Deletion of 39 nucleotides leading to an in frame deletion of amino acids 26-38.
Deletion of 39 nucleotides leading to an in frame deletion of amino acids 26-38.
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.
Cdc37e1E is a suppressor of eye phenotype of Rho1GMR.PH
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).
Disrupts sevB4 protein signalling.
Lethality cannot be rescued by up to four copies of Hsp83+t7.5.
No interaction with P{sev-svp1} or P{sev-svp2}.
Not rescued by: Hsp83+t7.5.