|Feature type||allele||Associated gene||Dmel\Vang|
|Also Known As||stbm6, stbm6cn, Vang6|
|Map ( GBrowse )|
|Allele class||loss of function allele|
What does this section display?
This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms).
What does this section not display?
This section does not currently display links that were removed or gene model changes.
Click the icon below to subscribe to this FlyBase record and receive updates automatically through your feed reader.
|All updates||Click here to see a list of all updates to this record from FB2010_08 and on.|
|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
2bp deletion at nucleotide 243, resulting in a frameshift at amino acid 81.
|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
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 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, 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.
Scer\GAL4hs.2sev, Vangstbm-6/Vang[+], shgdCR3h.Scer\UAS.T:Avic\GFP-rs has cell polarity defective phenotype, enhanceable by dgo[+]/dgo380
Vangstbm-6 has planar polarity defective | somatic clone phenotype, enhanceable | somatic clone by pwnunspecified
Vangstbm-6/Vang[+] is an enhancer of cell polarity defective phenotype of Scer\GAL4hs.2sev, dgo[+]/dgo380, shgdCR3h.Scer\UAS.T:Avic\GFP-rs
Vangstbm-6/Vang[+] is an enhancer of cell polarity defective phenotype of Scer\GAL4hs.2sev, shgdCR3h.Scer\UAS.T:Avic\GFP-rs
Vangstbm-6/Vang[+] is an enhancer of planar polarity defective phenotype of Scer\GAL4hs.2sev, dgoScer\UAS.cFa
|NOT Enhancer of|
Vangstbm-6/Vang[+] is a suppressor of planar polarity defective phenotype of Scer\GAL4hs.2sev, nmoScer\UAS.cUa
Vangstbm-6/Vangstbm-6 is a suppressor of planar polarity defective | somatic clone | cell non-autonomous phenotype of fz15
|NOT Suppressor of|
CG15283GD13108, Scer\GAL4en-e16E, Vangstbm-6/Vang[+], dgo[+]/dgo269 has planar polarity defective phenotype
|Phenotype Manifest In|
Scer\GAL4hs.2sev, Vangstbm-6/Vang[+], shgdCR3h.Scer\UAS.T:Avic\GFP-rs has ommatidium phenotype, enhanceable by dgo[+]/dgo380
Vangstbm-6 has trichome & adult abdomen | somatic clone | cell non-autonomous phenotype, suppressible by fz21/fz21
Vangstbm-6/Vang[+] is an enhancer of ommatidium phenotype of Scer\GAL4hs.2sev, dgo[+]/dgo380, shgdCR3h.Scer\UAS.T:Avic\GFP-rs
Vangstbm-6/Vang[+] is an enhancer of ommatidium phenotype of Scer\GAL4hs.2sev, shgdCR3h.Scer\UAS.T:Avic\GFP-rs
|NOT Enhancer of|
Vangstbm-6/Vangstbm-6 is a suppressor of trichome & abdomen | cell non-autonomous | somatic clone phenotype of fz15
|NOT Suppressor of|
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/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 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 background show no difference in the time of prehair initiation between single and double mutant tissue. fz 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 double mutant tissue.
As is seen with fz clones alone, fz 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 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/+.
|Complementation & Rescue Data|
|Stocks ( 1 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 11 )|
|Secondary FlyBase IDs|
|References ( 29 )|
|Generate a list of|
|List References by type|
|Recent research papers ( 3 )|