A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\aPKCk06403

General Information
SymbolDmel\aPKCk06403SpeciesD. melanogaster
NameFlyBase IDFBal0064438
Feature typealleleAssociated geneDmel\aPKC
Also Known AsDaPKCk06403, aPKC06403, l(2)k06403
Map ( GBrowse ) Untitled Document detailed view FBti0006743 FBti0035845 FBti0048688 FBti0125186_1 FBti0125186_2 FBti0023569 FBti0109181 FBti0046409 FBti0075459 FBti0066739 FBti0037374
Allele classloss of function allele, amorphic allele - genetic evidence
MutagenP-element activity
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Description
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FB2013_03
FB2013_02
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hide Nature of the Allele
Allele class
Mutagen
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
P{lacW} insertion in the third intron.
Caused by insertion
Cytology
hide Phenotypic Data
hide Phenotypic Class
hide Phenotype Manifest In
larval brain & neuroblast
mushroom body & neuron | somatic clone
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Statement
Reference
aPKC[k06403] mutant wing disc clones cannot be detected at the first instar larval stage. However, clones can be seen when induction takes place at the second instar larval stage, and these are positive for apoptosis. aPKC[ts]/aPKC[k06403] flies are viable at the permissive temperature (25[o]C) and adult flies appear morphologically normal. However, females are sterile, with no larvae hatching from laid eggs even when crossed with wild type males. Germline cyst encapsulation phenotypes are seen immediately after the mesenchymal-to-epithelial transition in region 3 of the germarium in aPKC[ts]/Df(2R)l4 mutant ovaries at the permissive temperature. The resulting follicular epithelium adherens junctions, apicobasal polarity and actin-myosin cytoskeleton appear normal. At the restrictive temperature (30[o]C) very few flies eclose from the pupal cases, with occasional escaper flies that exhibit abdominal dorsal closure defects. At 27-28[o]C (the semi-permissive temperature) viability is variable, but almost all flies show significant dorsal closure defects. aPKC[ts]/aPKC[k06403] third instar larval wing discs show a temperature sensitive induction of apoptosis. Whereas at the permissive temperatures (18[o]C and 25[o]C) there are low levels of cell extrusion and apoptosis, at the restrictive temperature (30[0]C) significantly higher levels of cell extrusion and apoptosis are seen, and the wings discs appear smaller than in controls. No phenotypes are seen in the heterozygous controls. At both the permissive and restrictive temperatures there is a significant decrease in the proportion of aPKC[ts]/aPKC[k06403] mutant wing disc cells with the correct planar spindle orientation compared to controls. The decrease is greater at 30[0]C than at 25[o]C. Embryos maternally mutant for aPKC[ts]/aPKC[k06403] fail to complete germ band extension (GBE), with a complete loss of epithelial integrity at the permissive temperature.
Homozygous tracheal terminal cells show a reduction in branching (primarily affecting class II and later-order branches) compared to wild type, a severe reduction in gas-filled lumen and an abnormal branch tip morphology.
aPKC[k06403] mutants display a mild defect in denticle belt formation.
Microtubules are disorganised but are not lost in homozygous follicle cell clones. Piling up of follicle cells and stretching or gaps in the epithelium are seen.
All aPKC[k06403] mutant adult Malpighian tubule renal and nephric stem cells (RNSCs) differentiate into renalcytes (RCs).
Occasional aPKC[psu265]/aPKC[k06403] and aPKC[psu417]/aPKC[k06403] adult escapers are seen. Embryos derived from homozygous female germ-line clones develop only scattered crumbs of cuticle. Epithelial cells in stage 7 embryos derived from homozygous female germ-line clones lose their columnar, monolayered organisation, rounding up and losing contact with each other. Homozygous follicle cell clones show extensive multilayering of the epithelium. An oocyte is specified in only 28% of germ-line clones.
Homozygous single neuroblast clones which are induced in first instar larvae and allowed to develop for 96 hours always contain a single large dpn-positive neuroblast (as do control single neuroblast clones). Progression through mitosis is delayed in aPKC[k06403] larval neuroblasts compared to wild-type neuroblasts; the transit from nuclear envelope breakdown to anaphase onset is 17.84 +/- 4.52 minutes in the mutant neuroblasts compared to 7.76 +/- 2.04 minutes in wild-type neuroblasts.
80% of homozygous female germline clones are arrested at stage 5 or 6 of oogenesis, but some germline clones do develop until stages 9 or 10.
Homozygous larvae have a reduced number of brain neuroblasts.
The transplantation of aPKCk06403 larval neuroblast clones into adult hosts does not cause tumor formation.
No aPKCk06403 homozygous clones can be recovered in the eyes of aPKCk06403 Scer\FRT; Scer\FLP1ey.PN adults and only a few very small clones can be recovered in the eye imaginal disc.
In aPKCExc55/aPKCk06403 mutant animals, there is a decrease in the number of synaptic boutons at the neuromuscular junction (NMJ). Muscle size remains normal.
When somatic clones are made in the follicular epithelium cell polarity defects are seen. These are more severe at the poles of the egg chamber than in lateral positions where polarity is often normal. Zonula adherens is also compromised in clones. Mutant follicle cells are also multilayered. most strikingly at the anterior and posterior poles. When mutant clones are made in the border cells no migration defects are seen.
Somatic clones of aPKCk06403 in the pupal retina are very small - consisting of only a few cells, suggesting a role in proliferation and/or survival of retinal cells.
Stage 15 homozygous embryos have normal epithelial and neuroblast polarity. Homozygous aPKCk06403 mutants die as late second instar larvae, they remain as second instar larvae for at least twice as long as normal. aPKCk06403 mutant second larval instar eye imaginal discs are not organised into an epithelial monolayer and appear to have lost epithelial polarity. They are also smaller than in wild-type. aPKCk06403 mutant clones exhibit a dramatic decrease in the number of neuronal progeny compared to wild-type. aPKCk06403 mushroom body clones contain 75-125 neurons, consisting primarily of early-born γ neurons (in contrast to wild-type clones, which contain 300-400 neurons, consisting of early-born γ neurons as well as later-born α- and β-neurons).
aPKCk06403 germ-line clones fail to differentiate an oocyte as indicated by the presence of polyploid nurse cell nuclei in germ-line mutant egg chambers. Depletion of aPKC function from the follicle cells leads to their multilayering, which disrupts the normal partitioning of germ-line nuclei to successively mature egg chambers caused by mispositioning of mutant follicle cells. IN aPKCk06403 mutant germ-line cysts ring canal distribution and spatioal distribution are indistinguishable from wild-type. No defects are seen in fusome morphology.
Homozygous aPKCk06403 and aPKCk06403/Df(2R)Jp1 embryos derived from heterozygous aPKCk06403/+ females do not form cuticle because they die before cuticle secretion begins (most die before or during cellularisation). The embryos show multilayering of the epithelium at gastrulation, the cells are extremely irregular in shape and apico-basal polarity of the epithelium is lost. Embryos that contain a zygotic wild-type allele of aPKC and are derived from aPKCk06403/+ females often die with characteristic head defects. At the anterior tip of the embryo, the epithelium is multilayered. Hemizygous embryos (that have a wild-type maternal contribution of aPKC) do not show obvious defects before germ band extension. The embryos form cuticles with severe head defects and large ventral holes, or lack ventral cuticle altogether.
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aPKCts/aPKCk06403 has increased cell death | heat sensitive phenotype, suppressible by raps[+]/raps193
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aPKCk06403/aPKC[+] is a suppressor of neuroanatomy defective | somatic clone phenotype of Zif1L15
aPKCk06403/aPKC[+] is a suppressor of visible | heat sensitive phenotype of peb1
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Statement
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Statement
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hideEnhanced by
Statement
Reference
hideSuppressed by
Statement
Reference
aPKCk06403 has denticle belt phenotype, suppressible by armF1α
aPKCts/aPKCk06403 has embryo | dorsal closure stage | heat sensitive phenotype, suppressible by raps[+]/raps193
aPKCts/aPKCk06403 has wing disc | third instar larval stage | heat sensitive phenotype, suppressible by raps[+]/raps193
hideEnhancer of
Statement
Reference
aPKCk06403/aPKC[+] is an enhancer of embryonic/larval cuticle phenotype of baz4
hideSuppressor of
Statement
Reference
aPKCk06403/aPKC[+] is a suppressor | partially of eye phenotype of Fmr1sev.PW
aPKCk06403/aPKC[+] is a suppressor | partially of neuroblast & larval brain & third instar larva phenotype of l(2)gl334
aPKCk06403/aPKC[+] is a suppressor | partially of ommatidium phenotype of Fmr1sev.PW
aPKCk06403/aPKC[+] is a suppressor of dorsal mesothoracic disc & epithelial cell phenotype of l(2)gl334
aPKCk06403/aPKC[+] is a suppressor of eye | heat sensitive phenotype of peb1
aPKCk06403/aPKC[+] is a suppressor of neuroblast | supernumerary | somatic clone phenotype of Zif1L15
aPKCk06403/aPKC[+] is a suppressor of NMJ bouton | larval stage phenotype of Fmr13
aPKCk06403/aPKC[+] is a suppressor of synapse & larval neuromuscular junction phenotype of Fmr13
aPKCk06403/aPKC[+] is a suppressor of ventral thoracic disc & epithelial cell phenotype of l(2)gl334
aPKCk06403/aPKC[+] is a suppressor of ventral thoracic disc phenotype of l(2)gl334
aPKCk06403/aPKC[+] is a suppressor of wing disc phenotype of l(2)gl334
aPKCk06403 is a suppressor of larval brain & neuroblast | supernumerary phenotype of l(2)gl334
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Statement
Reference
raps[193] dominantly suppresses the temperature sensitive induction of apoptosis seen in aPKC[ts]/aPKC[k06403] third instar larval wing discs at the semi-permissive temperature (28[o]C). However, this suppression does not occur at the restrictive temperature (30[o]C). raps[193] dominantly suppresses the abdominal dorsal closure defects seen in aPKC[ts]/aPKC[k06403] mutant flies at the semi-permissive temperature (28[o]C). However, this suppression did not occur at the restrictive temperature (30[o]C).
aPKC[k06403]/+ suppresses the increased number of type II neuroblasts and intermediate neural progenitor cells seen in l(2)gl[334]/l(2)gl[3644] larval brains.
arm[F1α]; aPKC[k06403] double mutants maintain some apical-basal polarity patterning, and while cell shapes are somewhat disrupted, cells appear to align in rows. arm[F1α]; sgg[M11]; aPKC[k06403] triple mutants exhibit significant denticle and cell disruption. Specifically, proper cell shapes and cell alignment are lost, and instead of organization into even rows, cells curved and formed denticle swirls.
The neuroblast overgrowth phenotype seen in Zif[1L15] mutant clones is significantly suppressed in a aPKC[k06403] heterozygous background.
The cuticle phenotype of dead embryos derived from baz[4]/+ embryos derived from a cross of baz[4]/+ females to wild-type males is enhanced if the females also carry one copy of aPKC[k06403].
Hyperplasia in adult Malpighian tubule clones expressing Ras85D[V12.Scer\UAS] (using the MARCM system, under the control of Scer\GAL80[αTub84B.PL] and Scer\GAL4[Scer\FRT.Act5C]) is not suppressed by making them also mutant for aPKC[k06403].
Larval tws[j11C8] mutant clones in an aPKC[k06403]/+ background contain an intermediate number of neuroblasts per clone, partially rescuing the single cell tws[j11C8] clone phenotype. The third instar optic lobe of tws[j11C8]/Df(3R)Exel6265 in a aPKC[k06403]/+ background have a partially reduced number of optic lobe neuroblasts, partially rescuing the tws[j11C8]/Df(3R)Exel6265 phenotype.
The giant fiber axon defects seen in adults expressing Gl[Δ.Scer\UAS] under the control of Scer\GAL4[A307] are partially suppressed by aPKC[k06403]/+.
The reduced size seen in l(2)gl4 L3 larval neuroblasts is not suppressed by aPKCk06403/aPKCk06403 and may in fact be slightly enhanced. l(2)gl334 aPKCk06403/l(2)gl334 + larvae exhibit essentially normal leg and wing imaginal disc morphology including disc size, columnar cell shape and an approximately normal apical membrane domain, at the early third instar stage. The increase in L3 larval brain volume seen in l(2)gl334/l(2)gl4 animals is partially suppressed by aPKCk06403/+. The increase in neuroblast number seen in homozygous l(2)gl334 third larval instar brains is partially suppressed by aPKCk06403/+. aPKCk06403 heterozygosity cannot suppress the l(2)gl4 "small neuroblast" phenotype.
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Reference
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Fails to complement
Rescued by
Comments
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Bloomington
Kyoto
hide Notes on Origin
Discoverer
I. Kiss.
hide Comments
Excision of the P{lacW} element can revert the lethality of aPKCk06403, indicating that the P{lacW} insertion is responsible for the aPKCk06403 phenotype.
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hide Synonyms & Secondary IDs ( 15 )
Reported As
Symbol Synonym
aPKCK06304
aPKCl(2)k06403
aPKC-zetak06403
l(2)k06403k06403
 
Name Synonym
Secondary FlyBase IDs
hide References ( 38 )
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hide Recent research papers ( 7 )
Leibfried et al., 2013, Development 140(2): 362--371
A Cdc42-regulated actin cytoskeleton mediates Drosophila oocyte polarization. [FBrf0220348]
Fletcher et al., 2012, Curr. Biol. 22(12): 1116--1122
Positive feedback and mutual antagonism combine to polarize crumbs in the Drosophila follicle cell epithelium. [FBrf0218646]
Guilgur et al., 2012, Development 139(3): 503--513
Drosophila aPKC is required for mitotic spindle orientation during symmetric division of epithelial cells. [FBrf0217157]
Haenfler et al., 2012, Dev. Biol. 365(1): 219--228
Cortical aPKC kinase activity distinguishes neural stem cells from progenitor cells by ensuring asymmetric segregation of Numb. [FBrf0218950]
Weber et al., 2012, Genetics 191(1): 145--162
Novel regulators of planar cell polarity: a genetic analysis in Drosophila. [FBrf0218210]
Jones and Metzstein, 2011, Genetics 189(1): 153--164
A Novel Function for the PAR Complex in Subcellular Morphogenesis of Tracheal Terminal Cells in Drosophila melanogaster. [FBrf0215238]
Kaplan et al., 2011, PLoS ONE 6(4): e18616
Complex Interactions between GSK3 and aPKC in Drosophila Embryonic Epithelial Morphogenesis. [FBrf0213424]