FlyBase Allele Report: Dmel\Dhc64C[4-19]

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.

(Schottenfeld-Roames and Ghabrial, 2012)

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.

(Yang et al., 2012)

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.

(Van De Bor et al., 2011)

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.

(Wang et al., 2011)

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.

(Li et al., 2010)

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.

(Liu et al., 2010)

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.

(Horne-Badovinac and Bilder, 2008)

The retrograde flux of mitochondria in the motor axons of Dhc64C^6-10/Dhc64C^4-19 larvae is reduced more than sixfold compared to wild-type larvae. Dhc64C^6-10/Dhc64C^4-19 nerves show axonal swellings although these do not appear to be the cause of the mitochondrial transport problems.

Dhc64C^4-19/+ nerves also show a significant reduction in the retrograde transport of mitochondria.

(Pilling et al., 2006)

The Dhc64C^4-19 allele has a mildly dominant effect on elongation cone stability in the testes of adult males. The average length of cysts is shortened in Dhc64C^4-19 testes, as the peak of the elongation cone (EC) distribution profile is shifted to the basal end.

(Ghosh-Roy et al., 2004)

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.

(Liu et al., 2000)

Dhc64C^4-19/Df(3L)10^H hemizygous larvae show lethality during late larval and pupal stages.

(Martin et al., 1999)

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.

(McGrail and Hays, 1997)

Strong allele. 75-80% of the lethality acts during larval stages. Low levels (3-12%) of embryonic lethality are observed.

(Gepner et al., 1996)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhancer of

Statement

Reference

Dhc64C[+]/Dhc64C^4-19 is an enhancer of abnormal planar polarity phenotype of Scer\GAL4^Bx-MS1096, kermit^UAS.cLa

(Lin and Katanaev, 2013)

Dhc64C^4-19 is an enhancer of visible | dominant phenotype of Egfr^E1

(Iyadurai et al., 2008)

Dhc64C^4-19 is an enhancer of visible phenotype of Hsap\HTT^{128Q.1-336.UAS}, Scer\GAL4^GMR.PU

(Kaltenbach et al., 2007)

Suppressor of

Statement

Reference

Dhc64C[+]/Dhc64C^4-19 is a suppressor of male semi-sterile phenotype of ctp^DIIA82

(Ghosh-Roy et al., 2004)

Dhc64C[+]/Dhc64C^4-19 is a suppressor of male semi-sterile phenotype of ctp^ins1

(Ghosh-Roy et al., 2004)

Dhc64C^4-19 is a suppressor of partially lethal - majority die | embryonic stage phenotype of BicD^D, stau^unspecified

(Navarro et al., 2004)

Dhc64C^4-19/stau^unspecified is a suppressor of partially lethal - majority die | embryonic stage phenotype of BicD^D

(Navarro et al., 2004)

Other

Statement

Reference

Dhc64C^4-19, Khc[+]/Khc^unspecified has paralytic | dominant | larval stage phenotype

(Martin et al., 1999)

Dhc64C^4-19, Klc^unspecified/Klc[+] has paralytic | dominant | larval stage phenotype

(Martin et al., 1999)

Dhc64C[+]/Dhc64C^4-19, Klc^unspecified has paralytic | dominant | larval stage phenotype

(Martin et al., 1999)

Dhc64C[+]/Dhc64C^4-19, Khc^unspecified has paralytic | dominant | larval stage phenotype

(Martin et al., 1999)

Phenotype Manifest In

NOT Enhanced by

Statement

Reference

Dhc64C^4-19 has mitochondrion | larval stage phenotype, non-enhanceable by Sod1^G85R

(Nemtsova et al., 2023)

Dhc64C^4-19 has larval multidendritic neuron phenotype, non-enhanceable by Sod1^G85R

(Nemtsova et al., 2023)

Dhc64C^4-19 has axon | larval stage phenotype, non-enhanceable by Sod1^G85R

(Nemtsova et al., 2023)

NOT suppressed by

Statement

Reference

Dhc64C^4-19 has mitochondrion | larval stage phenotype, non-suppressible by Sod1^G85R

(Nemtsova et al., 2023)

Dhc64C^4-19 has larval multidendritic neuron phenotype, non-suppressible by Sod1^G85R

(Nemtsova et al., 2023)

Dhc64C^4-19 has axon | larval stage phenotype, non-suppressible by Sod1^G85R

(Nemtsova et al., 2023)

Enhancer of

Statement

Reference

Dhc64C[+]/Dhc64C^4-19 is an enhancer of wing hair | increased number phenotype of Scer\GAL4^Bx-MS1096, kermit^UAS.cLa

(Lin and Katanaev, 2013)

Dhc64C[+]/Dhc64C^4-19 is an enhancer of spermatid phenotype of asun^f02815

(Anderson et al., 2009)

Dhc64C^4-19 is an enhancer of embryonic/larval cuticle phenotype of sdt^P10

(Horne-Badovinac and Bilder, 2008)

Dhc64C^4-19 is an enhancer of eye phenotype of Egfr^E1

(Iyadurai et al., 2008)

Dhc64C^4-19 is an enhancer of eye phenotype of Hsap\HTT^{128Q.1-336.UAS}, Scer\GAL4^GMR.PU

(Kaltenbach et al., 2007)

Dhc64C[+]/Dhc64C^4-19 is an enhancer of aster | embryonic cycle 5 phenotype of CycB^+t10

(Ji et al., 2002)

Dhc64C[+]/Dhc64C^4-19 is an enhancer of aster | embryonic cycle 6 phenotype of CycB^+t10

(Ji et al., 2002)

Dhc64C[+]/Dhc64C^4-19 is an enhancer of aster | embryonic cycle 7 phenotype of CycB^+t10

(Ji et al., 2002)

NOT Enhancer of

Statement

Reference

Dhc64C^4-19 is a non-enhancer of cystic bulge phenotype of ctp^exc39

(Ghosh-Roy et al., 2005)

Dhc64C^4-19 is a non-enhancer of nucleus & spermatid phenotype of ctp^exc39

(Ghosh-Roy et al., 2005)

Dhc64C^4-19 is a non-enhancer of cystic bulge phenotype of ctp^ins1

(Ghosh-Roy et al., 2005)

Dhc64C^4-19 is a non-enhancer of nucleus & spermatid phenotype of ctp^ins1

(Ghosh-Roy et al., 2005)

Suppressor of

Statement

Reference

Dhc64C[+]/Dhc64C^4-19 is a suppressor | partially of scutellar bristle phenotype of IKKε^DN.UAS, Scer\GAL4^sca.PU

(Otani et al., 2011)

Dhc64C[+]/Dhc64C^4-19 is a suppressor of spermatocyte fusome phenotype of ctp^ins1

(Ghosh-Roy et al., 2004)

Other

Statement

Reference

Dhc64C^4-19, Khc[+]/Khc^unspecified has posterior fascicle & axon phenotype

(Martin et al., 1999)

Dhc64C^4-19, Klc^unspecified/Klc[+] has posterior fascicle & axon phenotype

(Martin et al., 1999)

Dhc64C[+]/Dhc64C^4-19, Klc^unspecified has posterior fascicle & axon phenotype

(Martin et al., 1999)

Dhc64C[+]/Dhc64C^4-19, Khc^unspecified has posterior fascicle & axon phenotype

(Martin et al., 1999)

Additional Comments

Genetic Interactions

Statement

Reference

Bsg25D^null.R/Bsg25D^null.R, Dhc64C^4-19/+ stage 16 embryo myotubes present normal nuclear positioning.

(Rosen et al., 2019)

The presence of Dhc64C^4-19/+ enhances the multiple wing hair phenotype caused by expression of kermit^Scer\UAS.cLa under the control of Scer\GAL4^Bx-MS1096.

(Lin and Katanaev, 2013)

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%).

(Anderson et al., 2009)

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.

(Horne-Badovinac and Bilder, 2008)

The ctp^ins1/Y nuclear bundles and individualization complex phenotype is not affected by the Dhc64C^4-19 allele.

(Ghosh-Roy et al., 2005)

The sterility of ctp^ins1 male mutants is suppressed when they carry one copy of Dhc64C^4-19. The sterility of ctp^DIIA82 males is partially suppressed when they carry one copy of Dhc64C^4-19. The Dhc64C^4-19 mutation suppresses the testicular phenotype of ctp^ins1 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.

(Ghosh-Roy et al., 2004)

BicD^D stau^unspecified/Dhc64C^4-19 triple mutants exhibit a 39% hatch-rate, compared to BicD^D stau^unspecified double mutants, which exhibit a hatch-rate of 8%. This indicates suppression of the BicD^D stau^unspecified phenotype by Dhc64C^4-19.

(Navarro et al., 2004)

Dhc64C^4-19 Khc^unspecified and Dhc64C^4-19 Klc^unspecified double heterozygous larvae show a posterior paralysis phenotype. Axon swellings are seen.

(Martin et al., 1999)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Complements

Dhc64C^8-1

(Gepner et al., 1996)

Rescued by

Dhc64C^4-19 is rescued by Dhc64C^+tDN17

(McGrail and Hays, 1997)

Comments

Images (0)

Mutant

Wild-type

Stocks (3)

Bloomington

23863

w^*; Dhc64C^4-19 P{FRT(w^hs)}2A/TM6B, Tb¹

5274

mwh¹ Dhc64C^4-19 jv¹ ca¹/TM6B, Tb⁺ ca¹

Kyoto

108142

mwh¹ Dhc64C^4-19 jv¹ ca¹/TM6B, Tb¹ ca¹

Notes on Origin

Discoverer

Comments

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

(Gepner et al., 1996)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (8)

Reported As

Symbol Synonym

Dhc4-19

(Van De Bor et al., 2011)

Dhc64C 4-19

(Kreko-Pierce and Eaton, 2017)

Dhc64C^4-19

(Collins et al., 2017, Muñoz-Soriano et al., 2016, Schulman et al., 2014, Lin and Katanaev, 2013, Schottenfeld-Roames and Ghabrial, 2012, Yang et al., 2012, Li et al., 2010, Liu et al., 2010, Anderson et al., 2009, Christensen et al., 2008.4.15, Li et al., 2008, Pilling et al., 2006, Ghosh-Roy et al., 2005)

Dhc^4-19

(Nemtsova et al., 2023, Horne-Badovinac and Bilder, 2008, Iyadurai et al., 2008, Navarro et al., 2004, Ji et al., 2002)

dhc64C^4-19

(Chen et al., 2016, Beaven et al., 2015, Kang et al., 2014, Wang et al., 2011, Johnson et al., 2009, Zheng et al., 2008)

dhc64c^4-19

(Otani et al., 2011)

dhc^4-19

(Rosen et al., 2019, Das et al., 2016)

l(3)64Ca^4-19

Name Synonyms

Secondary FlyBase IDs

References (36)

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