Allele Dmel\Dhc64C^4-19

General Information
Symbol	Dmel\Dhc64C^4-19	Species	D. melanogaster
Name		FlyBase ID	FBal0048185
Feature type	allele	Associated gene	Dmel\Dhc64C
Also Known As	Dhc^4-19

Allele class	amorphic allele - genetic evidence, loss of function allele
Mutagen	ethyl methanesulfonate
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class	amorphic allele - genetic evidence (Martin et al., 1999, Pilling et al., 2006) loss of function allele (Gepner et al., 1996, McGrail and Hays, 1997)
Mutagen	ethyl methanesulfonate (Gepner et al., 1996)
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference Genomic Southern blotting revealed no polymorphism between the mutant and wild type chromosome. (Gepner et al., 1996)
Cytology
Phenotypic Data
Phenotypic Class
	cell lethal \| somatic clone (Gepner et al., 1996) cell shape defective \| adult stage \| somatic clone (Horne-Badovinac and Bilder, 2008) lethal \| embryonic stage (Liu et al., 2010) lethal \| larval stage \| recessive (Li et al., 2010) lethal \| recessive (McGrail and Hays, 1997, Gepner et al., 1996, Martin et al., 1999) neuroanatomy defective (with Dhc64C^6-10) (Liu et al., 2010) neuroanatomy defective \| somatic clone (Liu et al., 2000) neurophysiology defective (with Dhc64C^6-10) (Li et al., 2010)
Phenotype Manifest In
	adult mushroom body \| somatic clone (Liu et al., 2000) border follicle cell \| somatic clone (Van De Bor et al., 2011) dendrite \| somatic clone (Liu et al., 2000) embryonic/larval mushroom body \| somatic clone (Liu et al., 2000) embryonic/larval neuromuscular junction (with Dhc64C^6-10) (Li et al., 2010) follicle cell \| somatic clone (Horne-Badovinac and Bilder, 2008) mitochondrion (Pilling et al., 2006) mitochondrion (with Dhc64C^6-10) (Pilling et al., 2006) NMJ bouton (with Dhc64C^6-10) (Li et al., 2010) oocyte (McGrail and Hays, 1997) spermatid cyst (Ghosh-Roy et al., 2004) spermatocyte fusome (Ghosh-Roy et al., 2004) synapse (with Dhc64C^6-10) (Liu et al., 2010) terminal tracheal cell \| somatic clone (Schottenfeld-Roames and Ghabrial, 2012) type I neuroblast \| somatic clone (Wang et al., 2011)
Detailed Description
	Statement Reference 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) 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 the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Statement Reference Dhc64C^4-19 is an enhancer of visible \| dominant phenotype of Egfr^E1 (Iyadurai et al., 2008)
Suppressor of
Statement Reference Dhc64C[+]/Dhc64C^4-19 is a suppressor of male fertile \| poor phenotype of ctp^DIIA82 (Ghosh-Roy et al., 2004) Dhc64C[+]/Dhc64C^4-19 is a suppressor of male fertile \| poor phenotype of ctp^ins1 (Ghosh-Roy 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) Dhc64C^4-19 is a suppressor of partially lethal - majority die \| embryonic stage phenotype of BicD^D, stau^unspecified (Navarro et al., 2004)
Other
Statement Reference Dhc64C[+]/Dhc64C^4-19, Khc^unspecified 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^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)
Phenotype Manifest In
Enhancer of
Statement Reference 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) 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)
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 cystic bulge phenotype of ctp^ins1 (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 nucleus & spermatid phenotype of ctp^ins1 (Ghosh-Roy et al., 2005)
Suppressor of
Statement Reference Dhc64C[+]/Dhc64C^4-19 is a suppressor of spermatocyte fusome phenotype of ctp^ins1 (Ghosh-Roy et al., 2004)
Other
Statement Reference Dhc64C[+]/Dhc64C^4-19, Khc^unspecified 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^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)
Additional Comments
Genetic Interactions
Statement Reference 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 & 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
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 & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 5 )
Reported As
Symbol Synonym	Dhc4-19 (Van De Bor et al., 2011) Dhc64C^4-19 (Schottenfeld-Roames and Ghabrial, 2012, Pilling et al., 2006, Ghosh-Roy et al., 2005, Christensen et al., 2008.4.15, Anderson et al., 2009, Li et al., 2008, Liu et al., 2010, Li et al., 2010) dhc64C^4-19 (Zheng et al., 2008, Wang et al., 2011, Johnson et al., 2009) Dhc^4-19 (Ji et al., 2002, Navarro et al., 2004, Iyadurai et al., 2008, Horne-Badovinac and Bilder, 2008) l(3)64Ca^4-19
Name Synonym
Secondary FlyBase IDs

References ( 22 )

Generate a list of	All references relating to this allele ( 22 )

List References by type	Research paper ( 20 ) Review ( 1 ) Personal communication to FlyBase ( 1 )
Recent research papers ( 3 )
	Schottenfeld-Roames and Ghabrial, 2012, Nat. Cell Biol. 14(4): 386--393 Whacked and Rab35 polarize dynein-motor-complex-dependent seamless tube growth. [FBrf0217936] Van De Bor et al., 2011, Development 138(7): 1383--1393 Asymmetric localisation of cytokine mRNA is essential for JAK/STAT activation during cell invasiveness. [FBrf0213214] Wang et al., 2011, Dev. Cell 21(3): 520--533 An ana2/ctp/mud complex regulates spindle orientation in Drosophila neuroblasts. [FBrf0215580] Show all research papers ...
Recent reviews (0)
	All reviews listed in FlyBase were published before 2011 Show reviews ...

Allele Dmel\Dhc64C4-19

Allele Dmel\Dhc64C^4-19