1-like1/+ double heterozygous embryos show asymmetric cell division defects in "svp" cardiac progenitor cells that are significantly more severe than the additive effects of each of the two single heterozygotes. Defects in the symmetric cell divisions that give rise to the tin-expressing cardial cells are also significantly more severe in the double heterozygotes.

ponP65/+ ; Df(1)CHES-1-like1/+ double heterozygous embryos show asymmetric cell division defects in "svp" cardiac progenitor cells that are significantly more severe than the additive effects of each of the two single heterozygotes. Defects in the symmetric cell divisions that give rise to the tin-expressing cardial cells in the double heterozygotes are not significantly different from the additive effects of each of the two single heterozygotes.

tin346/+ ; Df(1)CHES-1-like1/+ double heterozygous embryos show asymmetric cell division defects in "svp" cardiac progenitor cells that are significantly more severe than the additive effects of each of the two single heterozygotes. Defects in the symmetric cell divisions that give rise to the tin-expressing cardial cells are also significantly more severe in the double heterozygotes.

NOT in combination with other aberrations

Homozygotes and hemizygotes are viable and fertile.

The cardial cells (CCs) are unevenly distributed in mutant embryos: hemisegments having localised increases or decreases in CC number, occasional enlarged CC nuclei and CCs that are misaligned either with other CCs within a hemisegment or with their counterparts across the dorsal midline are seen.

Cell divisions defects underlie the cardiac defects seen in the embryos. Defects in the asymmetric cell division that in wild-type causes an "svp" progenitor cell to give rise to one svp-expressing CC and one svp-expressing pericardial cell (PC) are seen: in some cases the progenitor produces two svp-expressing CCs. In other cases karyokinesis defects are seen during the asymmetric division of the "svp" progenitor cell: the posterior-most svp-expressing CC nuclei in each hemisegment are arrested in the process of dividing, and the two nuclei are unable to dissociate. This does not change the number of svp-expressing CCs, but results in a reduction in the number of associated svp-expressing PCs. Karyokinesis defects are also seen in the the symmetrically dividing tin-expressing CCs, resulting in localised reduction in the number of these cells. Additional cell divisions sometimes occur in the tin-expressing CCs.

Stocks (0)
Notes on Origin
Discoverer
 
Balancer / Genotype Variants of the Aberration
 
Separable Components
 
Other Comments
 
Synonyms and Secondary IDs (2)
Reported As
Symbol Synonym
CHES-1-like1
Name Synonyms
Secondary FlyBase IDs
  • FBal0267970
References (4)