A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\Vangstbm-6

General Information
SymbolDmel\Vangstbm-6SpeciesD. melanogaster
NameFlyBase IDFBal0062423
Feature typealleleAssociated geneDmel\Vang
Also Known Asstbm6, stbm6cn, Vang6
Map ( GBrowse ) GBrowse View Helpdetailed view FBal0062423 FBal0088604 FBal0088602 FBal0088603
Allele classloss of function allele
MutagenX ray
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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
sequence variant
comment=Reported in FBrf0102026 to be a 2bp deletion at nucleotide 243 creating a frameshift mutation at amino acid 81; position of mutation on reference sequence inferred by FlyBase curator based on author statement (using GB:AF044208)
evidence=experimental
Associated Sequence Data
DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
UniProtKB/Swiss-Prot
UniProtKB/TrEMBL
Progenitor genotype
Nature of the lesion
Statement
Reference
2bp deletion at nucleotide 243, resulting in a frameshift at amino acid 81.
Cytology
hide Phenotypic Data
hide Phenotypic Class
hide Phenotype Manifest In
macrochaeta & prothoracic segment
trichome & adult abdomen
trichome & adult abdomen | somatic clone
trichome & adult abdomen | somatic clone | cell non-autonomous
trichome & adult head
trichome & adult thorax
trichome & pleural membrane
trichome & pleural membrane | somatic clone
trichome & pleural membrane | somatic clone | cell non-autonomous
hide Detailed Description
Statement
Reference
Homozygous larvae show increased crossing of dendrites in the dendritic arbor of the ddaC class IV neurons compared to wild type.
The angle and direction of rotation of ommatidia is randomised in mutant eyes.
The directional preferences of growing microtubules in mutant wing cells is not significantly different from that seen in wild type at 24 hours after puparium formation.
In wild-type wings, the ratio of non-hexagonally shaped cells relative to hexagonally shaped cells is around 11%, whereas in Vang[stbm-6] homozygous mutant wings this ratio increases to 30%. Vang[stbm-6] mutant wings display strong hair orientation defects, but very few if any multiple hairs.
Overall length of the tracheal dorsal trunk is normal in hemizygous stage 16 embryos.
Vang[stbm-6] mutant border cells are predominantly found at the lagging edge of border cell clusters compared to wild-type cells that show a strong preference to migrate at the leading edge of the cluster. Border cell clusters from Vang[stbm-6] mutants show an average of 37 actin protrusions, reduced compared to the average of 94.8 in wild-type clusters. In border cell clusters where both polar follicle cells are mutant for fz[15] there is no preference for non-mutant border cells to take up the leading edge positions in the cluster, which is observed when polar cells are wild-type. In border cell clusters where only one polar follicle cell is mutant for fz[15], this mutant cell displays no preference for position at the front or back of the cluster.
Homozygotes show defects in ommatidial polarity.
The hexagonal packing of intervein cells, which usually occurs between wing development stage P2B (when the first morphological signs of veins appear (FBrf0005070), and the middle of P2C (before hair formation (FBrf0005070)) is disrupted in Vangstbm-6/Vangstbm-6 flies.
In Vangstbm-6 mutant pupae, the mitotic spindles of dividing sensory organ precursor cells in the developing notum are not aligned with the anterior-posterior axis, but instead are randomly oriented.
Vangstbm-6 flies are viable with a planar polarity phenotype in the tergites which resembles that seen in fz- flies: they are disheveled, especially in the anterior parts of the anterior compartment, but have largely normal polarity elsewhere. Similarly, in the pleura, polarity is generally disordered, as in fz-, except that there is a weak tendency for the hairs to be organized into zones of alternating polarity along the antero-posterior axis. The hairs in the middle of the anterior compartment tend to be reversed, with the remaining hairs being more normally polarised. Within Vangstbm-6 somatic clones in the adult abdomen the rows of hairs are jumbled and poorly oriented: some hairs point straight upwards, especially those in clones in anterior regions of the anterior compartment. Disruption of polarity extends a few cells anterior to these clones. This non-autonomous effect is variable, usually including patches with some hairs that are reversed. Reversal anterior to clones is more consistent and extensive for clones in the pleura, but is unaffected by position on the anteroposterior axis and can extend across the A-P compartment boundary.
Vangstbm-6 homozygous embryos fail to hatch, exhibiting a phenotype similar to unfertilized eggs.
Mutants show no significant disruption of ovarian morphology.
Homozygotes are viable, although many embryos die between 0-4 hours after egg laying. Homozygotes have rough eyes, due to misalignment of the normally parallel rows of ommatidia. The majority of ommatidia in the eye are correctly assembled, and the misaligned eye lattice is due to aberrant orientation of ommatidial units, which can be in several orientations: normal (46%), reversed dorsoventrally (35%), reversed anteroposteriorly (7%) or reversed both dorsoventrally and anteroposteriorly (7%). In addition, although most ommatidia rotate the normal 90o, some undergo partial or no rotation (3%). Photoreceptors R3 and R4 are bilaterally symmetrical in 2% of ommatidia, abolishing the chirality of these ommatidia. These ommatidia show a rectangular rather than the normal trapezoidal arrangement of rhabdomeres. The pigment cell lattice is also disrupted, as a consequence of ommatidial misorientation. The eyes contain a normal complement of primary pigment cells, bristles and cone cells, although a few ommatidia are missing one cone cell. The number of secondary and tertiary pigment cells is often correct, except at the vertices of partially or unrotated ommatidia, where there is an excess of these cell types. Ommatidial assembly is normal in homozygous eye discs, but rotation of the ommatidia is delayed, and some ommatidia initiate rotation in the wrong direction. The polarity of many thoracic bristles is abnormal in homozygous adults, and the leg bristles are oriented perpendicular to the leg. Hair polarity is disrupted throughout the body, for example surrounding the eye and on the wings and thorax. Extra tarsal segments or partial duplications are frequently seen in tarsal segments 3 and 4, and occasionally in tarsal segment 2. The wings are held out.
In mutant eyes some ommatidia show normal polarity, many show inversions on the anterior-posterior and dorsal ventral axis so consequently the equator is abolished.
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Statement
Reference
hideSuppressed by
Statement
Reference
hideEnhancer of
Statement
Reference
Vangstbm-6/Vang[+] is an enhancer of visible phenotype of Scer\GAL4hs.2sev, dgoScer\UAS.cFa
Vangstbm-6 is an enhancer of visible | recessive phenotype of Rab2351
hideNOT Enhancer of
Statement
Reference
Vangstbm-6/Vang[+] is a non-enhancer of visible phenotype of Scer\GAL4en-e16E, kermitGS2053
hideSuppressor of
Statement
Reference
Vangstbm-6/Vang[+] is a suppressor of planar polarity defective phenotype of bdgGMREP
hideNOT Suppressor of
Statement
Reference
Vangstbm-6/Vang[+] is a non-suppressor of visible phenotype of Scer\GAL4en-e16E, kermitGS2053
hideOther
Statement
Reference
hide Phenotype Manifest In
hideEnhanced by
Statement
Reference
Vangstbm-6 has ommatidium phenotype, enhanceable by bdg164/bdg164
Vangstbm-6 has trichome & adult abdomen phenotype, enhanceable | somatic clone by pwnunspecified
hideSuppressed by
Statement
Reference
Vangstbm-6 has trichome & adult abdomen | somatic clone | cell non-autonomous phenotype, suppressible by fz21/fz21
Vangstbm-6 has wing hair | somatic clone phenotype, suppressible by fz21
hideEnhancer of
Statement
Reference
Vangstbm-6/Vang[+] is an enhancer of wing cell | adult stage | heat sensitive phenotype of shi1
Vangstbm-6 is an enhancer of ommatidium phenotype of nmoP1
Vangstbm-6 is an enhancer of ommatidium phenotype of pkpk.sev
Vangstbm-6 is an enhancer of wing hair phenotype of Rab2351
hideNOT Enhancer of
Statement
Reference
Vangstbm-6/Vang[+] is a non-enhancer of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053
hideSuppressor of
Statement
Reference
Vangstbm-6/Vang[+] is a suppressor of ommatidium phenotype of bdgGMREP
Vangstbm-6/Vangstbm-6 is a suppressor of trichome & abdomen | cell non-autonomous | somatic clone phenotype of fz15
Vangstbm-6/Vangstbm-6 is a suppressor of trichome & adult abdomen | somatic clone | cell non-autonomous phenotype of Scer\GAL4αTub84B.PL, fzScer\UAS.cSa
hideNOT Suppressor of
Statement
Reference
Vangstbm-6/Vang[+] is a non-suppressor of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053
Vangstbm-6 is a non-suppressor of wing hair | somatic clone phenotype of fz21
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Statement
Reference
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hide Genetic Interactions
Statement
Reference
Vang[stbm-6]/+ significantly enhances both the eye and wing defects induced by the overexpression of dgo[Scer\UAS.cFa] under the control of Scer\GAL4[hs.2sev].
stan[E59]/Vang[stbm-6] double heterozygous larvae show increased crossing of dendrites in the dendritic arbor of the ddaC class IV neurons compared to wild type (neither single heterozygote shows this phenotype). fry[1]/Vang[stbm-6] double heterozygous larvae show increased crossing of dendrites in the dendritic arbor of the ddaC class IV neurons compared to wild type (neither single heterozygote shows this phenotype).
Vang[stbm-6]/+ suppresses the ommatidial over-rotation phenotype which is caused by expression of nmo[Scer\UAS.cUa] under the control of Scer\GAL4[hs.2sev].
Many ommatidia do not rotate at all and remain oriented parallel to the equator in Vang[stbm-6] nmo[P1] double mutants.
The double mutant combination Vang[stbm-6], Rab23[51] displays a very high number of multiple wing hairs and strong hair orientation defects.
Vang[stbm-6] clones in the pupal wing in a uniformly fz[21] background show no difference in the time of prehair initiation between single and double mutant tissue. fz[21] clones in the pupal wing in a uniformly Vang[stbm-6] background show prehairs initiating sooner in Vang[stbm-6] mutant tissue than in Vang[stbm-6] ; fz[21] double mutant tissue.
As is seen with fz[21] clones alone, fz[21] Vang[stbm-6] double mutant clones non-autonomously reorient the wing hairs of neighbouring wild type cells so that they point towards the clone.
Homozygosity for bdg[164] enhances the ommatidial polarity defects caused by homozygosity for Vang[stbm-6]. The ommatidial polarity defects seen in bdg[GMREP] homozygotes are dominantly suppressed by Vang[stbm-6].
Both a dgo380/+ and a Vangstbm-6/+ background enhances the ommatidial rotation phenotype of Scer\GAL4hs.2sev>shgdCR3h.Scer\UAS.T:Avic\GFP-rs eyes; a dgo380/+, Vangstbm-6/+ double mutant background further enhances this phenotype.
The formation of holes in wings due to temperature shift of shi1/shi1 animals during pupal stages is moderately enhanced by Vangstbm-6/+.
The loss of polarity seen in Vangstbm-6 somatic clones in the adult abdomen is enhanced by pwnunspecified. The loss of cell polarity seen adjacent to these clones is suppressed by fz21/fz21.
hide Xenogenetic Interactions
Statement
Reference
hide Complementation & Rescue Data
Rescued by
Comments
VangScer\UAS.T:Avic\GFP-m6; Scer\GAL4neur-P72 rescues oriented cell division in the pupal notum of Vangstbm-6 mutant animals.
hide Stocks ( 1 )
Bloomington
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Discoverer
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hide Synonyms & Secondary IDs ( 11 )
Reported As
Symbol Synonym
Vangstbm6c
Name Synonym
Secondary FlyBase IDs
  • FBal0062421
hide References ( 29 )
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hide Recent research papers ( 3 )
Weber et al., 2012, Genetics 191(1): 145--162
Novel regulators of planar cell polarity: a genetic analysis in Drosophila. [FBrf0218210]
Matsubara et al., 2011, Genes Dev. 25(18): 1982--1996
The seven-pass transmembrane cadherin Flamingo controls dendritic self-avoidance via its binding to a LIM domain protein, Espinas, in Drosophila sensory neurons. [FBrf0215818]
Mirkovic et al., 2011, Nat. Struct. Mol. Biol. 18(6): 665--672
Nemo kinase phosphorylates β-catenin to promote ommatidial rotation and connects core PCP factors to E-cadherin-β-catenin. [FBrf0213849]