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General Information
Symbol
Dmel\pnrVX6
Species
D. melanogaster
Name
FlyBase ID
FBal0032468
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Mutagen
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
uncharacterized change in nucleotide sequence
Linked to:
XhoI-EcoRI restriction fragment
Comment:
Deletion with breakpoints within this EcoRI, XhoI fragment
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
Deletion that breaks in the first intron and removes the entire C-terminal part of the gene leaving only nine amino acids of the coding region.
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 ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference
pnrVX6/pnrMD237 transheterozygous adults displaying thoracic clefts and loss of dorsocentral mechanosensory macrochaetae, as compared to wild-type controls.
Class I abdominal dorsal multidendritic ddaD and ddaE neurons from pnrVX6 mutant somatic clones in third instar larvae present misoriented dendrite branch terminals, as compared to controls.
pnrVX6/+ ; Df(3R)Exel6157/+ double heterozygous embryos show asymmetric cell division defects in "svp" cardiac progenitor cells that are not significantly different from the additive effects of each of the two single heterozygotes. Defects in the symmetric cell divisions that give rise to the tin-expressing cardial cells in the double heterozygotes are not significantly different from the additive effects of each of the two single heterozygotes. pnrVX6/+ ; Df(1)CHES-1-like1/+ double heterozygous embryos show asymmetric cell division defects in "svp" cardiac progenitor cells that are not significantly different from the additive effects of each of the two single heterozygotes. Defects in the symmetric cell divisions that give rise to the tin-expressing cardial cells in the double heterozygotes are not significantly different from the additive effects of each of the two single heterozygotes.
pnrVX6/pnrMD237 flies lack the dorsocentral bristles.
Heterozygotes have a normal number of scutellar bristles.
Herozygotes exhibit a significant decrease in lifespan, as compared to controls.
pnrVX6/+ flies have the normal number of dorsocentral bristles.
Homozygous pnrVX6 and trans-heterozygous pnrMD237/pnrVX6 mutants lack dorsocentral bristles.
Less than 1% of pnrVX6/+ flies show any dorsocentral bristle loss.
In pnrVX6 mutant embryos, only remnants of the heart and lymph gland appear to be present.
pnrVX6 mutant embryos have reduced levels of both myocardial and pericardial cells.
Eye development occurs normally in heterozygous flies. Homozygous clones in the eye disc and adult eye show dorsal eye enlargements.
In stage-15 pnrVX6 mutant embryos, the lymph gland, cardioblasts and pericardial nephrocytes fail to develop from the cardiogenic mesoderm.
In mutant embryos cardioblasts almost never develop, a strong decrease in pericardial cells is also seen.
During mid-stage 11 mutant embryos exhibit a loss of cardiac precursors, cardiogenesis appear not to be initiated. By stage 16 a loss of pericardial cells are seen.
Homozygous clones in the eye result in dorsal eye enlargements or ectopic eye, due to a change of dorsal eye fate to ventral. Eye discs homozygous for pnrVX6 (generated using the "EGUF" method to remove all eye disc cells except the homozygous pnrVX6 clone cells) show dorsal overgrowths in the disc and in adult eyes.
The amnioserosa cells appear morphologically normal until the end of embryogenesis in mutant animals. Germband retraction is normal. Homozygous larvae have a characteristic basket shape and dorsal closure defects. The abdominal region of the cuticle lacks the most dorsal pattern elements (the dorsal triangles), which appear to be replaced by dorsolateral spinules.
Homozygous somatic clones in the lateral (LAT) notal region proliferate and differentiate normally, very few clones are seen in the medial (MED) notal region the few that are seen, are in the process of invaginating from the surrounding tissue. Those clones that extended to both regions differentiate normally in the LAT region but form necrotic tissue in the MED region. In some cases invaginated tissue can be seen to differentiate notum structures. In addition some clones found associated with the LAT region, usually near the MED/LAT border, form invaginating vesicles or outgrowths. In these cases the normal LAT pattern is not altered. Very few clones are seen in the medial abdomen region, as compared to the lateral abdomen. Those clones that are in the medial region are always abnormal. dpo not integrate with wild-type cells and form vesicles that segregate from the surrounding tissue. Nevertheless, they differentiate bristles and cuticle of abdominal character.
Homozygous clones in the eye disc only produce a phenotype when they are at the dorsal margin of the eye disc. These clones result in an ectopic field of differentiating photoreceptors anterior to the main eye field. In adult flies this results in the formation of an ectopic eye field in the dorsal head cuticle, which can either be separate from or fused with the normal eye. These ectopic eye fields do not arise exclusively from mutant cells within the clone itself, but also contain wild-type cells. Duplication of the antenna is also frequently observed. In some cases a dramatic loss of the eye and an absence of differentiating photoreceptors in the eye disc is seen, resulting from the loss of all pnr function, in animals carrying very large homozygous clones in the eye. Most animals carrying large clones in the eye die as late pupae, and their heads are sometimes entirely missing. Homozygous dorsal and ventral clones in the eye which lie close to the equator do not show any polarity defects. Only the largest and most dorsal clones, up to eight ommatidial rows from the equator, are abnormal. Ommatidial clusters in the equatorial regions of these clones adopt a ventral polarity and chirality, and more dorsally, the formation of an ectopic equator is seen. This new equator forms within the clone rather than at its boundary and the polarity inversion does not strictly follow the borders of the clone. On one hand, some mutant clusters near the margins of the clone show normal dorsal polarity, and on the other, wild-type ommatidia adjacent to a mutant clone sometimes show chirality changes.
In female D.simulans/D.melanogaster hybrids heterozygous for pnrVX6 the posterior scutellar bristle, anterior dorsocentral bristle, posterior postalar bristle and the posterior dorsocentral bristle are lost at a high frequency compared to female D.simulans/D.melanogaster hybrid controls, when grown at both 18oC and 25oC (though the effect is stronger at 25oC. In female D.simulans/D.melanogaster hybrids heterozygous for pnrVX6 and Df(1)sc-B57, the posterior and anterior scutellar bristles and the posterior and anterior dorsocentral bristles are lost at a high frequency compared to female D.simulans/D.melanogaster hybrid with pnrVX6 or Df(1)sc-B57 alone.
In(3R)iab6G/pnrVX6 flies are lethal as pupae and have strong imaginal defects. Mitotic clones in the thorax adjacent to the thoracic midline cause a sizeable bilateral cleft involving most of the scutum causing the entire scutellum to disappear.
Cells of the amnioserosa and part of the dorsal epidermis die. The phenotype in clones is similar to that of pnrD1.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Enhancer of
Statement
Reference
pnr[+]/pnrVX6 is an enhancer of visible | adult stage phenotype of Bxhdp58-1
pnr[+]/pnrVX6 is an enhancer of visible | adult stage phenotype of BxhdpR590
pnr[+]/pnrVX6 is an enhancer of visible | adult stage phenotype of Bxhdp185-1
Suppressor of
Statement
Reference
pnr[+]/pnrVX6 is a suppressor of visible | recessive | somatic clone phenotype of Lrev6-3
pnr[+]/pnrVX6 is a suppressor | partially of visible | dominant phenotype of L2
Other
Phenotype Manifest In
Enhanced by
Statement
Reference
NOT Enhanced by
Statement
Reference
pnrVX6 has adult heart phenotype, non-enhanceable by tin346/tin[+]
pnrVX6 has adult heart phenotype, non-enhanceable by Df(3R)GC14/+
pnrVX6 has adult heart phenotype, non-enhanceable by H15nmr-614/H15[+]
pnrVX6 has adult heart phenotype, non-enhanceable by Df(2L)Exel6012/+
pnrVX6 has cardioblast phenotype, non-enhanceable by pntS012309
Suppressed by
NOT suppressed by
Statement
Reference
pnrVX6 has adult heart phenotype, non-suppressible by tin346/tin[+]
pnrVX6 has adult heart phenotype, non-suppressible by Df(3R)GC14/+
pnrVX6 has adult heart phenotype, non-suppressible by H15nmr-614/H15[+]
pnrVX6 has adult heart phenotype, non-suppressible by Df(2L)Exel6012/+
pnrVX6 has cardioblast phenotype, non-suppressible by pntS012309
Enhancer of
Statement
Reference
pnrVX6 is an enhancer of thorax phenotype of ChiE
Suppressor of
NOT Suppressor of
Other
Additional Comments
Genetic Interactions
Statement
Reference
Expression of XNPdsRNA.Scer\UAS.Sym under the control of Scer\GAL4pnr-MD237 partially rescues the lethality of pnrVX6/pnrMD237 such that 33% of the animals survive. Expression of XNPUY3132 under the control of Scer\GAL4455.2 enhances the penetrance of the scutellar phenotypes seen in pnrVX6 heterozygotes.
The increase in heart arrest/fibrillation upon electrical pacing that is seen in pnrVX6/+ adults is not significantly altered by tin346/+ or Df(3R)GC14/+. The increase in heart arrest/fibrillation upon electrical pacing that is seen in pnrVX6/+ adults is not significantly altered by H15nmr-614/+ or Df(2L)Exel6012/+. The increase in heart arrest/fibrillation upon electrical pacing that is seen in pnrVX6/+ adults is not rescued by expression of tinScer\UAS.cRa under the control of either Scer\GAL4how-24B or Scer\GAL4Mef2.PR. The increase in heart arrest/fibrillation upon electrical pacing that is seen in pnrVX6/+ adults is not rescued by expression of tinScer\UAS.cRa under the simultaneous control of both Scer\GAL4twi.PG and Scer\GAL4how-24B. The cardiac arrhythmias seen in pnrVX6/+ adults are also not rescued in these animals. The increase in heart arrest/fibrillation upon electrical pacing that is seen in pnrVX6/+ adults is ameliorated by expression of H15Scer\UAS.cQa under the simultaneous control of both Scer\GAL4twi.PG and Scer\GAL4how-24B. The increase in heart arrest/fibrillation upon electrical pacing that is seen in pnrVX6/+ adults is ameliorated by expression of midScer\UAS.cQb under the simultaneous control of both Scer\GAL4twi.PG and Scer\GAL4how-24B. The cardiac arrhythmias seen in pnrVX6/+ adults are also rescued in these animals. The increase in heart arrest/fibrillation upon electrical pacing that is seen in pnrVX6/+ adults is ameliorated by expression of midScer\UAS.cQb under the control of either Scer\GAL4Mef2.PR or Scer\GAL4tin.CΔ4. The cardiac arrhythmias seen in pnrVX6/+ adults are also rescued in animals expressing midScer\UAS.cQb under the control of Scer\GAL4tin.CΔ4.
pnrVX6/+ dominantly suppresses the missing thoracic bristle phenotype of CtBPScer\UAS.cSa, Scer\GAL4ap-md544 flies.
Bxhdp-n60/Y ; pnrVX6/+ flies show loss of dorsocentral bristles. sensE2/pnrVX6 double heterozygotes show loss of dorsocentral bristles.
Flies lacking a copy of pnrVX6 and CtBPrev19 show no significant difference in the number of dorsocentral bristles compared to pnrVX6/+
One copy of pnrVX6 enhances the dorsocentral bristle loss seen in hemizygous Bxhdp185-1 mutant males. 90% of flies lack the anterior pair of bristles. One copy of pnrVX6 enhances the dorsocentral bristle loss seen in hemizygous Bxhdp58-1 mutant males. 90% of flies lack the anterior pair of bristles. One copy of pnrVX6 enhances the dorsocentral bristle loss seen in hemizygous BxhdpR590 mutant males. 90% of flies lack the anterior pair of bristles. No dorsocentral bristle loss is seen in flies hemizygous for Bx2 and heterozygous for pnrVX6. No dorsocentral bristle loss is seen in flies hemizygous for Bx1002 and heterozygous for pnrVX6.
The slight increase in lymph gland size seen in Zfrp8SM206/+ larvae is dominantly suppressed by pnrVX6.
Df(3L)29A6; Df(3L)DocA, pnrVX6 stage 16 embryos have a reduced number of cardioblasts compared to wild type; Df(3L)29A6; Df(3L)DocA, pnrVX6, tin346 embryos have even fewer cardioblasts and form only short regions of the dorsal vessel. Df(3L)29A6; pnrVX6, tin346 show a milder loss of cardioblasts.
The dorsal eye enlargements caused by homozygous pnrVX6 clones are no longer seen in the flies are also carrying Lrev6-3/+.
pnrVX6, pntS012309 double mutant embryos lack cardioblasts and pericardial cells and are phenotypically indistinguishable from pnrVX6 embryos.
Expression of CG46146Scer\UAS.cCa under the control of Scer\GAL4ey.PH in eye discs homozygous for pnrVX6 (generated using the "EGUF" method to remove all eye disc cells except the homozygous pnrVX6 clone cells) results in a small eye phenotype due to a reduction of the eye on both dorsal and ventral eye margins in nearly 20% of flies. This double mutant phenotype is different from either single mutant phenotype. The polarity of most of the ommatidia in the small eye is dorsal, along with a few ventral or with a polarity defect. Expression of SerBd.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4ey.PH at 25[o]C in eye discs homozygous for pnrVX6 (generated using the "EGUF" method to remove all eye disc cells except the homozygous pnrVX6 clone cells) results in a complete loss of the eye in 99% of flies, compared to 50% of flies showing complete loss of the eye or a very small eye when SerBd.Scer\UAS.T:Hsap\MYC is expressed under the control of Scer\GAL4ey.PH at 25[o]C in a wild-type background.
Ubiquitous expression of araScer\UAS.cGa under the control of Scer\GAL4unspecified abolishes photoreceptor differentiation, which is not restored if the flies also carry clones of pnrVX6. Large pnrVX6 clones in the eye, which would be expected to produce an ectopic eye field in a wild-type background, show no photoreceptor differentiation in discs if they are also expressing wgScer\UAS.cAa under the control of Scer\GAL4ey.PH.
The addition of pnrVX6/+ to heterozygous ChiE flies gives flies that exhibit a thoracic cleft.
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Expression of pnrScer\UAS.β under the control of Scer\GAL4pnr-MD237 results in poor rescue (0.4 bristles per thorax) of the loss of dorsocentral bristles seen in pnrVX6/pnrMD237 flies. Expression of pnrSA.Scer\UAS.β under the control of Scer\GAL4pnr-MD237 results in significant rescue (4.6 bristles per thorax) of the loss of dorsocentral bristles seen in pnrVX6/pnrMD237 flies.
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments
Class 2 pnr allele: lethal recessive allele. Allelic series according to the extent of the dorsal hole: pnr1 > Df(3R)sbd45 = pnrVX6 = pnrVP8 = pnrD1 > pnrD3.
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (46)