FlyBase Allele Report: Dmel\pnr[VX6]

pnr^VX6/pnr^MD237 transheterozygous adults displaying thoracic clefts and loss of dorsocentral mechanosensory macrochaetae, as compared to wild-type controls.

(Immarigeon et al., 2019)

Class I abdominal dorsal multidendritic ddaD and ddaE neurons from pnr^VX6 mutant somatic clones in third instar larvae present misoriented dendrite branch terminals, as compared to controls.

(Hattori et al., 2013)

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-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.

(Ahmad et al., 2012)

15% of pnr^VX6/pnr^MD237 animals survive.

(Valadez-Graham et al., 2012)

pnr^VX6/pnr^MD237 flies lack the dorsocentral bristles.

(Yang et al., 2012)

Heterozygotes have a normal number of scutellar bristles.

(Bronstein et al., 2010)

Herozygotes exhibit a significant decrease in lifespan, as compared to controls.

(Qian and Bodmer, 2009)

pnr^VX6/+ flies have the normal number of dorsocentral bristles.

(Biryukova and Heitzler, 2008)

Homozygous pnr^VX6 and trans-heterozygous pnr^MD237/pnr^VX6 mutants lack dorsocentral bristles.

(Fromental-Ramain et al., 2008)

Less than 1% of pnr^VX6/+ flies show any dorsocentral bristle loss.

(Zenvirt et al., 2008)

In pnr^VX6 mutant embryos, only remnants of the heart and lymph gland appear to be present.

(Han and Olson, 2005)

pnr^VX6 mutant embryos have reduced levels of both myocardial and pericardial cells.

(Qian et al., 2005)

Eye development occurs normally in heterozygous flies. Homozygous clones in the eye disc and adult eye show dorsal eye enlargements.

(Singh et al., 2005)

In stage-15 pnr^VX6 mutant embryos, the lymph gland, cardioblasts and pericardial nephrocytes fail to develop from the cardiogenic mesoderm.

(Mandal et al., 2004)

In mutant embryos cardioblasts almost never develop, a strong decrease in pericardial cells is also seen.

(Alvarez et al., 2003)

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.

(Klinedinst and Bodmer, 2003)

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 pnr^VX6 (generated using the "EGUF" method to remove all eye disc cells except the homozygous pnr^VX6 clone cells) show dorsal overgrowths in the disc and in adult eyes.

(Singh and Choi, 2003)

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.

(Herranz and Morata, 2001)

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.

(Calleja et al., 2000)

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.

(Maurel-Zaffran and Treisman, 2000)

In female D.simulans/D.melanogaster hybrids heterozygous for pnr^VX6 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 18^oC and 25^oC (though the effect is stronger at 25^oC. In female D.simulans/D.melanogaster hybrids heterozygous for pnr^VX6 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 pnr^VX6 or Df(1)sc-B57 alone.

(Skaer and Simpson, 2000)

In(3R)iab6^G/pnr^VX6 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.

(Heitzler et al., 1996)

Cells of the amnioserosa and part of the dorsal epidermis die. The phenotype in clones is similar to that of pnr^D1.

(Ramain et al., 1993)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

pnr^MD237/pnr^VX6 has partially lethal - majority die phenotype, suppressible | partially by Scer\GAL4^pnr-MD237/XNP^RNAi.UAS.Sym

(Valadez-Graham et al., 2012)

pnr^VX6 has visible | somatic clone phenotype, suppressible by L[+]/L^rev6-3

(Singh et al., 2005)

Enhancer of

Statement

Reference

pnr[+]/pnr^VX6 is an enhancer of visible | adult stage phenotype of Bx^hdp58-1

(Zenvirt et al., 2008)

pnr[+]/pnr^VX6 is an enhancer of visible | adult stage phenotype of Bx^hdpR590

(Zenvirt et al., 2008)

pnr[+]/pnr^VX6 is an enhancer of visible | adult stage phenotype of Bx^hdp185-1

(Zenvirt et al., 2008)

Suppressor of

Statement

Reference

pnr[+]/pnr^VX6 is a suppressor of visible | dominant phenotype of L²

(Singh et al., 2005)

pnr[+]/pnr^VX6 is a suppressor of visible | recessive | somatic clone phenotype of L^rev6-3

(Singh et al., 2005)

Other

Statement

Reference

Scer\GAL4^Act5C.PU, XNP^UY3132, pnr^VX6 has lethal phenotype

(Valadez-Graham et al., 2012)

pnr[+]/pnr^VX6, sens^E2 has visible | dominant phenotype

(Asmar et al., 2008)

Bx^hdp-n60, pnr[+]/pnr^VX6 has visible phenotype

(Asmar et al., 2008)

Df(3L)29A6, Df(3L)DocA, pnr^VX6, tin³⁴⁶ has lethal phenotype

(Reim and Frasch, 2005)

Df(3L)DocA, pnr^VX6, tin³⁴⁶ has viable phenotype

(Reim and Frasch, 2005)

PRAS40^UAS.cCa, Scer\GAL4^ey.PH, pnr^VX6 has visible | somatic clone phenotype

(Singh and Choi, 2003)

Chi^E, pnr^VX6 has lethal phenotype

(Ramain et al., 2000)

Phenotype Manifest In

Enhanced by

Statement

Reference

pnr^VX6 has scutellum phenotype, enhanceable by XNP^UY3132/Scer\GAL4^455.2

(Valadez-Graham et al., 2012)

NOT Enhanced by

Statement

Reference

pnr^VX6 has adult heart phenotype, non-enhanceable by tin³⁴⁶/tin[+]

(Qian and Bodmer, 2009)

pnr^VX6 has adult heart phenotype, non-enhanceable by Df(3R)GC14/+

(Qian and Bodmer, 2009)

pnr^VX6 has adult heart phenotype, non-enhanceable by H15^nmr-614/H15[+]

(Qian and Bodmer, 2009)

pnr^VX6 has adult heart phenotype, non-enhanceable by Df(2L)Exel6012/+

(Qian and Bodmer, 2009)

pnr^VX6 has dorsal vessel wall cell phenotype, non-enhanceable by pnt^S012309

(Alvarez et al., 2003)

pnr^VX6 has embryonic pericardial cell phenotype, non-enhanceable by pnt^S012309

(Alvarez et al., 2003)

Suppressed by

Statement

Reference

pnr^VX6 has adult heart phenotype, suppressible by Scer\GAL4^twi.PG/Scer\GAL4^how-24B/H15^UAS.cQa

(Qian and Bodmer, 2009)

pnr^VX6 has adult heart phenotype, suppressible by mid^UAS.cQb/Scer\GAL4^twi.PG/Scer\GAL4^how-24B

(Qian and Bodmer, 2009)

pnr^VX6 has adult heart phenotype, suppressible by mid^UAS.cQb/Scer\GAL4^Mef2.PR

(Qian and Bodmer, 2009)

pnr^VX6 has adult heart phenotype, suppressible by mid^UAS.cQb/Scer\GAL4^tin.CΔ4

(Qian and Bodmer, 2009)

pnr^VX6 has eye | dorsal | somatic clone phenotype, suppressible by L[+]/L^rev6-3

(Singh et al., 2005)

pnr^VX6 has eye disc | somatic clone phenotype, suppressible by Scer\GAL4^ey.PH/wg^UAS.cAa

(Maurel-Zaffran and Treisman, 2000)

pnr^VX6 has photoreceptor neuron | ectopic | somatic clone phenotype, suppressible by Scer\GAL4^ey.PH/wg^UAS.cAa

(Maurel-Zaffran and Treisman, 2000)

NOT suppressed by

Statement

Reference

pnr^VX6 has adult heart phenotype, non-suppressible by tin³⁴⁶/tin[+]

(Qian and Bodmer, 2009)

pnr^VX6 has adult heart phenotype, non-suppressible by Df(3R)GC14/+

(Qian and Bodmer, 2009)

pnr^VX6 has adult heart phenotype, non-suppressible by H15^nmr-614/H15[+]

(Qian and Bodmer, 2009)

pnr^VX6 has adult heart phenotype, non-suppressible by Df(2L)Exel6012/+

(Qian and Bodmer, 2009)

pnr^VX6 has adult heart phenotype, non-suppressible by tin^UAS.cRa/Scer\GAL4^how-24B

(Qian and Bodmer, 2009)

pnr^VX6 has adult heart phenotype, non-suppressible by tin^UAS.cRa/Scer\GAL4^Mef2.PR

(Qian and Bodmer, 2009)

pnr^VX6 has adult heart phenotype, non-suppressible by tin^UAS.cRa/Scer\GAL4^twi.PG/Scer\GAL4^how-24B

(Qian and Bodmer, 2009)

pnr^VX6 has embryonic pericardial cell phenotype, non-suppressible by pnt^S012309

(Alvarez et al., 2003)

pnr^VX6 has dorsal vessel wall cell phenotype, non-suppressible by pnt^S012309

(Alvarez et al., 2003)

Enhancer of

Statement

Reference

pnr[+]/pnr^VX6 is an enhancer of anterior dorsocentral bristle phenotype of Bx^hdp58-1

(Zenvirt et al., 2008)

pnr[+]/pnr^VX6 is an enhancer of anterior dorsocentral bristle phenotype of Bx^hdpR590

(Zenvirt et al., 2008)

pnr[+]/pnr^VX6 is an enhancer of anterior dorsocentral bristle phenotype of Bx^hdp185-1

(Zenvirt et al., 2008)

pnr^VX6 is an enhancer of thorax phenotype of Chi^E

(Ramain et al., 2000)

Suppressor of

Statement

Reference

pnr[+]/pnr^VX6 is a suppressor of scutellar bristle | increased number phenotype of Ssdp^L7

(Bronstein et al., 2010)

pnr[+]/pnr^VX6 is a suppressor | partially of posterior scutellar bristle | adult stage phenotype of CtBP^UAS.cSa, Scer\GAL4^ap-md544

(Stern et al., 2009)

pnr[+]/pnr^VX6 is a suppressor | partially of anterior scutellar bristle | adult stage phenotype of CtBP^UAS.cSa, Scer\GAL4^ap-md544

(Stern et al., 2009)

pnr[+]/pnr^VX6 is a suppressor | partially of posterior dorsocentral bristle | adult stage phenotype of CtBP^UAS.cSa, Scer\GAL4^ap-md544

(Stern et al., 2009)

pnr[+]/pnr^VX6 is a suppressor | partially of anterior dorsocentral bristle | adult stage phenotype of CtBP^UAS.cSa, Scer\GAL4^ap-md544

(Stern et al., 2009)

pnr[+]/pnr^VX6 is a suppressor of embryonic/larval lymph gland phenotype of Zfrp8^SM206

(Minakhina et al., 2007)

pnr[+]/pnr^VX6 is a suppressor of eye | ventral phenotype of L²

(Singh et al., 2005)

pnr[+]/pnr^VX6 is a suppressor of eye | ventral | somatic clone phenotype of L^rev6-3

(Singh et al., 2005)

NOT Suppressor of

Statement

Reference

pnr^VX6 is a non-suppressor | somatic clone of photoreceptor neuron phenotype of Scer\GAL4^unspecified, ara^UAS.cGa

(Maurel-Zaffran and Treisman, 2000)

Other

Statement

Reference

pnr[+]/pnr^VX6, sens^E2 has dorsocentral bristle phenotype

(Asmar et al., 2008)

Bx^hdp-n60, pnr[+]/pnr^VX6 has dorsocentral bristle phenotype

(Asmar et al., 2008)

Df(3L)29A6, Df(3L)DocA, pnr^VX6 has dorsal vessel wall cell phenotype

(Reim and Frasch, 2005)

Df(3L)29A6, pnr^VX6, tin³⁴⁶ has dorsal vessel wall cell phenotype

(Reim and Frasch, 2005)

Df(3L)29A6, Df(3L)DocA, pnr^VX6, tin³⁴⁶ has dorsal vessel wall cell phenotype

(Reim and Frasch, 2005)

Df(3L)29A6, Df(3L)DocA, pnr^VX6, tin³⁴⁶ has embryonic/larval dorsal vessel phenotype

(Reim and Frasch, 2005)

PRAS40^UAS.cCa, Scer\GAL4^ey.PH, pnr^VX6 has eye | somatic clone phenotype

(Singh and Choi, 2003)

Chi^E, pnr^VX6 has thorax phenotype

(Ramain et al., 2000)

Chi[+]/Chi^E, pnr^VX6 has thorax phenotype

(Ramain et al., 2000)

Additional Comments

Genetic Interactions

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.

(Valadez-Graham et al., 2012)

The increase in heart arrest/fibrillation upon electrical pacing that is seen in pnr^VX6/+ adults is not significantly altered by tin³⁴⁶/+ 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.

(Qian and Bodmer, 2009)

pnr^VX6/+ dominantly suppresses the missing thoracic bristle phenotype of CtBP^Scer\UAS.cSa, Scer\GAL4^ap-md544 flies.

(Stern et al., 2009)

Bx^hdp-n60/Y ; pnr^VX6/+ flies show loss of dorsocentral bristles.

sens^E2/pnr^VX6 double heterozygotes show loss of dorsocentral bristles.

(Asmar et al., 2008)

Flies lacking a copy of pnr^VX6 and CtBP^rev19 show no significant difference in the number of dorsocentral bristles compared to pnr^VX6/+

(Biryukova and Heitzler, 2008)

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 Bx² and heterozygous for pnr^VX6.

No dorsocentral bristle loss is seen in flies hemizygous for Bx¹⁰⁰² and heterozygous for pnr^VX6.

(Zenvirt et al., 2008)

The slight increase in lymph gland size seen in Zfrp8^SM206/+ larvae is dominantly suppressed by pnr^VX6.

(Minakhina et al., 2007)

Df(3L)29A6; Df(3L)DocA, pnr^VX6 stage 16 embryos have a reduced number of cardioblasts compared to wild type; Df(3L)29A6; Df(3L)DocA, pnr^VX6, tin³⁴⁶ embryos have even fewer cardioblasts and form only short regions of the dorsal vessel. Df(3L)29A6; pnr^VX6, tin³⁴⁶ show a milder loss of cardioblasts.

(Reim and Frasch, 2005)

The dorsal eye enlargements caused by homozygous pnr^VX6 clones are no longer seen in the flies are also carrying L^rev6-3/+.

(Singh et al., 2005)

pnr^VX6, pnt^S012309 double mutant embryos lack cardioblasts and pericardial cells and are phenotypically indistinguishable from pnr^VX6 embryos.

(Alvarez et al., 2003)

Expression of CG46146^Scer\UAS.cCa under the control of Scer\GAL4^ey.PH in eye discs homozygous for pnr^VX6 (generated using the "EGUF" method to remove all eye disc cells except the homozygous pnr^VX6 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 Ser^{Bd.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^ey.PH at 25[o]C in eye discs homozygous for pnr^VX6 (generated using the "EGUF" method to remove all eye disc cells except the homozygous pnr^VX6 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 Ser^{Bd.Scer\UAS.T:Hsap\MYC} is expressed under the control of Scer\GAL4^ey.PH at 25[o]C in a wild-type background.

(Singh and Choi, 2003)

Ubiquitous expression of ara^Scer\UAS.cGa under the control of Scer\GAL4^unspecified abolishes photoreceptor differentiation, which is not restored if the flies also carry clones of pnr^VX6. Large pnr^VX6 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 wg^Scer\UAS.cAa under the control of Scer\GAL4^ey.PH.

(Maurel-Zaffran and Treisman, 2000)

The addition of pnr^VX6/+ to heterozygous Chi^E flies gives flies that exhibit a thoracic cleft.

(Ramain et al., 2000)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

pnr^MD237/pnr^VX6 is rescued by pnr^SA.UAS.β/Scer\GAL4^pnr-MD237

(Yang et al., 2012)

Partially rescued by

pnr^VX6 is partially rescued by pnr^UAS.cHa/Scer\GAL4^twi.PG/Scer\GAL4^how-24B

(Qian and Bodmer, 2009)

pnr^VX6 is partially rescued by pnr^UAS.cHa/Scer\GAL4^Mef2.PR

(Qian and Bodmer, 2009)

pnr^VX6 is partially rescued by pnr^UAS.cHa/Scer\GAL4^tin.CΔ4

(Qian and Bodmer, 2009)

pnr^VX6 is partially rescued by pnr^UAS.cHa/Scer\GAL4^how-24B

(Qian and Bodmer, 2009)

pnr^VX6 is partially rescued by pnr^UAS.cHa/Scer\GAL4^da.G32

(Klinedinst and Bodmer, 2003)

pnr^VX6 is partially rescued by Scer\GAL4^zen.Kr.PF/pnr^UAS.cHa

(Klinedinst and Bodmer, 2003)

pnr^VX6 is partially rescued by pnr^UAS.cHa/Scer\GAL4^twi.PG/Scer\GAL4^how-24B

(Klinedinst and Bodmer, 2003)

Not rescued by

pnr^MD237/pnr^VX6 is not rescued by pnr^UAS.β/Scer\GAL4^pnr-MD237

(Yang et al., 2012)

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.

(Yang et al., 2012)

Images (0)

Mutant

Wild-type

Stocks (3)

Bloomington

6334

w^*; P{neoFRT}82B pnr^VX6/TM6B, Tb⁺

603840

w^*; P{neoFRT}82B pnr^VX6 e^s tin³⁴⁶ ca¹/TM3, P{eve-lacZ8.0}AG1, Sb¹

Kyoto

101673

kar² ry⁵⁰⁶ pnr^VX6 P{neoFRT}82B / TM3, Sb¹ Tb^*

Notes on Origin

Discoverer

Comments

Class 2 pnr allele: lethal recessive allele. Allelic series according to the extent of the dorsal hole: pnr¹ > Df(3R)sbd45 = pnr^VX6 = pnr^VP8 = pnr^D1 > pnr^D3.

(Heitzler et al., 1996)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (3)

Reported As

Symbol Synonym

Name Synonyms

Secondary FlyBase IDs

References (50)

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