|Feature type||allele||Associated gene||Dmel\Dhc64C|
|Also Known As||Dhc4-19|
|Allele class||amorphic allele - genetic evidence, loss of function allele|
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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|
The terminal cells in Dhc64C[4-19] mutant trachea have thin cytoplasmic branches that lack air filling. Seamless tubes do not extend into these branches, although acetylated microtubules often do. Formation of filopodia at branch tips is disrupted and ectopic seamless tubes that are not air filled are detected near the nucleus. Discontinuous apical membrane fragments are found in terminal branches lacking seamless tubes and are associated with microtubule tracts.
Border cell clusters composed entirely of homozygous cells do not migrate and are found at the anterior tip of the egg chamber at late stage 9. In mosaic clusters in which the polar follicle cells are homozygous, the number of outer border cells is reduced compared to wild type. In mosaic clusters in which all the outer border cells are homozygous and the polar cells are wild-type, migration of the cluster is normal and the cluster contains the normal number of outer border cells.
Homozygous larval neuroblast clones show a spindle misorientation phenotype in metaphase. Neuroblast overproliferation is seen in type I but not in type II neuroblast clones.
Homozygous Dhc64C[4-19] mutant animals do not develop to third instar stage. In Dhc64C[4-19]/Dhc64C[6-10] mutant third instar larvae, amplitudes of evoked excitatory junctional potentials (EJPs) in abdominal muscles (a measure of the extent of neurotransmitter release) are indistinguishable from wild-type for at least 30 minutes of low-frequency electrical stimulation (0.5 Hz) of motor neurons. The amplitude and frequency of spontaneous miniature EJPs (mEJPs) in the mutants are not significantly different from that of wild-type. In contrast, Dhc64C[4-19]/Dhc64C[6-10] mutants are unable to sustain normal levels of neurotransmission during high-frequency electrical stimulation. EJP amplitudes in the mutants declined abnormally rapidly within five minutes of stimulation at 10 Hz. There is an upturn in EJP amplitudes after switching from 10 to 0.5 Hz stimulation in the mutants. The EJP response does not reach wild-type levels in the mutants even one hundred seconds after switching from high- to low-frequency stimulation. The total amount of the lipophilic dye FM 1-43 taken up into boutons during 10 Hz stimulation is significantly reduced in BicD[r5]/Df(2L)TW119 mutants, compared with controls. Potassium-induced unloading of FM1-43 (pre-loaded into an internalised vesicle population during stimulation) is defective in Dhc64C[4-19]/Dhc64C[6-10] mutants.
Dhc64C[6-10]/Dhc64C[4-19] hypomorphic heterozygous mutants appear normal and display neuromuscular junctions indistinguishable from wild-type. At 7 and 9 hours after puparium formation there is no obvious change in synaptic vesicle distribution (compared to a redistribution in wild-type). These mutants also show considerably larger synaptic areas compared to wild-type.
Homozygous Dhc64C[4-19] follicle cell clones, induced by driving Scer\FLP1[Scer\UAS.cUa] under the control of the Scer\GAL4[e22c] driver, show rounding and multilayering, predominantly at the posterior of the egg chamber. Gaps are seen in the epithelium.
The retrograde flux of mitochondria in the motor axons of Dhc64C6-10/Dhc64C4-19 larvae is reduced more than sixfold compared to wild-type larvae. Dhc64C6-10/Dhc64C4-19 nerves show axonal swellings although these do not appear to be the cause of the mitochondrial transport problems. Dhc64C4-19/+ nerves also show a significant reduction in the retrograde transport of mitochondria.
The Dhc64C4-19 allele has a mildly dominant effect on elongation cone stability in the testes of adult males. The average length of cysts is shortened in Dhc64C4-19 testes, as the peak of the elongation cone (EC) distribution profile is shifted to the basal end.
Homozygous mushroom body neuroblast clones are reduced in size compared to control clones when examined in larvae or adults. The clones show a progressive reduction in BrdU incorporation during larval life, in contrast to wild-type clones, which generate new neurons at all times examined. Homozygous mushroom body neuroblast clones examined at the larval stage show a significant reduction of dendritic complexity compared to wild type. Single cell homozygous clones in the mushroom body examined in adults have defects in dendritic growth and branching. Axons in homozygous mushroom body neuroblast and single- and two-cell clones have axonal swellings which are preferentially located at the axon termini.
Mosaic egg chambers fail to produce mature eggs, the oocyte fails to differentiate and each of the cells adopt the nurse cell fate. The initial polarity of the germ line cyst is disrupted as shown by the disorganised pattern of ring canals. Dhc64C+tDN17 can rescue the production of normal fertilised eggs.
Strong allele. 75-80% of the lethality acts during larval stages. Low levels (3-12%) of embryonic lethality are observed.
Dhc64C4-19/stauunspecified is a suppressor of partially lethal - majority die | embryonic stage phenotype of BicDD
|Phenotype Manifest In|
|NOT Enhancer of|
A single copy of Dhc64C[4-19] introduced into the Mat89Bb[f02815] background significantly increases the incidence of multi-nucleated spermatids (from 64% to 93%).
Reducing the number of copies of Dhc64C[4-19] (embryos examined could carry between 0 and 2 copies) enhances the cuticle phenotype seen in hemizygous sdt[P10]. Embryos generally have only a single patch or fragments of cuticle compared to the two patches typically seen in sdt[P10] mutants alone.
The ctpins1/Y nuclear bundles and individualization complex phenotype is not affected by the Dhc64C4-19 allele.
The sterility of ctpins1 male mutants is suppressed when they carry one copy of Dhc64C4-19. The sterility of ctpDIIA82 males is partially suppressed when they carry one copy of Dhc64C4-19. The Dhc64C4-19 mutation suppresses the testicular phenotype of ctpins1 males; these double mutants have greater numbers of ECs within each cyst and a higher proportion of these are intact. However, the EC distribution profile is not altered.
BicDD stauunspecified/Dhc64C4-19 triple mutants exhibit a 39% hatch-rate, compared to BicDD stauunspecified double mutants, which exhibit a hatch-rate of 8%. This indicates suppression of the BicDD stauunspecified phenotype by Dhc64C4-19.
|Complementation & Rescue Data|
|Stocks ( 3 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 5 )|
|Secondary FlyBase IDs|
|References ( 22 )|
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|Recent research papers ( 3 )|
|Recent reviews (0)|
|All reviews listed in FlyBase were published before 2011|