Genomic Southern blotting revealed no polymorphism between the mutant and wild type chromosome.
Embryos derived from Dhc64C6-6/Dhc64C6-8 females that develop to nuclear cycle 14 fail to undergo normal furrow formation that is seen between adjacent nuclei in wild-type embryos at this stage. These embryos also accumulate fewer Golgi bodies in the apical cytoplasm compared to wild-type embryos at this stage, despite the presence of intact microtubules.
Dhc64C6-6/Dhc64C6-8 adults are recovered in equal proportion to nonmutant siblings, indicating that this heteroallelic combination is not less viable than wild type. 94% of embryos derived from Dhc64C6-6/Dhc64C6-8 females mated to wild-type males fail to survive beyond the end of embryogenesis. Most of these embryos fail to cellularise properly and cannot complete gastrulation. Approximately 5.7% of the remaining embryos survive through hatching, with 1.4% of these embryos failing to complete larval development. The approximately 3% of embryos that complete larval development survive to adulthood. Two predominant mitotic defects, free centrosomes and multipolar spindle arrays, are found in syncytial blastoderm embryos derived from Dhc64C6-6/Dhc64C6-8 females mated to wild-type males that are arrested early in embryogenesis. Free centrosomes are seen either singly or in numbers. The free centrosomes can arise during both early and late nuclear cycles by different pathways that are independent of cell cycle stage. First, centrosomes are seen departing the nuclear envelope during prophase. The detachment of centrosomes from bipolar and multipolar spindles is also seen. Spindles are seen lacking one or both centrosomes at their poles. The mean distance between centrosomes and the associated spindle poles is 1.8μm, significantly higher than wild type. Centrosome migration is abnormal in these embryos. Spindle configurations are often excessively curved and the normally uniform spacing between spindles within the syncytium is disrupted. Multipolar spindle arrays are seen, which most commonly arise from fusion of a number of neighbouring spindles. Spindle-associated or single free centrosomes are also capable of inducing ectopic spindle poles on adjacent mitotic arrays. Abnormal spindles in which an apparently normal half-spindle containing a single centrosome, spindle pole and chromatin is flanked by an abnormally blunt-ended pole lacking a detectable centrosome are also seen. The mitotic defects are detected during very early nuclear cycles. The syncytial nuclear divisions of embryos derived from Dhc64C6-6/Dhc64C6-8 females mated to wild-type males show poor synchrony.
Lethality acts during larval, pupal or pharate adult phase. Low levels (3-12%) of embryonic lethality are observed.
Dhc64C6-6/Dhc64C6-8 is an enhancer of lethal | embryonic stage phenotype of baz4
Dhc64C6-6/Dhc64C6-8 is an enhancer of abnormal cell polarity phenotype of baz4
Dhc64C[+]/Dhc64C6-8 is an enhancer of visible | dominant phenotype of DCTN1-p150Gl-1
Dhc64C6-6/Dhc64C6-8 is an enhancer of embryonic/first instar larval cuticle phenotype of baz4
Dhc64C[+]/Dhc64C6-8 is an enhancer of eye phenotype of DCTN1-p150Gl-1
Dhc64C[+]/Dhc64C6-8 is an enhancer of ommatidium phenotype of DCTN1-p150Gl-1
Dhc64C6-6/Dhc64C6-8 is rescued by Dhc64C+tDN17
Dhc64C6-8 is rescued by Dhc64C+tDN17
Complements Dhc64C8-1. Intragenic complementation relationships involve Dhc64C5-6, Dhc64C6-6, Dhc64C6-8, Dhc64C6-10, Dhc64C6-12 and Dhc64C8-1.