A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\pnrVX6

General Information
SymbolDmel\pnrVX6SpeciesD. melanogaster
NameFlyBase IDFBal0032468
Feature typealleleAssociated geneDmel\pnr
Map ( GBrowse ) GBrowse View Helpdetailed view FBal0032463 FBal0032462 FBal0032457 FBal0032468
Allele classamorphic allele - genetic evidence, loss 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
uncharacterized change in nucleotide sequence
comment=Deletion with breakpoints within this EcoRI, XhoI fragment
evidence=experimental
linked_to=XhoI-EcoRI_rfrag
Associated Sequence Data
DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
UniProtKB/Swiss-Prot
UniProtKB/TrEMBL
Progenitor genotype
Nature of the lesion
Statement
Reference
Deletion of most of the coding sequence.
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.
Cytology
hide Phenotypic Data
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Statement
Reference
pnr[VX6]/+ ; 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. pnr[VX6]/+ ; Df(1)CHES-1-like[1]/+ 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.
pnr[VX6]/pnr[MD237] flies lack the dorsocentral bristles.
Heterozygotes have a normal number of scutellar bristles.
Heterozygous adults show an increase in heart arrest/fibrillation compared to control flies upon electrical pacing of the heart. The severity of the defect increases with age. Heterozygous flies show an increase in irregular heart rate with progressive bradycardia compared with the controls. The mean diastolic interval length is increased compared to controls.
pnr[VX6]/+ flies have the normal number of dorsocentral bristles.
Less than 1% of pnr[VX6]/+ 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.
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hideSuppressed by
Statement
Reference
pnrVX6 has visible | somatic clone phenotype, suppressible by L[+]/Lrev6-3
hideEnhancer 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 Bxhdp185-1
pnr[+]/pnrVX6 is an enhancer of visible | adult stage phenotype of BxhdpR590
hideSuppressor of
Statement
Reference
pnr[+]/pnrVX6 is a suppressor | partially of visible | dominant phenotype of L2
pnr[+]/pnrVX6 is a suppressor of visible | recessive | somatic clone phenotype of Lrev6-3
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Statement
Reference
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Statement
Reference
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Statement
Reference
pnrVX6 has adult heart phenotype, non-enhanceable by Df(2L)Exel6012/+
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 tin346/tin[+]
pnrVX6 has cardioblast phenotype, non-enhanceable by pntS012309
hideSuppressed by
Statement
Reference
pnrVX6 has eye | dorsal | somatic clone phenotype, suppressible by L[+]/Lrev6-3
hideNOT suppressed by
Statement
Reference
pnrVX6 has adult heart phenotype, non-suppressible by Df(2L)Exel6012/+
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 tin346/tin[+]
pnrVX6 has cardioblast phenotype, non-suppressible by pntS012309
hideEnhancer of
Statement
Reference
pnrVX6 is an enhancer of thorax phenotype of ChiE
hideSuppressor of
Statement
Reference
pnr[+]/pnrVX6 is a suppressor | partially of eye | ventral phenotype of L2
pnr[+]/pnrVX6 is a suppressor of eye | ventral | somatic clone phenotype of Lrev6-3
pnr[+]/pnrVX6 is a suppressor of scutellar bristle | supernumerary phenotype of SsdpL7
hideNOT Suppressor of
Statement
Reference
hideOther
Statement
Reference
Chi[+]/ChiE, pnrVX6 has thorax phenotype
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Statement
Reference
Expression of XNP[dsRNA.Scer\UAS.Sym] under the control of Scer\GAL4[pnr-MD237] partially rescues the lethality of pnr[VX6]/pnr[MD237] such that 33% of the animals survive. Expression of XNP[UY3132] under the control of Scer\GAL4[455.2] enhances the penetrance of the scutellar phenotypes seen in pnr[VX6] heterozygotes.
The increase in heart arrest/fibrillation upon electrical pacing that is seen in pnr[VX6]/+ adults is not significantly altered by tin[346]/+ or Df(3R)GC14/+. The increase in heart arrest/fibrillation upon electrical pacing that is seen in pnr[VX6]/+ adults is not significantly altered by H15[nmr-614]/+ or Df(2L)Exel6012/+. The increase in heart arrest/fibrillation upon electrical pacing that is seen in pnr[VX6]/+ adults is not rescued by expression of tin[Scer\UAS.cRa] under the control of either Scer\GAL4[how-24B] or Scer\GAL4[Mef2.PR]. The increase in heart arrest/fibrillation upon electrical pacing that is seen in pnr[VX6]/+ adults is not rescued by expression of tin[Scer\UAS.cRa] under the simultaneous control of both Scer\GAL4[twi.PG] and Scer\GAL4[how-24B]. The cardiac arrhythmias seen in pnr[VX6]/+ adults are also not rescued in these animals. The increase in heart arrest/fibrillation upon electrical pacing that is seen in pnr[VX6]/+ adults is ameliorated by expression of H15[Scer\UAS.cQa] under the simultaneous control of both Scer\GAL4[twi.PG] and Scer\GAL4[how-24B]. The increase in heart arrest/fibrillation upon electrical pacing that is seen in pnr[VX6]/+ adults is ameliorated by expression of mid[Scer\UAS.cQb] under the simultaneous control of both Scer\GAL4[twi.PG] and Scer\GAL4[how-24B]. The cardiac arrhythmias seen in pnr[VX6]/+ adults are also rescued in these animals. The increase in heart arrest/fibrillation upon electrical pacing that is seen in pnr[VX6]/+ adults is ameliorated by expression of mid[Scer\UAS.cQb] under the control of either Scer\GAL4[Mef2.PR] or Scer\GAL4[tin.CΔ4]. The cardiac arrhythmias seen in pnr[VX6]/+ adults are also rescued in animals expressing mid[Scer\UAS.cQb] under the control of Scer\GAL4[tin.CΔ4].
pnr[VX6]/+ dominantly suppresses the missing thoracic bristle phenotype of CtBP[Scer\UAS.cSa], Scer\GAL4[ap-md544] flies.
Bx[hdp-n60]/Y ; pnr[VX6]/+ flies show loss of dorsocentral bristles. sens[E2]/pnr[VX6] double heterozygotes show loss of dorsocentral bristles.
Flies lacking a copy of pnr[VX6] and CtBP[rev19] show no significant difference in the number of dorsocentral bristles compared to pnr[VX6]/+
One copy of pnr[VX6] enhances the dorsocentral bristle loss seen in hemizygous Bx[hdp185-1] mutant males. 90% of flies lack the anterior pair of bristles. One copy of pnr[VX6] enhances the dorsocentral bristle loss seen in hemizygous Bx[hdp58-1] mutant males. 90% of flies lack the anterior pair of bristles. One copy of pnr[VX6] enhances the dorsocentral bristle loss seen in hemizygous Bx[hdpR590] mutant males. 90% of flies lack the anterior pair of bristles. No dorsocentral bristle loss is seen in flies hemizygous for Bx[2] and heterozygous for pnr[VX6]. No dorsocentral bristle loss is seen in flies hemizygous for Bx[1002] and heterozygous for pnr[VX6].
The slight increase in lymph gland size seen in Zfrp8[SM206]/+ larvae is dominantly suppressed by pnr[VX6].
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 LScer\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 25oC 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 25oC 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.
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Rescued by
Partially rescued by
Not rescued by
Comments
Expression of pnr[Scer\UAS.β] under the control of Scer\GAL4[pnr-MD237] results in poor rescue (0.4 bristles per thorax) of the loss of dorsocentral bristles seen in pnr[VX6]/pnr[MD237] flies. Expression of pnr[SA.Scer\UAS.β] under the control of Scer\GAL4[pnr-MD237] results in significant rescue (4.6 bristles per thorax) of the loss of dorsocentral bristles seen in pnr[VX6]/pnr[MD237] flies.
hide Stocks ( 2 )
Bloomington
Kyoto
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Discoverer
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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.
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hide Synonyms & Secondary IDs ( 3 )
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hide Recent research papers ( 4 )
Ahmad et al., 2012, Dev. Cell 23(1): 97--111
Two forkhead transcription factors regulate the division of cardiac progenitor cells by a polo-dependent pathway. [FBrf0218973]
Valadez-Graham et al., 2012, Nucleic Acids Res. 40(4): 1460--1474
XNP/dATRX interacts with DREF in the chromatin to regulate gene expression. [FBrf0217551]
Yang et al., 2012, Development 139(2): 325--334
The kinase Sgg modulates temporal development of macrochaetes in Drosophila by phosphorylation of Scute and Pannier. [FBrf0216991]
Ryu et al., 2011, Dev. Dyn. 240(1): 86--96
Tinman is a direct activator of midline in the drosophila dorsal vessel. [FBrf0212547]
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