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General Information
Symbol
Dmel\Cdc37e1E
Species
D. melanogaster
Name
FlyBase ID
FBal0029088
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Mutagen
    Nature of the Allele
    Allele class
    Mutagen
    Mutations Mapped to the Genome
     
    Type
    Location
    Additional Notes
    References
    Comment:

    Deletion of 39 nucleotides leading to an in frame deletion of amino acids 26-38.

    Associated Sequence Data
    DNA sequence
    Protein sequence
     
     
    Progenitor genotype
    Cytology
    Nature of the lesion
    Statement
    Reference

    Deletion of 39 nucleotides leading to an in frame deletion of amino acids 26-38.

    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

    Cdc37e1E/Cdc37e6B animals die as third instar larvae. Mutant larvae have spermatids with a phenotype characteristic of cytokinesis failure: 4 nuclei associated with a single mitochondrial derivative. In addition these spermatids have nuclei of variable size, suggesting aberrant chromosome distribution at meiotic division. Time lapse video analysis of Cdc37e1E/Cdc37e6B spermatocyte meiosis reveals numerous defects. Anaphase I chromosomes are poorly condensed and often fail to align in a proper metaphase plate. The overall distance between the two centrosomes at metaphase is shorter than in control cells and the overall shape of the mutant spindle is stumpier. During metaphase, the homologues split apart asynchronously and the first signs of splitting are earlier than in control cells. During anaphase, segregation mistakes are obvious, with chromosomes acquiring an amphitelic orientation, i.e. both sister kinetochores orientated to opposite poles. Premature sister chromatid separation takes place as the amphitelic chromosomes segregate their chromatids during anaphase I. Single chromatids are also observed at different positions within the anaphase spindle. After segregation the chromatin decondenses and the daughter nuclei are formed, but no sign of furrow constriction is detected and cytokinesis does not occur, giving rise to binucleated cells that sometimes contain additional micronuclei. Several aspects of microtubule organization are disrupted in Cdc37e1E/Cdc37e6B mutant spermatocytes: the kinetochore fibers are reduced both in size and in density compared with wild-type; at late anaphase the dense bundles of microtubules that run along the membrane at the area where furrowing will occur in the control are absent; no central spindle is formed; the contractile ring (midbody) is absent.

    Slight suppressor effect on Src42AKR.hs.2sev.

    External Data
    Interactions
    Show genetic interaction network for Enhancers & Suppressors
    Phenotypic Class
    Phenotype Manifest In
    Enhancer of
    Statement
    Reference

    Cdc37[+]/Cdc37e1E is an enhancer of phenotype of sevB4

    Suppressor of
    Statement
    Reference

    Cdc37e1E is a suppressor of eye phenotype of Rho1GMR.PH

    Additional Comments
    Genetic Interactions
    Statement
    Reference

    Suppression of the rough eye phenotype caused by two insertions of P{GMR-Rho1}, tertiary and secondary pigment cells surround rhabdomeres of near normal morphology and a significant number of ommatidia are apparent.

    No effect on the rough eye phenotype (formation of extra R7 cells) caused by P{sev-svp2} and no effect on the P{ro-svp1} rough eye phenotype (loss of one or more outer photoreceptors from many of the ommatidia).

    Mutations at Cdc37 dominantly enhance the abdominal phenotype of cdc2E1-24/cdc2216P, causing profound derangement of abdominal structures, missing bristles, and fused segments. Mutations at Cdc37 also reduced the temperature at which the inviability of cdc2E1-24/cdc2216P takes effect.

    Disrupts sevB4 protein signalling.

    Xenogenetic Interactions
    Statement
    Reference
    Complementation and Rescue Data
    Comments

    Lethality cannot be rescued by up to four copies of Hsp83+t7.5.

    Images (0)
    Mutant
    Wild-type
    Stocks (0)
    Notes on Origin
    Discoverer
    Comments
    Comments
    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (3)
    Reported As
    Symbol Synonym
    Cdc37e1E
    Name Synonyms
    Secondary FlyBase IDs
      References (8)