|Feature type||allele||Associated gene||Dmel\Dhc64C|
|Also Known As||dhc6-6, Dhc6-6|
|Allele class||loss of function allele, hypomorphic allele - genetic evidence|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Genomic Southern blotting revealed no polymorphism between the mutant and wild type chromosome.
|Phenotype Manifest In|
Dhc64C6-6/Dhc64C6-12 mutant clonal prefollicular cysts show premature mitochondrial accumulation at the middle of the fusome compared to wild-type cysts. The Balbiani body is reduced in the oocytes that develop from these clones.
Dhc64C6-6/Dhc64C6-8 trans-heterozygous mutants are adult viable. Dhc64C6-6/Dhc64C6-8 mutants (m/z mutants) produce large sheets of embryonic cuticle, indicative of relatively normal epithelial polarity.
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.
Ooplasmic streaming still occurs in stage 9 Dhc64C6-6/Dhc64C6-12 oocytes but it is significantly slower than normal.
Ovaries from Dhc64C6-6/Dhc64C6-12 females show a range of phenotypes, including the failure of the oocyte to differentiate.
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. Dhc64C6-6/Df(3L)10H hemizygous larval neuroblasts frequently show a reduced affinity of centrosomes for spindle poles. Spindle microtubule bundles are often disrupted and curved.
Dhc64C6-6/Dhc64C6-12 transheterozygous ovaries produce mature eggs, however, the eggs are fragile and show variable defects in size, shape and number and orientation of the chorionic appendages.
Lethality acts during larval, pupal or pharate adult phase. Low levels (3-12%) of embryonic lethality are observed.
|Phenotype Manifest In|
The baz4/+ phenotype is enhanced in homozygous, heterozygous or trans-heterozygous Dhc64C6-6 or Dhc64C6-8 mutants, resulting in larger cuticle holes and an overall loss of cuticle.
Dhc64C6-6 is a strong dominant suppressor of the Lis-1E415 homozygous phenotype, resulting in fertility, proper oocyte nucleus positioning and near normal oocyte growth.
|Complementation & Rescue Data|
|Fails to complement|
|Stocks ( 1 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 9 )|
|Secondary FlyBase IDs|
|References ( 22 )|
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|Recent research papers ( 1 )|