Allele Dmel\pnrVX6
| General Information | |||
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| Symbol | Dmel\pnrVX6 | Species | D. melanogaster |
| Name | FlyBase ID | FBal0032468 | |
| Feature type | allele | Associated gene | Dmel\pnr |
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| Allele class | amorphic allele - genetic evidence, loss of function allele | ||
| Mutagen | X ray | ||
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| Description |
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| FB2013_03 | |||
| FB2013_02 | |||
| All updates | Click here to see a list of all updates to this record from FB2010_08 and on. | ||
Nature of the Allele
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| 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
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EMBL / GenBank | DNA sequence Protein sequence Name | ||
| UniProtKB/Swiss-Prot | |||
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| 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 | |||
Phenotypic Data
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Phenotypic Class
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Phenotype Manifest In
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Detailed Description
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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. 15% of pnr[VX6]/pnr[MD237] animals survive. 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. | |||
External Data
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Interactions
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Phenotypic Class
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Suppressed by | |||
Statement Reference pnrMD237/pnrVX6 has partially lethal - majority die phenotype, suppressible | partially by Scer\GAL4pnr-MD237/XNPdsRNA.Scer\UAS.Sym | |||
Enhancer of | |||
Statement Reference | |||
Suppressor of | |||
Statement Reference | |||
Other | |||
Statement Reference | |||
Phenotype Manifest In
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Enhanced by | |||
Statement Reference | |||
NOT Enhanced by | |||
Statement Reference | |||
Suppressed by | |||
Statement Reference pnrVX6 has adult heart phenotype, suppressible by midScer\UAS.cQb/Scer\GAL4twi.PG/Scer\GAL4how-24B/Scer\GAL4how-24B pnrVX6 has adult heart phenotype, suppressible by Scer\GAL4twi.PG/Scer\GAL4how-24B/Scer\GAL4how-24B/H15Scer\UAS.cQa pnrVX6 has photoreceptor cell | ectopic | somatic clone phenotype, suppressible by Scer\GAL4ey.PH/wgScer\UAS.cAa | |||
NOT suppressed by | |||
Statement Reference pnrVX6 has adult heart phenotype, non-suppressible by tinScer\UAS.cRa/Scer\GAL4how-24B/Scer\GAL4how-24B pnrVX6 has adult heart phenotype, non-suppressible by tinScer\UAS.cRa/Scer\GAL4twi.PG/Scer\GAL4how-24B/Scer\GAL4how-24B | |||
Enhancer of | |||
Statement Reference | |||
Suppressor of | |||
Statement Reference pnr[+]/pnrVX6 is a suppressor | partially of anterior dorsocentral bristle | adult stage phenotype of CtBPScer\UAS.cSa, Scer\GAL4ap-md544 pnr[+]/pnrVX6 is a suppressor | partially of anterior scutellar bristle | adult stage phenotype of CtBPScer\UAS.cSa, Scer\GAL4ap-md544 pnr[+]/pnrVX6 is a suppressor | partially of posterior dorsocentral bristle | adult stage phenotype of CtBPScer\UAS.cSa, Scer\GAL4ap-md544 pnr[+]/pnrVX6 is a suppressor | partially of posterior scutellar bristle | adult stage phenotype of CtBPScer\UAS.cSa, Scer\GAL4ap-md544 | |||
NOT Suppressor of | |||
Statement Reference pnrVX6 is a non-suppressor | somatic clone of photoreceptor cell phenotype of Scer\GAL4unspecified, araScer\UAS.cGa | |||
Other | |||
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Additional Comments
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Genetic Interactions
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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. 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. | |||
Xenogenetic Interactions
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Statement Reference | |||
Complementation & Rescue Data
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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. | ||
Stocks
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| Bloomington | |||
| Kyoto | |||
Notes on Origin
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Comments
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External Crossreferences & Linkouts
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Synonyms & Secondary IDs
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| Reported As | |||
| Symbol Synonym | pnrvx6 pnrVX6 PnrVX6 | ||
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References
( 37 ) | |||
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Recent research papers ( 4 ) | |||
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Recent reviews (0)
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| All reviews listed in FlyBase were published before 2011 | |||

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