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General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Key Links
Nature of the Allele
Mutations Mapped to the Genome
Additional Notes
Associated Sequence Data
DNA sequence
Protein sequence
Progenitor genotype
Nature of the lesion

Genomic Southern blotting revealed no polymorphism between the mutant and wild type chromosome.

Expression Data
Reporter Expression
Additional Information
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Modifiers Based on Experimental Evidence ( 1 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
Disease-implicated variant(s)
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description

Cultured primary neurons derived from homozygous Dhc64C4-19 embryos have a significantly increased axon length compared to wild-type controls.

The terminal cells in Dhc64C4-19 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.

Severe delays in border cell migration are seen in follicle cell clones in which several of the migratory border cells, but none of the polar cells, are mutant. In mixed border cell clusters, the mutant cells are always at the back of the migrating cluster.

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 Dhc64C4-19 mutant animals do not develop to third instar stage.

In Dhc64C4-19/Dhc64C6-10 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, Dhc64C4-19/Dhc64C6-10 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 BicDr5/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 Dhc64C4-19/Dhc64C6-10 mutants.

Dhc64C6-10/Dhc64C4-19 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 Dhc64C4-19 follicle cell clones, induced by driving Scer\FLP1Scer\UAS.cUa under the control of the Scer\GAL4e22c 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.

Dhc64C4-19/Df(3L)10H hemizygous larvae show lethality during late larval and pupal stages.

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.

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

Dhc64C[+]/Dhc64C4-19 is an enhancer of spermatid phenotype of asunf02815

Dhc64C4-19 is an enhancer of eye phenotype of EgfrE1

Dhc64C[+]/Dhc64C4-19 is an enhancer of aster | embryonic cycle 5 phenotype of CycB+t10

Dhc64C[+]/Dhc64C4-19 is an enhancer of aster | embryonic cycle 6 phenotype of CycB+t10

Dhc64C[+]/Dhc64C4-19 is an enhancer of aster | embryonic cycle 7 phenotype of CycB+t10

NOT Enhancer of

Dhc64C4-19 is a non-enhancer of cystic bulge phenotype of ctpexc39

Dhc64C4-19 is a non-enhancer of nucleus & spermatid phenotype of ctpexc39

Dhc64C4-19 is a non-enhancer of cystic bulge phenotype of ctpins1

Dhc64C4-19 is a non-enhancer of nucleus & spermatid phenotype of ctpins1

Suppressor of

Dhc64C[+]/Dhc64C4-19 is a suppressor of spermatocyte fusome phenotype of ctpins1


Dhc64C[+]/Dhc64C4-19, Klcunspecified has posterior fascicle & axon phenotype

Dhc64C4-19, Khc[+]/Khcunspecified has posterior fascicle & axon phenotype

Dhc64C4-19, Klcunspecified/Klc[+] has posterior fascicle & axon phenotype

Dhc64C[+]/Dhc64C4-19, Khcunspecified has posterior fascicle & axon phenotype

Additional Comments
Genetic Interactions

Bsg25Dnull.R/Bsg25Dnull.R, Dhc64C4-19/+ stage 16 embryo myotubes present normal nuclear positioning.

The presence of Dhc64C4-19/+ enhances the multiple wing hair phenotype caused by expression of kermitScer\UAS.cLa under the control of Scer\GAL4Bx-MS1096.

A single copy of Dhc64C4-19 introduced into the Mat89Bbf02815 background significantly increases the incidence of multi-nucleated spermatids (from 64% to 93%).

Reducing the number of copies of Dhc64C4-19 (embryos examined could carry between 0 and 2 copies) enhances the cuticle phenotype seen in hemizygous sdtP10. Embryos generally have only a single patch or fragments of cuticle compared to the two patches typically seen in sdtP10 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.

Dhc64C4-19 Khcunspecified and Dhc64C4-19 Klcunspecified double heterozygous larvae show a posterior paralysis phenotype. Axon swellings are seen.

Xenogenetic Interactions
Complementation and Rescue Data
Images (0)
Stocks (3)
Notes on Origin

Clones are only generated in the presence of P{Dhc+}.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (8)
References (35)