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General Information
Symbol
Dmel\pntΔ88
Species
D. melanogaster
Name
FlyBase ID
FBal0035437
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
pntD88, pntdelta88
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Small deletion that covers 3' end of pnt.

Deletion of the entire P-element and flanking sequences, deletion of the entire P1 transcript and 3' exons of the P2 transcript.

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

embryonic/larval dorsal branch & terminal tracheal cell | somatic clone

Detailed Description
Statement
Reference

pntΔ88 mutant embryos show a significant increase in the overall number of cardioblasts (both generic and ostial cardioblasts), as compared to controls.

Oenocytes are completely absent in pntΔ88 homozygous stage 15 embryos, unlike in heterozygous or wild-type controls.

pntP1-82/pntΔ88 or pntP1-90/pntΔ88 mutant larval brains have a significant increase in the number of Asense-negative type II neuroblasts, but a significant decrease in the number of intermediate neural progenitors.

Adult midgut intestinal stem cell somatic MARCM clones homozygous for pntΔ88 display growth defects and never grow past the 2-cell stage. The rate of mitosis upon infection with Pseudomonas entomophila in the mosaic midgut is decreased compared to controls.

pntΔ88/pnt1277 flies have weakly rough eyes.

Supernumerary tracheal fusion cells are present in the dorsal trunk of pntΔ88 embryos.

Homozygous bract cells are never seen in somatic clones induced in the leg, while homozygous bristles are recovered.

Mutant embryos have gaps in the dorsal trunk. The tracheal cells of heterozygotes show moderate lack-of-migration defects in 44% of embryos, and show severe ectopic lack-of-migration defects in 15% of embryos.

pntΔ88/pnt1277 flies have rough eyes and show a loss of photoreceptor cells.

In control stage 15 embryos, the anterior and posterior lateral trunks (Lta and Ltp, respectively) from adjacent segments are joined. In contrast, gaps occur between the Lta and Ltp in stage 15 homozygous pntΔ88 embryos.

By stage 15, in control embryos, tracheal ganglionic cells and branches enter the ventral nerve cord (VNC) toward the central nervous system (CNS) midline. In contrast, in homozygous pntΔ88 embryos, tracheal ganglionic branches and cells rarely enter the VNC when present and are truncated, but in most cases are absent.

Homozygous pntΔ88 embryos show significant losses in the continuity of tracheal tubules (gaps and breaks) and constrictions in the dorsal trunk. Dorsal branch formation does not occur in some metameres in homozygous pntΔ88 mutants.

Homozygous pntΔ88 mutant fat body clones do not exhibit any mitochondrial phenotypes.

Many pntΔ88/pnt1277 ommatidia over- or under-rotate; the variance (s.d.) in degree of rotation is greater than in wild type in adult eyes.

Eggs derived from egg chambers containing complete homozygous follicle cell clones have a single thick dorsal appendages.

Eggs derived from females with mosaic pntΔ88 egg chambers have a single dorsal appendage.

pnt1277/pntΔ88 eye discs show polarity defects (6.7% of ommatidial clusters are inverted and 6% are symmetrical).

pnt1230/pntΔ88 eye discs show chirality defects in 26.4% of ommatidial clusters.

pntKG04968/pntΔ88 eye discs show chirality defects in 9.5% of ommatidial clusters.

pntΔ88 Minute clones in the eye disc fail to form the arcs and rosettes of cells in the morphogenetic furrow that are seen in wild-type eye discs. Some clones show small clusters of cells within the furrow while other clones contain no clustering.

The tracheal branches of pntΔ88 embryos do not show breaks.

pnt1277/pntΔ88 display a weak rough eye phenotype.

Homozygous clones in the dorsal tracheal branches fail to develop as terminal cells.

pntΔ88 homozygous clones in the dorsal air sac primordium grow and normally but never contribute to the tip of the primordium.

In pntΔ88 stage 15 embryos, the genital disc precursor cells are completely missing.

In pntΔ88 embryos, migration of all primary tracheal branches is incomplete. pnt737/pntΔ88 transheterozygotes show a less severe phenotype in which nearly all branches are affected.

In mutant embryos midline glial cells fail to migrate in between the segmental commissure.

Only 23% of cuticles from pntΔ88 homozygous embryos show fusion of at least one pair of denticle belts.

Mutant embryos have ectopic cardioblasts that form enlarged hearts comprising disorganised rows of cardioblasts. The ectopic cardioblasts appear to be restricted to the posterior domain.

In pntΔ88 embryos, the anterior and posterior sensory fascicles are spaced further apart at the CNS-PNS transition zone compared with wild type.

In pntΔ88 mutant somatic clones in the 3rd instar eye disc, photoreceptors R2-R5 fail to undergo or differentiation. Within pntΔ88 mutant somatic clones there is a failure of G1 arrest in the furrow: all cells except R8s re-enter the cell cycle. However, many of these cells do not progress past G2 (in clones only about 40% of wild-type numbers of postmitotic cells are seen posterior to the furrow). Consequently, the mitotic index is reduced in these clones. Those cells entering mitosis in these clones, tend to do so later than in wild-type (more posterior to the furrow).

The arrangement of glial cells is irregular in the central nervous system of mutant embryos.

The second mitotic wave is absent in pntΔ88 clones in the eye. The cells are arrested in G2.

Despite the absence of secondary and tertiary tracheal branches in pntΔ88 mutant embryos, the tip cells of migrating branches in these embryos have numerous filpodia as in wild-type.

pntΔ88 mutant embryos have an estimated 85 cells in each Malpighian tubule cell (as opposed to about 125 in wild-type).

pnt1277/pntΔ88 show reduced number of R7 photoreceptors.

Homozygous embryos show some loss of VA2 muscle precursor cells (81% of hemisegments contain VA2 precursor cells).

The size of the primary branches of the tracheal system is largely unaffected in mutant embryos.

Formation of eve-expressing progenitors in the mesoderm is variably reduced in mutant embryos. The formation of eve-expressing pericardial cells and muscle DA1 is reduced in mutant embryos.

Heterozygotes have wild-type wings.

The third midgut chamber is greatly reduced in size in homozygous embryos. The central and posterior constrictions that form this chamber form normally, but are located more closely together than in the wild-type gut. 85% of embryos fail to form the anterior constriction completely; the constriction initiates at its normal site but does not significantly constrict the midgut. Elongation of gastric caecae is not seen in these embryos. The number of visceral mesoderm (VM) cells in the third midgut chamber is reduced compared to wild-type, while the first, second and fourth midgut chambers contain normal numbers of cells. Defects in VM cell segregation are seen immediately after the stage 12 mitosis, producing a junction in the central midgut. By stage 16, VM cells are often scattered around the surface of the midgut, in contrast to the ordered files of cells seen in wild-type embryos. pnt05484Δ33/pntΔ88 and pnt07825Δ78/pntΔ88 embryos have wild-type midgut development.

Homozygous embryos have a reduced number of cells in both the anterior and posterior Malpighian tubules compared to wild-type embryos.

The central nervous system (CNS) is narrower than normal and the commissures are thicker than normal and incompletely separated in pntΔ88 embryos.

Exit glial cells fail to extend cellular processes to properly ensheath the two nerve bundles. pnt ttk double mutant flies display an additive CNS phenotype combining characteristics of both phenotypic traits.

The Bolwig's nerve defasciculates and becomes misrouted during its growth from P1 to P2. The aberrant BN branches grow on the surface of the optic lobe anlagen and their endings reach various ectopic positions during mid-stage 16.

Segmental commissures are fused in mutant embryos.

pnt2/pntΔ88 embryos exhibit subtle ventral defects. Leg and eye/antenna pnt2/pntΔ88 mutant discs can be in vivo cultured. Wing and haltere discs cannot.

Segmental commissures appear fused in homozygous embryos. 90% of the ommatidia in pntΔ88/pnt1277 flies lack the R7 photoreceptor and/or some outer photoreceptor cells.

pntΔ88/pntT6 combination is viable, 25% ommatidia are missing R7 cells.

Eggs laid by mosaic females (generated using Scer\FRT/Scer\FLP1 recombination system) that have a clone of mutant follicle cells in the dorsal-anterior region or a clone that covers the entire follicle cell layer exhibit a single broad dorsal appendage 4 times wider than a wild type appendage. This is not a fusion of the two appendages but cells from the middle region taking on an appendage-producing cell fate. The majority of these eggs hatch and develop into fertile adults. Eggs from females with a germline homozygous for pntΔ88 do not exhibit defects in the dorsal appendages or any discernible embryonic phenotype.

Heterozygotes with pnt1277 lack one to three photoreceptor cells in most ommatidia. The R7 precursor can be rescued by pnt P2 transcript expressed by sev enhancers but the mutant phenotype is enhanced by pntT151A.Scer\UAS expressed by sev enhancers.

Mutants show fused commissures and disrupted trachea. Longitudinal glia do not form the typical flat sheet on the dorsal side of the CNS, but cells of rounded appearance are evident, partly sitting on top of one another. Some of these cells have glial-type morphology, with lobulated nuclei, that nevertheless fail to flatten and ensheath the longitudinal connectives.

CNS and tracheal phenotype.

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

pnt1277/pntΔ88 has visible phenotype, suppressible by Bap170hfl1/Bap170[+]

NOT suppressed by
Statement
Reference
Enhancer of
Statement
Reference

pnt[+]/pntΔ88 is an enhancer of visible phenotype of Scer\GAL4hs.2sev, edlUAS.cYa

pnt[+]/pntΔ88 is an enhancer of visible phenotype of cswlf

NOT Enhancer of
Statement
Reference

pnt[+]/pntΔ88 is a non-enhancer of visible | dominant phenotype of Bx1

Suppressor of
Statement
Reference

pnt[+]/pntΔ88 is a suppressor of visible phenotype of Scer\GAL4Tub.PU, cswN308D.UASp

pnt[+]/pntΔ88 is a suppressor of visible phenotype of fafBX4

NOT Suppressor of
Statement
Reference

pnt[+]/pntΔ88 is a non-suppressor of visible | dominant phenotype of Bx1

Other
Phenotype Manifest In
Enhanced by
Statement
Reference
NOT Enhanced by
Suppressed by
NOT suppressed by
Enhancer of
Statement
Reference

pnt[+]/pntΔ88 is an enhancer of eye phenotype of rauf04153/Df(2L)rauΔ

pnt[+]/pntΔ88 is an enhancer of ommatidium phenotype of Scer\GAL4hs.2sev, edlUAS.cYa

pnt[+]/pntΔ88 is an enhancer of ommatidium phenotype of cswlf

NOT Enhancer of
Statement
Reference

pnt[+]/pntΔ88 is a non-enhancer of ommatidium phenotype of Scer\GAL4hs.2sev, nmoUAS.cUa

pnt[+]/pntΔ88 is a non-enhancer of wing margin phenotype of Bx1

pnt[+]/pntΔ88 is a non-enhancer of wing vein phenotype of cswlf

Suppressor of
Statement
Reference

pntΔ88 is a suppressor of heart primordium phenotype of edlk06602

pnt[+]/pntΔ88 is a suppressor of wing vein | ectopic phenotype of Scer\GAL4Tub.PU, cswN308D.UASp

pntΔ88 is a suppressor | partially of ommatidium phenotype of aosrlt

pnt[+]/pntΔ88 is a suppressor of photoreceptor cell R1 | ectopic phenotype of fafBX4

pnt[+]/pntΔ88 is a suppressor of photoreceptor cell R2 | ectopic phenotype of fafBX4

pnt[+]/pntΔ88 is a suppressor of photoreceptor cell R3 | ectopic phenotype of fafBX4

pnt[+]/pntΔ88 is a suppressor of photoreceptor cell R4 | ectopic phenotype of fafBX4

pnt[+]/pntΔ88 is a suppressor of photoreceptor cell R5 | ectopic phenotype of fafBX4

pntΔ88 is a suppressor of phenotype of JraAsp.hs.sev

NOT Suppressor of
Statement
Reference

pnt[+]/pntΔ88 is a non-suppressor of ommatidium phenotype of Scer\GAL4hs.2sev, nmoUAS.cUa

pnt[+]/pntΔ88 is a non-suppressor of wing margin phenotype of Bx1

pntΔ88 is a non-suppressor of ommatidium phenotype of Rac1V12.hs.sev

Other
Additional Comments
Genetic Interactions
Statement
Reference

edlk06602, pntΔ88 double mutant embryos show an increase in the number of cardioblasts, which is similar to what is observed in pntΔ88 single mutants and unlike the decrease observed in edlk06602 single mutants.

The expression of midUAS.cRa under the control of Scer\GAL4tin.cBa in a pntΔ88 mutant background converts many of the extra ostial cardioblasts into generic cardioblasts.

The growth of intestinal stem cell somatic MARCM clones expressing cicKK100838 under the control of Scer\GAL4tub.PU in the adult midgut is significantly impaired by combination with pntΔ88 in homozygous state.

The extra wing vein phenotype caused by expression of CG4096KK108644 under the control of Scer\GAL4Act5C.PU is not suppressed if the flies also carry pntΔ88.

The penetrance of the tracheal lumen defect seen in Vhl1/+ embryos is not modified by pntΔ88/+.

Bap170hfl1/+ suppresses the loss of photoreceptor cells seen in pntΔ88/pnt1277 flies.

Expression of Bap170C1.Scer\UAS under the control of Scer\GAL4elav.PU enhances the rough eye phenotype and loss of photoreceptor cells seen in pntΔ88/pnt1277 flies.

In contrast to single heterozygous pntΔ88 or jing1 mutants, double heterozygous embryos show tracheal ganglionic branch defects.

In contrast to single heterozygous pntΔ88 or jing3 mutants, double heterozygous embryos show tracheal ganglionic branch defects.

jing3/pntΔ88 double heterozygotes show significant losses in the continuity of tracheal tubules (gaps and breaks) and constrictions in the dorsal trunk (Dt), similar to the homozygous phenotypes of jing3 and less severe than that of homozygous vvldfr-E82.

Dorsal branches are absent, truncated or broken in jing3/pntΔ88 double heterozygotes.

ed1X5 dominantly enhances the phenotype of mis-rotation of ommatidia that is seen in pntΔ88/pnt1277 animals.

fredH24 dominantly suppresses the phenotype of mis-rotation of ommatidia that is seen in pntΔ88/pnt1277 animals.

Expression of Egfr::toract.Scer\UAS under the control of Scer\GAL4αTub84B.PL does not rescue the lack of arcs and rosettes in the morphogenetic furrow of eye discs with pntΔ88 Minute clones.

The rough eye phenotype of flies expressing GugScer\UAS.cCa under the control of Scer\GAL4GMR.PF is enhanced in both a pnt1277/pntΔ88 and a pnt1277/pnt07825 background.

kni6/+, pntΔ88/+ embryos form rudimentary tracheal branches.

The rough eye phenotype caused by expression of edlScer\UAS.cYa under the control of Scer\GAL4hs.2sev is enhanced by pntΔ88/+.

Ras85DV12.Scer\UAS; Scer\GAL4GMR.PF increases the number of cells in G2 arrest posterior the furrow in pntΔ88 mutant clones to 100%. This effect is also seen with Ras85DV12.S35.Scer\UAS, but not with Ras85DV12.G37.Scer\UAS or Ras85DV12.C40.Scer\UAS. Within pntΔ88 mutant clones in the eye disc in a BacA\p35GMR.PH background, caspase activation is seen posterior to column 8, relative to the morphogenetic furrow. There is no increase in caspase activation outside of these clones.

pntΔ88 has no detectable effects on the neuronal defects seen in embryos expressing gcmScer\UAS.cHa under the control of Scer\GAL4sca-T3.

Expression of stgScer\UAS.cNa (under the control of Scer\GAL4αTub84B.PL) in pntΔ88 clones in the eye disc completely rescues the second mitotic wave.

Weakly enhances the eye phenotype produced by activated arm constructs. (either armS44Y.GMR or armS56F.GMR).

Expression of csw::Src64Bsrc90.Scer\UAS under the control of Scer\GAL4twi.PG does not affect the loss of VA2 muscle precursor cells seen in pntΔ88 embryos (82% of hemisegments have VA2 cells).

The cswlf/Y rough eye phenotype is dominantly enhanced by pntΔ88. The cswlf/Y wing vein gap phenotype is not enhanced by pntΔ88.

S104E Df(2R)CX1 double heterozygotes show notching of the wing margin.

The width of the CNS is closer to wild-type if pntΔ88 embryos are also mutant for Df(3L)H99, although commissure separation remains incomplete.

Dominantly suppresses the extra outer photoreceptor cell phenotype seen in fafBX4 homozygotes.

pntΔ88/pntT6 phenotype is dominantly enhanced by prosJO1, leading to roughening of the external eye.

pntΔ88/pnt1277 completely suppresses the ectopic R7 rough eye phenotype of JraAsp.hs.sev.

Xenogenetic Interactions
Statement
Reference

The pntΔ88 midline glia phenotype is partially rescued when Ggal\ets1Scer\UAS.cAa, ALV\v-etsScer\UAS.cAa or Ggal\ets2Scer\UAS.cAa is expressed using Scer\GAL4sli.PS. The eye phenotype of pntΔ88/pnt1277 flies is partially rescued when Ggal\ets2Scer\UAS.cAa or ALV\v-etsScer\UAS.cAa is expressed using Scer\GAL4hs.2sev.

Complementation and Rescue Data
Partially rescued by
Comments

Scer\GAL4sli.PS-mediated expression of pntP2.Scer\UAS or pntP1.Scer\UAS rescues the fused commissure phenotype. Expression of pntT151A.Scer\UAS fails to rescue the phenotype.

Scer\GAL4sli.PS-mediated expression of pntP2.Scer\UAS or pntP1.Scer\UAS rescues the pntΔ88 fused commissure phenotype. Expression of pntT151A.Scer\UAS fails to rescue the pntΔ88 fused commissure phenotype.

The eye phenotype of pntΔ88/pnt1277 flies is partially rescued when pntP1.Scer\UAS is expressed using Scer\GAL4hs.2sev at 17oC.

The R7 precursor can be rescued by pnt P2 transcript expressed by sev enhancers but the mutant phenotype is enhanced by pntT151A.Scer\UAS expressed by sev enhancers.

Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments

Analysis of excess cardioblast phenotype provides an allelic series:pntS012309, pnt2 > pntRR112, pntrM254 > pntΔ88, pnt07825.

No interaction with P{sev-svp1} or P{sev-svp2} exists.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
References (105)