FlyBase Allele Report: Dmel\pnt[Δ88]

pnt^Δ88 mutant embryos show a significant increase in the overall number of cardioblasts (both generic and ostial cardioblasts), as compared to controls.

(Schwarz et al., 2018)

Oenocytes are completely absent in pnt^Δ88 homozygous stage 15 embryos, unlike in heterozygous or wild-type controls.

(Wang et al., 2017)

pnt^P1-82/pnt^Δ88 or pnt^P1-90/pnt^Δ88 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.

(Xie et al., 2016)

Adult midgut intestinal stem cell somatic MARCM clones homozygous for pnt^Δ88 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.

(Jin et al., 2015)

pnt^Δ88/pnt¹²⁷⁷ flies have weakly rough eyes.

(Tchankouo-Nguetcheu et al., 2014)

Supernumerary tracheal fusion cells are present in the dorsal trunk of pnt^Δ88 embryos.

(Caviglia and Luschnig, 2013)

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

(Mou et al., 2012)

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.

(Hsouna et al., 2010)

pnt^Δ88/pnt¹²⁷⁷ flies have rough eyes and show a loss of photoreceptor cells.

(Rendina et al., 2010)

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 pnt^Δ88 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 pnt^Δ88 embryos, tracheal ganglionic branches and cells rarely enter the VNC when present and are truncated, but in most cases are absent.

Homozygous pnt^Δ88 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 pnt^Δ88 mutants.

(Sonnenfeld et al., 2010)

Homozygous pnt^Δ88 mutant fat body clones do not exhibit any mitochondrial phenotypes.

(Baltzer et al., 2009)

Many pnt^Δ88/pnt¹²⁷⁷ ommatidia over- or under-rotate; the variance (s.d.) in degree of rotation is greater than in wild type in adult eyes.

(Fetting et al., 2009)

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

(Lachance et al., 2009)

Eggs derived from females with mosaic pnt^Δ88 egg chambers have a single dorsal appendage.

(Zartman et al., 2009)

pnt¹²⁷⁷/pnt^Δ88 eye discs show polarity defects (6.7% of ommatidial clusters are inverted and 6% are symmetrical).

pnt¹²³⁰/pnt^Δ88 eye discs show chirality defects in 26.4% of ommatidial clusters.

pnt^KG04968/pnt^Δ88 eye discs show chirality defects in 9.5% of ommatidial clusters.

(Weber et al., 2008)

pnt^Δ88 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.

(Brown et al., 2006)

The tracheal branches of pnt^Δ88 embryos do not show breaks.

(Cela and Llimargas, 2006)

pnt¹²⁷⁷/pnt^Δ88 display a weak rough eye phenotype.

(Charroux et al., 2006)

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

(Ghabrial and Krasnow, 2006)

pnt^Δ88 homozygous clones in the dorsal air sac primordium grow and normally but never contribute to the tip of the primordium.

(Cabernard and Affolter, 2005)

In pnt^Δ88 stage 15 embryos, the genital disc precursor cells are completely missing.

(Chen et al., 2005)

In pnt^Δ88 embryos, migration of all primary tracheal branches is incomplete. pnt⁷³⁷/pnt^Δ88 transheterozygotes show a less severe phenotype in which nearly all branches are affected.

(Myat et al., 2005)

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

(Pielage et al., 2004)

Only 23% of cuticles from pnt^Δ88 homozygous embryos show fusion of at least one pair of denticle belts.

(Urban et al., 2004)

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.

(Alvarez et al., 2003)

In pnt^Δ88 embryos, the anterior and posterior sensory fascicles are spaced further apart at the CNS-PNS transition zone compared with wild type.

(Sepp and Auld, 2003)

In pnt^Δ88 mutant somatic clones in the 3rd instar eye disc, photoreceptors R2-R5 fail to undergo or differentiation. Within pnt^Δ88 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).

(Yang and Baker, 2003)

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

(Yuasa et al., 2003)

The second mitotic wave is absent in pnt^Δ88 clones in the eye. The cells are arrested in G2.

(Baonza et al., 2002)

Despite the absence of secondary and tertiary tracheal branches in pnt^Δ88 mutant embryos, the tip cells of migrating branches in these embryos have numerous filpodia as in wild-type.

(Ribeiro et al., 2002)

pnt^Δ88 mutant embryos have an estimated 85 cells in each Malpighian tubule cell (as opposed to about 125 in wild-type).

(Sudarsan et al., 2002)

pnt¹²⁷⁷/pnt^Δ88 show reduced number of R7 photoreceptors.

(Bai et al., 2001)

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

(Johnson Hamlet and Perkins, 2001)

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

(Beitel and Krasnow, 2000)

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.

(Halfon et al., 2000)

Heterozygotes have wild-type wings.

(Nagaraj et al., 1999)

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. pnt^05484Δ33/pnt^Δ88 and pnt^07825Δ78/pnt^Δ88 embryos have wild-type midgut development.

(Bilder et al., 1998)

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

(Kerber et al., 1998)

The central nervous system (CNS) is narrower than normal and the commissures are thicker than normal and incompletely separated in pnt^Δ88 embryos.

(Dong and Jacobs, 1997)

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.

(Giesen et al., 1997)

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.

(Schmucker et al., 1997)

Segmental commissures are fused in mutant embryos.

(Scholz et al., 1997, Scholz et al., 1997)

pnt²/pnt^Δ88 embryos exhibit subtle ventral defects. Leg and eye/antenna pnt²/pnt^Δ88 mutant discs can be in vivo cultured. Wing and haltere discs cannot.

(Simcox, 1997)

Segmental commissures appear fused in homozygous embryos. 90% of the ommatidia in pnt^Δ88/pnt¹²⁷⁷ flies lack the R7 photoreceptor and/or some outer photoreceptor cells.

(Albagli et al., 1996)

pnt^Δ88/pnt^T6 combination is viable, 25% ommatidia are missing R7 cells.

(Kauffmann et al., 1996)

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 pnt^Δ88 do not exhibit defects in the dorsal appendages or any discernible embryonic phenotype.

(Morimoto et al., 1996)

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 pnt^{T151A.Scer\UAS} expressed by sev enhancers.

(Brunner et al., 1994)

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.

(Klaes et al., 1994)

CNS and tracheal phenotype.

(Scholz et al., 1993)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

pnt¹²⁷⁷/pnt^Δ88 has visible phenotype, enhanceable by Scer\GAL4^elav.PU/Bap170^C1.UAS

(Rendina et al., 2010)

pnt^Δ88 has abnormal mitotic cell cycle | somatic clone phenotype, enhanceable by Ras85D^V12.UAS/Scer\GAL4^GMR.PF

(Yang and Baker, 2003)

NOT Enhanced by

Statement

Reference

pnt^Δ88 has increased cell number | embryonic stage phenotype, non-enhanceable by edl^k06602

(Schwarz et al., 2018)

Suppressed by

Statement

Reference

pnt¹²⁷⁷/pnt^Δ88 has visible phenotype, suppressible by Bap170^hfl1/Bap170[+]

(Rendina et al., 2010)

NOT suppressed by

Statement

Reference

pnt^Δ88 has increased cell number | embryonic stage phenotype, non-suppressible by edl^k06602

(Schwarz et al., 2018)

Enhancer of

Statement

Reference

pnt[+]/pnt^Δ88 is an enhancer of neoplasia | larval stage | somatic clone phenotype of Ras85D^V12.UAS, Scer\GAL4^Act.PU

(Ito and Igaki, 2021)

pnt[+]/pnt^Δ88 is an enhancer of visible phenotype of Scer\GAL4^hs.2sev, edl^UAS.cYa

(Yamada et al., 2003)

pnt[+]/pnt^Δ88 is an enhancer of visible phenotype of csw^lf

(Firth et al., 2000)

NOT Enhancer of

Statement

Reference

pnt[+]/pnt^Δ88 is a non-enhancer of abnormal planar polarity phenotype of Scer\GAL4^hs.2sev, nmo^UAS.cUa

(Mirkovic et al., 2011)

pnt[+]/pnt^Δ88 is a non-enhancer of visible | dominant phenotype of Bx¹

(Bejarano et al., 2008)

Suppressor of

Statement

Reference

pnt^Δ88 is a suppressor of decreased cell number | embryonic stage phenotype of edl^k06602

(Schwarz et al., 2018)

pnt[+]/pnt^Δ88 is a suppressor of visible phenotype of Scer\GAL4^Tub.PU, csw^N308D.UASp

(Oishi et al., 2006)

pnt^Δ88 is a suppressor of abnormal cell polarity phenotype of aos^rlt

(Gaengel and Mlodzik, 2003)

pnt[+]/pnt^Δ88 is a suppressor of visible phenotype of faf^BX4

(Isaksson et al., 1997)

NOT Suppressor of

Statement

Reference

pnt^Δ88 is a non-suppressor of visible phenotype of AdamTS-B^KK108644, Scer\GAL4^Act5C.PU

(Butchar et al., 2012)

pnt[+]/pnt^Δ88 is a non-suppressor of abnormal planar polarity phenotype of Scer\GAL4^hs.2sev, nmo^UAS.cUa

(Mirkovic et al., 2011)

pnt[+]/pnt^Δ88 is a non-suppressor of visible | dominant phenotype of Bx¹

(Bejarano et al., 2008)

pnt^Δ88 is a non-suppressor of abnormal neuroanatomy phenotype of Scer\GAL4^sca-T3, gcm^UAS.cHa

(Yuasa et al., 2003)

Other

Statement

Reference

Scer\GAL4^Tub.PU, cic^KK100838, pnt^Δ88 has decreased cell number | somatic clone phenotype

(Jin et al., 2015)

hry²⁶, pnt^Δ88 has partially lethal phenotype

(Bianchi-Frias et al., 2004)

hryⁱ²², pnt^Δ88 has partially lethal phenotype

(Bianchi-Frias et al., 2004)

hryⁱ²²/h[+], pnt^Δ88 has partially lethal phenotype

(Bianchi-Frias et al., 2004)

h[+]/hry²⁶, pnt^Δ88 has partially lethal phenotype

(Bianchi-Frias et al., 2004)

Df(2R)CX1, pnt^Δ88 has visible | dominant phenotype

(Nagaraj et al., 1999)

Phenotype Manifest In

Enhanced by

Statement

Reference

pnt¹²⁷⁷/pnt^Δ88 has eye photoreceptor cell phenotype, enhanceable by Scer\GAL4^elav.PU/Bap170^C1.UAS

(Rendina et al., 2010)

pnt¹²⁷⁷/pnt^Δ88 has eye phenotype, enhanceable by Scer\GAL4^elav.PU/Bap170^C1.UAS

(Rendina et al., 2010)

pnt¹²⁷⁷/pnt^Δ88 has ommatidium phenotype, enhanceable by ed[+]/ed^1X5

(Fetting et al., 2009)

pnt^T6/pnt^Δ88 has ommatidium phenotype, enhanceable by pros[+]/pros^JO1

(Kauffmann et al., 1996)

NOT Enhanced by

Statement

Reference

pnt^Δ88 has embryonic heart ostial cardioblast | increased number phenotype, non-enhanceable by edl^k06602

(Schwarz et al., 2018)

pnt^Δ88 has embryonic cardioblast | increased number phenotype, non-enhanceable by edl^k06602

(Schwarz et al., 2018)

pnt¹²⁷⁷/pnt^Δ88 has eye phenotype, non-enhanceable by Ptp61F[+]/Ptp61F^4-10

(Tchankouo-Nguetcheu et al., 2014)

pnt¹²⁷⁷/pnt^Δ88 has eye phenotype, non-enhanceable by Ptp61F^UAS.cBa/Scer\GAL4^GMR.PU

(Tchankouo-Nguetcheu et al., 2014)

pnt^Δ88 has muscle cell of ventral acute muscle 2 | precursor phenotype, non-enhanceable by Scer\GAL4^twi.PG/csw^{UAS.Tag:Myr(Src64B)}

(Johnson Hamlet and Perkins, 2001)

Suppressed by

Statement

Reference

pnt¹²⁷⁷/pnt^Δ88 has eye photoreceptor cell phenotype, suppressible by Bap170^hfl1/Bap170[+]

(Rendina et al., 2010)

pnt¹²⁷⁷/pnt^Δ88 has ommatidium phenotype, suppressible by fred[+]/fred^H24

(Fetting et al., 2009)

pnt^Δ88 has mitotic cell cycle | somatic clone phenotype, suppressible by stg^UAS.cNa/Scer\GAL4^αTub84B.PL

(Baonza et al., 2002)

pnt^Δ88 has eye disc | somatic clone phenotype, suppressible by stg^UAS.cNa/Scer\GAL4^αTub84B.PL

(Baonza et al., 2002)

pnt¹²⁷⁷/pnt^Δ88 has photoreceptor cell R7 phenotype, suppressible by ed^slH8/ed^1X5

(Bai et al., 2001)

pnt¹²⁷⁷/pnt^Δ88 has ommatidium phenotype, suppressible by ed^slH8/ed^1X5

(Bai et al., 2001)

pnt^Δ88 has larval ventral nerve cord phenotype, suppressible by Df(3L)H99

(Dong and Jacobs, 1997)

pnt^Δ88 has eye photoreceptor cell phenotype, suppressible by ALV\v-ets^UAS.cAa/Scer\GAL4^hs.2sev

(Albagli et al., 1996)

pnt^Δ88 has midline glial cell phenotype, suppressible by ALV\v-ets^UAS.cAa/Scer\GAL4^sli.PS

(Albagli et al., 1996)

pnt^Δ88 has eye photoreceptor cell phenotype, suppressible by Scer\GAL4^hs.2sev/Ggal\ets2^UAS.cAa

(Albagli et al., 1996)

pnt^Δ88 has midline glial cell phenotype, suppressible by Ggal\ets1^UAS.cAa/Scer\GAL4^sli.PS

(Albagli et al., 1996)

pnt^Δ88 has midline glial cell phenotype, suppressible by Scer\GAL4^sli.PS/Ggal\ets2^UAS.cAa

(Albagli et al., 1996)

NOT suppressed by

Statement

Reference

pnt^Δ88 has embryonic heart ostial cardioblast | increased number phenotype, non-suppressible by edl^k06602

(Schwarz et al., 2018)

pnt^Δ88 has embryonic cardioblast | increased number phenotype, non-suppressible by edl^k06602

(Schwarz et al., 2018)

pnt¹²⁷⁷/pnt^Δ88 has eye phenotype, non-suppressible by Ptp61F[+]/Ptp61F^4-10

(Tchankouo-Nguetcheu et al., 2014)

pnt¹²⁷⁷/pnt^Δ88 has eye phenotype, non-suppressible by Ptp61F^UAS.cBa/Scer\GAL4^GMR.PU

(Tchankouo-Nguetcheu et al., 2014)

pnt^Δ88 has ommatidial precursor cluster | somatic clone phenotype, non-suppressible by Egfr::tor^act.UAS/Scer\GAL4^αTub84B.PL

(Brown et al., 2006)

pnt^Δ88 has muscle cell of ventral acute muscle 2 | precursor phenotype, non-suppressible by Scer\GAL4^twi.PG/csw^{UAS.Tag:Myr(Src64B)}

(Johnson Hamlet and Perkins, 2001)

Enhancer of

Statement

Reference

pnt[+]/pnt^Δ88 is an enhancer of eye-antennal disc | somatic clone phenotype of Ras85D^V12.UAS, Scer\GAL4^Act.PU

(Ito and Igaki, 2021)

pnt[+]/pnt^Δ88 is an enhancer of eye phenotype of rau^f04153/Df(2L)rau^Δ

(Sieglitz et al., 2013)

pnt¹²⁷⁷/pnt^Δ88 is an enhancer of interommatidial bristle phenotype of Gug^UAS.cCa, Scer\GAL4^GMR.PF

(Charroux et al., 2006)

pnt[+]/pnt^Δ88 is an enhancer of ommatidium phenotype of Scer\GAL4^hs.2sev, edl^UAS.cYa

(Yamada et al., 2003)

pnt[+]/pnt^Δ88 is an enhancer of ommatidium phenotype of csw^lf

(Firth et al., 2000)

NOT Enhancer of

Statement

Reference

pnt[+]/pnt^Δ88 is a non-enhancer of ommatidium phenotype of Scer\GAL4^hs.2sev, nmo^UAS.cUa

(Mirkovic et al., 2011)

pnt[+]/pnt^Δ88 is a non-enhancer of wing margin phenotype of Bx¹

(Bejarano et al., 2008)

pnt[+]/pnt^Δ88 is a non-enhancer of wing vein phenotype of csw^lf

(Firth et al., 2000)

Suppressor of

Statement

Reference

pnt^Δ88 is a suppressor of embryonic cardioblast phenotype of edl^k06602

(Schwarz et al., 2018)

pnt^Δ88 is a suppressor of embryonic heart ostial cardioblast phenotype of edl^k06602

(Schwarz et al., 2018)

pnt^Δ88 is a suppressor of heart primordium phenotype of edl^k06602

(Schwarz et al., 2018)

pnt[+]/pnt^Δ88 is a suppressor of embryonic/larval ganglionic tracheal branch phenotype of seq^Z1241

(Araújo and Casanova, 2011)

pnt[+]/pnt^Δ88 is a suppressor of wing vein | ectopic phenotype of Scer\GAL4^Tub.PU, csw^N308D.UASp

(Oishi et al., 2006)

pnt[+]/pnt^Δ88 is a suppressor of eye phenotype of Scer\GAL4^GMR.PF, fred^RNAi.UAS

(Chandra et al., 2003)

pnt^Δ88 is a suppressor of ommatidium phenotype of aos^rlt

(Gaengel and Mlodzik, 2003)

pnt[+]/pnt^Δ88 is a suppressor of photoreceptor cell R1 | ectopic phenotype of faf^BX4

(Isaksson et al., 1997)

pnt[+]/pnt^Δ88 is a suppressor of photoreceptor cell R2 | ectopic phenotype of faf^BX4

(Isaksson et al., 1997)

pnt[+]/pnt^Δ88 is a suppressor of photoreceptor cell R3 | ectopic phenotype of faf^BX4

(Isaksson et al., 1997)

pnt[+]/pnt^Δ88 is a suppressor of photoreceptor cell R4 | ectopic phenotype of faf^BX4

(Isaksson et al., 1997)

pnt[+]/pnt^Δ88 is a suppressor of photoreceptor cell R5 | ectopic phenotype of faf^BX4

(Isaksson et al., 1997)

pnt^Δ88 is a suppressor of photoreceptor cell R6 | ectopic phenotype of faf^BX4

(Isaksson et al., 1997)

pnt^Δ88 is a suppressor of phenotype of Jra^Asp.hs.sev

(Treier et al., 1995)

NOT Suppressor of

Statement

Reference

pnt^Δ88 is a non-suppressor of wing vein | ectopic phenotype of AdamTS-B^KK108644, Scer\GAL4^Act5C.PU

(Butchar et al., 2012)

pnt[+]/pnt^Δ88 is a non-suppressor of ommatidium phenotype of Scer\GAL4^hs.2sev, nmo^UAS.cUa

(Mirkovic et al., 2011)

pnt[+]/pnt^Δ88 is a non-suppressor of wing margin phenotype of Bx¹

(Bejarano et al., 2008)

pnt^Δ88 is a non-suppressor of larval neuron phenotype of Scer\GAL4^sca-T3, gcm^UAS.cHa

(Yuasa et al., 2003)

pnt^Δ88 is a non-suppressor of ommatidium phenotype of Rac1^V12.hs.sev

(Fanto et al., 2000)

Other

Statement

Reference

Scer\GAL4^tin.cBa, mid^UAS.cRa, pnt^Δ88 has embryonic cardioblast phenotype

(Schwarz et al., 2018)

Scer\GAL4^Tub.PU, cic^KK100838, pnt^Δ88 has adult midgut | somatic clone phenotype

(Jin et al., 2015)

Scer\GAL4^Tub.PU, cic^KK100838, pnt^Δ88 has intestinal stem cell | somatic clone | adult stage phenotype

(Jin et al., 2015)

jing[+]/jing³, pnt^Δ88 has adult dorsal tracheal branch | embryonic stage phenotype

(Sonnenfeld et al., 2010)

jing[+]/jing³, pnt^Δ88 has embryonic/larval tracheal section | embryonic stage phenotype

(Sonnenfeld et al., 2010)

jing¹, pnt[+]/pnt^Δ88 has tracheal lateral trunk posterior branch primordium | embryonic stage 15 phenotype

(Sonnenfeld et al., 2010)

jing¹, pnt[+]/pnt^Δ88 has embryonic/larval ganglionic tracheal branch | embryonic stage 15 phenotype

(Sonnenfeld et al., 2010)

jing³, pnt[+]/pnt^Δ88 has tracheal lateral trunk posterior branch primordium | embryonic stage 15 phenotype

(Sonnenfeld et al., 2010)

jing³, pnt[+]/pnt^Δ88 has embryonic/larval ganglionic tracheal branch | embryonic stage 15 phenotype

(Sonnenfeld et al., 2010)

kni⁶, pnt^Δ88 has presumptive embryonic/larval tracheal system phenotype

(Myat et al., 2005)

kni[+]/kni⁶, pnt^Δ88 has presumptive embryonic/larval tracheal system phenotype

(Myat et al., 2005)

Df(2R)CX1, pnt^Δ88 has wing phenotype

(Nagaraj et al., 1999)

Additional Comments

Genetic Interactions

Statement

Reference

edl^k06602, pnt^Δ88 double mutant embryos show an increase in the number of cardioblasts, which is similar to what is observed in pnt^Δ88 single mutants and unlike the decrease observed in edl^k06602 single mutants.

The expression of mid^UAS.cRa under the control of Scer\GAL4^tin.cBa in a pnt^Δ88 mutant background converts many of the extra ostial cardioblasts into generic cardioblasts.

(Schwarz et al., 2018)

The growth of intestinal stem cell somatic MARCM clones expressing cic^KK100838 under the control of Scer\GAL4^tub.PU in the adult midgut is significantly impaired by combination with pnt^Δ88 in homozygous state.

(Jin et al., 2015)

The extra wing vein phenotype caused by expression of CG4096^KK108644 under the control of Scer\GAL4^Act5C.PU is not suppressed if the flies also carry pnt^Δ88.

(Butchar et al., 2012)

The penetrance of the tracheal lumen defect seen in Vhl¹/+ embryos is not modified by pnt^Δ88/+.

(Hsouna et al., 2010)

Bap170^hfl1/+ suppresses the loss of photoreceptor cells seen in pnt^Δ88/pnt¹²⁷⁷ flies.

Expression of Bap170^C1.Scer\UAS under the control of Scer\GAL4^elav.PU enhances the rough eye phenotype and loss of photoreceptor cells seen in pnt^Δ88/pnt¹²⁷⁷ flies.

(Rendina et al., 2010)

In contrast to single heterozygous pnt^Δ88 or jing¹ mutants, double heterozygous embryos show tracheal ganglionic branch defects.

In contrast to single heterozygous pnt^Δ88 or jing³ mutants, double heterozygous embryos show tracheal ganglionic branch defects.

jing³/pnt^Δ88 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 vvl^dfr-E82.

Dorsal branches are absent, truncated or broken in jing³/pnt^Δ88 double heterozygotes.

(Sonnenfeld et al., 2010)

ed^1X5 dominantly enhances the phenotype of mis-rotation of ommatidia that is seen in pnt^Δ88/pnt¹²⁷⁷ animals.

fred^H24 dominantly suppresses the phenotype of mis-rotation of ommatidia that is seen in pnt^Δ88/pnt¹²⁷⁷ animals.

(Fetting et al., 2009)

Expression of Egfr::tor^act.Scer\UAS under the control of Scer\GAL4^αTub84B.PL does not rescue the lack of arcs and rosettes in the morphogenetic furrow of eye discs with pnt^Δ88 Minute clones.

(Brown et al., 2006)

The rough eye phenotype of flies expressing Gug^Scer\UAS.cCa under the control of Scer\GAL4^GMR.PF is enhanced in both a pnt¹²⁷⁷/pnt^Δ88 and a pnt¹²⁷⁷/pnt⁰⁷⁸²⁵ background.

(Charroux et al., 2006)

kni⁶/+, pnt^Δ88/+ embryos form rudimentary tracheal branches.

(Myat et al., 2005)

The rough eye phenotype caused by expression of edl^Scer\UAS.cYa under the control of Scer\GAL4^hs.2sev is enhanced by pnt^Δ88/+.

(Yamada et al., 2003)

Ras85D^V12.Scer\UAS; Scer\GAL4^GMR.PF increases the number of cells in G2 arrest posterior the furrow in pnt^Δ88 mutant clones to 100%. This effect is also seen with Ras85D^{V12.S35.Scer\UAS}, but not with Ras85D^{V12.G37.Scer\UAS} or Ras85D^{V12.C40.Scer\UAS}. Within pnt^Δ88 mutant clones in the eye disc in a BacA\p35^GMR.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.

(Yang and Baker, 2003)

pnt^Δ88 has no detectable effects on the neuronal defects seen in embryos expressing gcm^Scer\UAS.cHa under the control of Scer\GAL4^sca-T3.

(Yuasa et al., 2003)

Expression of stg^Scer\UAS.cNa (under the control of Scer\GAL4^αTub84B.PL) in pnt^Δ88 clones in the eye disc completely rescues the second mitotic wave.

(Baonza et al., 2002)

Weakly enhances the eye phenotype produced by activated arm constructs. (either arm^S44Y.GMR or arm^S56F.GMR).

(Freeman and Bienz, 2001)

Expression of csw::Src64B^{src90.Scer\UAS} under the control of Scer\GAL4^twi.PG does not affect the loss of VA2 muscle precursor cells seen in pnt^Δ88 embryos (82% of hemisegments have VA2 cells).

(Johnson Hamlet and Perkins, 2001)

The csw^lf/Y rough eye phenotype is dominantly enhanced by pnt^Δ88. The csw^lf/Y wing vein gap phenotype is not enhanced by pnt^Δ88.

(Firth et al., 2000)

S^104E Df(2R)CX1 double heterozygotes show notching of the wing margin.

(Nagaraj et al., 1999)

The width of the CNS is closer to wild-type if pnt^Δ88 embryos are also mutant for Df(3L)H99, although commissure separation remains incomplete.

(Dong and Jacobs, 1997)

Dominantly suppresses the extra outer photoreceptor cell phenotype seen in faf^BX4 homozygotes.

(Isaksson et al., 1997)

pnt^Δ88/pnt^T6 phenotype is dominantly enhanced by pros^JO1, leading to roughening of the external eye.

(Kauffmann et al., 1996)

pnt^Δ88/pnt¹²⁷⁷ completely suppresses the ectopic R7 rough eye phenotype of Jra^Asp.hs.sev.

(Treier et al., 1995)

Xenogenetic Interactions

Statement

Reference

The pnt^Δ88 midline glia phenotype is partially rescued when Ggal\ets1^Scer\UAS.cAa, ALV\v-ets^Scer\UAS.cAa or Ggal\ets2^Scer\UAS.cAa is expressed using Scer\GAL4^sli.PS. The eye phenotype of pnt^Δ88/pnt¹²⁷⁷ flies is partially rescued when Ggal\ets2^Scer\UAS.cAa or ALV\v-ets^Scer\UAS.cAa is expressed using Scer\GAL4^hs.2sev.

(Albagli et al., 1996)

Complementation and Rescue Data

Fails to complement

pnt¹³¹³

(Ghabrial et al., 2011)

pnt¹⁹⁸

(Ghabrial et al., 2011)

pnt⁷³⁷

(Myat et al., 2005)

Rescued by

pnt^Δ88/pnt² is rescued by pnt^GFP.FPTB

(Boisclair Lachance et al., 2014)

pnt^Δ88/Df(3R)Exel9012 is rescued by pnt^GFP.FPTB

(Boisclair Lachance et al., 2014)

pnt^Δ88 is rescued by Scer\GAL4^sli.PS/pnt^P1.UAS

(Scholz et al., 1997)

pnt^Δ88 is rescued by pnt^P2.UAS/Scer\GAL4^sli.PS

(Scholz et al., 1997)

pnt^Δ88 is rescued by Scer\GAL4^sli.PS/pnt^P1.UAS

(Scholz et al., 1997)

pnt^Δ88 is rescued by pnt^P2.UAS/Scer\GAL4^sli.PS

(Scholz et al., 1997)

Partially rescued by

pnt¹²⁷⁷/pnt^Δ88 is partially rescued by Scer\GAL4^hs.2sev/pnt^P1.UAS

(Albagli et al., 1996)

Not rescued by

pnt^Δ88 is not rescued by pnt^T151A.UAS/Scer\GAL4^sli.PS

(Scholz et al., 1997)

pnt^Δ88 is not rescued by pnt^T151A.UAS/Scer\GAL4^sli.PS

(Scholz et al., 1997)

Comments

Scer\GAL4^sli.PS-mediated expression of pnt^P2.Scer\UAS or pnt^P1.Scer\UAS rescues the fused commissure phenotype. Expression of pnt^{T151A.Scer\UAS} fails to rescue the phenotype.

(Scholz et al., 1997)

Scer\GAL4^sli.PS-mediated expression of pnt^P2.Scer\UAS or pnt^P1.Scer\UAS rescues the pnt^Δ88 fused commissure phenotype. Expression of pnt^{T151A.Scer\UAS} fails to rescue the pnt^Δ88 fused commissure phenotype.

(Scholz et al., 1997)

The eye phenotype of pnt^Δ88/pnt¹²⁷⁷ flies is partially rescued when pnt^P1.Scer\UAS is expressed using Scer\GAL4^hs.2sev at 17^oC.

(Albagli et al., 1996)

The R7 precursor can be rescued by pnt P2 transcript expressed by sev enhancers but the mutant phenotype is enhanced by pnt^{T151A.Scer\UAS} expressed by sev enhancers.

(Brunner et al., 1994)

Images (0)

Mutant

Wild-type

Stocks (2)

861

106100

Notes on Origin

Discoverer

Comments

Analysis of excess cardioblast phenotype provides an allelic series:pnt^S012309, pnt² > pnt^RR112, pnt^rM254 > pnt^Δ88, pnt⁰⁷⁸²⁵.

(Alvarez et al., 2003)

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

(Begemann et al., 1995)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (8)

Reported As

Symbol Synonym

Pnt^Δ88

(Mora et al., 2013)

pnt⁸⁸

(Baker et al., 2009, Brown and Freeman, 2003)

pnt^AE88

(Albagli et al., 1996)

pnt^D88

(Ghabrial et al., 2011, Salzer et al., 2010, Mirkovic and Mlodzik, 2006, Fanto, 2000, Fanto et al., 2000)

pnt^delta88

(Chen et al., 2005, Rogers et al., 2005, Yagi and Hayashi, 1997)

pnt^Δ88

(Bollepogu Raja et al., 2024, Wang et al., 2024, Ito and Igaki, 2021, Mendoza-Garcia et al., 2021, Wolfstetter et al., 2020, Wu et al., 2020, Chai et al., 2019, Zhou et al., 2019, Boisclair Lachance et al., 2018, Duncan et al., 2018, Newcomb et al., 2018, Schwarz et al., 2018, Davis and Rebay, 2017, Wang et al., 2017, Sato et al., 2016, Xie et al., 2016, Jin et al., 2015, Boisclair Lachance et al., 2014, Tchankouo-Nguetcheu et al., 2014, Caviglia and Luschnig, 2013, Shwartz et al., 2013, Sieglitz et al., 2013, Avet-Rochex et al., 2012, Butchar et al., 2012, Mou et al., 2012, Robertson et al., 2012, Technau et al., 2012, Araújo and Casanova, 2011, Hwang and Rulifson, 2011, Mirkovic et al., 2011, Moses et al., 2011, Hsouna et al., 2010, Jiang et al., 2010, Rendina et al., 2010, Sonnenfeld et al., 2010, Baltzer et al., 2009, Fetting et al., 2009, Franzdóttir et al., 2009, Lachance et al., 2009, Zartman et al., 2009, Bejarano et al., 2008, Weber et al., 2008, de Navascués and Modolell, 2007, Letizia et al., 2007, Maeda et al., 2007, Brown et al., 2006, Cela and Llimargas, 2006, Charroux et al., 2006, Ghabrial and Krasnow, 2006, Liu et al., 2006, Oishi et al., 2006, Sellin et al., 2006, Cabernard and Affolter, 2005, Firth and Baker, 2005, Meignin et al., 2004)

pointed⁸⁸

(Pielage et al., 2004)

Δ88

(Weber et al., 2012)

Name Synonyms

Secondary FlyBase IDs

References (120)

Report Sections

Open Close