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General Information
Symbol
Dmel\Vangstbm-6
Species
D. melanogaster
Name
FlyBase ID
FBal0062423
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
stbm6, Vang6, stbm6cn, Vangstbm6, stbmnull
Key Links
Mutagen
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Comment:

Reported 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 (using A of ATG of GB:AF044208 as position 1).

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

2bp deletion at nucleotide 243, resulting in a frameshift at amino acid 81.

Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 1 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
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

Detailed Description
Statement
Reference

Vangstbm-6 testes have slightly (but significantly) fewer waste bags and normal individualization complexes (ICs) while they have a similar number of abnormal ICs when compared to controls.

VangEGFP.C, Vangstbm-6 individuals exhibit normal wings with normal trichome polarity.

Vangarm.PU, Vangstbm-6 individuals exhibit wing trichome orientation defects only in the proximal regions.

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 Vangstbm-6 homozygous mutant wings this ratio increases to 30%.

Vangstbm-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.

Vangstbm-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 Vangstbm-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 fz15 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 fz15, this mutant cell displays no preference for position at the front or back of the cluster.

Homozygotes show defects in ommatidial polarity.

Vangstbm-6/VangA3 adults show defects in ommatidial patterning, with ommatidia pointing in random directions with randomised chirality.

Homozygous clones in the pupal wing (32 hours after puparium formation) cause neighbouring cells to point their trichomes away from the clone.

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.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Suppressed by
Statement
Reference
NOT suppressed by
Enhancer of
NOT Enhancer of
Statement
Reference

Vangstbm-6/Vang[+] is a non-enhancer of abnormal neuroanatomy | dominant | adult stage phenotype of tapGal4

Vangstbm-6/Vang[+] is a non-enhancer of abnormal planar polarity phenotype of fwsev.Tag:HA

Vangstbm-6/Vang[+] is a non-enhancer of visible phenotype of Scer\GAL4en-e16E, kermitGS2053

Suppressor of
NOT Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Enhanced by
Statement
Reference

Vangstbm-6 has ommatidium phenotype, enhanceable by bdg164/bdg164

Vangstbm-6 has trichome & adult abdomen phenotype, enhanceable | somatic clone by pwnunspecified

Suppressed by
Statement
Reference

Vangstbm-6 has wing hair | somatic clone phenotype, suppressible by fz21

Vangstbm-6 has trichome & adult abdomen | somatic clone | cell non-autonomous phenotype, suppressible by fz21/fz21

NOT suppressed by
Enhancer of
Statement
Reference

Vangstbm-6/Vang[+] is an enhancer of ommatidium phenotype of Scer\GAL4hs.2sev, dgoUAS.cFa

Vangstbm-6/Vang[+] is an enhancer of wing hair phenotype of Scer\GAL4hs.2sev, dgoUAS.cFa

Vangstbm-6 is an enhancer of ommatidium phenotype of nmoP1

Vangstbm-6 is an enhancer of wing hair phenotype of Rab2351

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 pkpk.sev

NOT Enhancer of
Statement
Reference

Vangstbm-6/Vang[+] is a non-enhancer of ommatidium phenotype of fwsev.Tag:HA

Vangstbm-6/Vang[+] is a non-enhancer of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053

Suppressor of
Statement
Reference

Vangstbm-6/Vang[+] is a suppressor of ommatidium phenotype of Scer\GAL4hs.2sev, nmoUAS.cUa

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, fzUAS.cSa

NOT Suppressor of
Statement
Reference

Vangstbm-6/Vang[+] is a non-suppressor of ommatidium phenotype of fwsev.Tag:HA

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

Other
Additional Comments
Genetic Interactions
Statement
Reference

Vangstbm-6, dgo380, pkpk-sple-13 and dsh3, Vangstbm-6, dgo380, pkpk-sple-13 triple and quadruple heterozygotes exhibit mild wing trichome orientation defects in proximal regions.

Vangstbm-6/+ does not significantly enhance frequency of mushroom body beta lobe axon overgrowth defects in tapGal4/+ brains.

One copy of Vangstbm-6 enhances the axonal projection defects seen in the αlobes of DAAMEx1 mutant mushroom bodies. The β lobe defects are also enhanced but not as strongly.

Vangstbm-6/+ has no effect on the planar cell polarity phenotype in the eye caused by expression of two copies of fwsev.T:Ivir\HA1.

Vangstbm-6/+ does not affect the multiple wing hair phenotype caused by expression of kermitScer\UAS.cLa under the control of Scer\GAL4Bx-MS1096.

Vangstbm-6/+ significantly enhances both the eye and wing defects induced by the overexpression of dgoScer\UAS.cFa under the control of Scer\GAL4hs.2sev.

stanE59/Vangstbm-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).

fry1/Vangstbm-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).

Vangstbm-6/+ suppresses the ommatidial over-rotation phenotype which is caused by expression of nmoScer\UAS.cUa under the control of Scer\GAL4hs.2sev.

Many ommatidia do not rotate at all and remain oriented parallel to the equator in Vangstbm-6 nmoP1 double mutants.

The double mutant combination Vangstbm-6, Rab2351 displays a very high number of multiple wing hairs and strong hair orientation defects.

Vangstbm-6 clones in the pupal wing in a uniformly fz21 background show no difference in the time of prehair initiation between single and double mutant tissue.

fz21 clones in the pupal wing in a uniformly Vangstbm-6 background show prehairs initiating sooner in Vangstbm-6 mutant tissue than in Vangstbm-6 ; fz21 double mutant tissue.

As is seen with fz21 clones alone, fz21 Vangstbm-6 double mutant clones non-autonomously reorient the wing hairs of neighbouring wild type cells so that they point towards the clone.

Homozygosity for bdg164 enhances the ommatidial polarity defects caused by homozygosity for Vangstbm-6.

The ommatidial polarity defects seen in bdgGMREP homozygotes are dominantly suppressed by Vangstbm-6.

Vangstbm-6/Vangstbm-6 fz15/fz21 clones in the pupal wing (32 hours after puparium formation) have negligible effects on the polarity of trichomes in neighbouring cells. Trichome polarity is also relatively unperturbed within the double mutant clones.

stanE59 Vangstbm-6 double mutant clones in the pupal wing (23 hours after puparium formation) do not affect polarity of trichomes in surrounding wild-type tissue.

dsh3 Vangstbm-6/Vangstbm-6 clones in the pupal wing (32 hours after puparium formation) cause neighbouring cells to point their trichomes away from the clone, as occurs with Vangstbm-6/Vangstbm-6 single mutant clones in the pupal wing.

pkpk-sple-13 Vangstbm-6/Vangstbm-6 clones in the pupal wing (32 hours after puparium formation) cause neighbouring cells to point their trichomes away from the clone, as occurs with Vangstbm-6/Vangstbm-6 single mutant clones in the pupal wing.

dgo380 Vangstbm-6/Vangstbm-6 clones in the pupal wing (32 hours after puparium formation) cause neighbouring cells to point their trichomes away from the clone, as occurs with Vangstbm-6/Vangstbm-6 single mutant clones in the pupal wing.

Clones expressing fzScer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4Act5C.PI in a Vangstbm-6 background do not affect the polarity of trichomes in the surrounding non-clonal tissue.

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.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Comments

VangAct5C.T:Avic\GFP-EYFP can rescue the wing planar polarity defects seen in Vangstbm-6/VangA3 animals. Expression at 6 hours after puparium formation (APF) results in only minor polarity defects in the rescued wings. The rescue progressively worsens if expression is induced between 12 and 24 hours APF, with expression induced at 30 hours APF providing no rescue.

Vangsev.PS partially rescues the ommatidial patterning defects of Vangstbm-6/VangA3 adults. The ommatidial misrotation defect is largely rescued, but the dorsoventral inversion phenotype is not rescued.

VangScer\UAS.T:Avic\GFP-m6; Scer\GAL4neur-P72 rescues oriented cell division in the pupal notum of Vangstbm-6 mutant animals.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (14)
References (50)