FlyBase Allele Report: Dmel\pins[P89]

General Information

Symbol

Dmel\pins^P89

Species

D. melanogaster

Name

FlyBase ID

FBal0104444

Feature type

allele

Associated gene

Dmel\pins

Associated Insertion(s)

Carried in Construct

Also Known As

pins⁸⁹

Key Links

Allele class

loss of function allele

Mutagen

Delta2-3 transposase

Nature of the Allele

Allele class

loss of function allele

(Cai et al., 2003)

Mutagen

Delta2-3 transposase

(Yu et al., 2000)

Progenitor genotype

P{EP}EP3559

(Yu et al., 2000)

Cytology

Description

Excision of the P{EP} element resulting in a deletion which removes part of the raps coding region.

(Yu et al., 2000)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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 ( 1 )

Disease

Evidence

References

model of brain cancer

CEA with pins^P62

(Caussinus and Gonzalez, 2005)

model of cancer

CEA with pins^P62

(Janic et al., 2010)

Modifiers Based on Experimental Evidence ( 0 )

Disease

Interaction

References

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

centrosome (with pins^P62)

(Rebollo et al., 2007)

embryonic neuroblast & spindle

(Yu et al., 2000)

ganglion mother cell GMC4-2a

(Yu et al., 2003)

intermediate neuronal progenitor | third instar larval stage

(Zhang et al., 2016)

larval RP2 motor neuron

(Yu et al., 2000)

larval RP2 motor neuron | ectopic

(Yu et al., 2003, Yu et al., 2000)

mitotic cell cycle & spindle

(Yu et al., 2000)

mitotic domain 9 & spindle

(Yu et al., 2003, Yu et al., 2000)

neuroblast

(Cai et al., 2003)

neuroblast | third instar larval stage

(Zhang et al., 2016)

RP2sib neuron

(Yu et al., 2003, Yu et al., 2000)

Detailed Description

Statement

Reference

pins^P89 third instar larvae show a decrease in the number of brain neuroblasts compared to wild-type. They also display defects in asymmetric protein segregation in neuroblasts and intermediate neural progenitors (secondary neuroblasts) in metaphase although both the neuroblasts and secondary neuroblasts divide symmetrically in the end with correctly segregated mira protein (presumably due to 'telophase rescue').

(Zhang et al., 2016)

raps^P62/raps^P89 mutant neuroblasts exhibit rotation of approximately 100[o] between the first and second mitoses and a further 80[o] between the second and third. Thus, altogether, the division axis of this cell rotated ~180[o] over the course of three consecutive divisions.

(Januschke and Gonzalez, 2010)

The first stages of centrosome movement in raps^P89/raps^P62/ larval neuroblasts occur as in wild type; a highly correlated behaviour is seen, as the centrosomes move in parallel toward the cortex, where they remain until one of them starts moving around the cell. However, when this movement of one centrosome starts to occur, the mutant neuroblasts show a clear difference from wild type; in the mutant neuroblasts, although migration of the centrosome is first restricted to one side of the cell, later on migration takes place throughout the entire cell, such that the trajectories of both centrosomes become fully intermingled. At this stage in the mutant neuroblasts, the cortical aster is disassembled.

(Rebollo et al., 2007)

The transplantation of raps^P89/raps^P62 larval neuroblast clones into the abdomen of adult hosts causes tumor growth, with clones growing to 100 times their original size thereby severely damaging and displacing the host's organs. Although genome stability is not grossly affected shortly after transplantation, 40-day-old tumors show karyotype defects such as segmental aneuploidy. Additionally, 15-20% of cells within the tumors have supernumerary centrosomes and these cells tend to be hyperploid.

(Caussinus and Gonzalez, 2005)

Embryos lacking both maternal and zygotic raps^P89 are antigen minus and are phenotypically indistinguishable from germline clones derived from alleles raps^P120 and raps^P17. The great majority of raps^P89 mutant neuroblasts undergo unequal divisions; however, 15% (n = 120) divide with symmetric mitotic spindles and generate equal-sized daughter cells.

(Cai et al., 2003)

Mitotic spindle in the neuroblast cells of mitotic domain 9 raps^P89 mutant embryos fail to reorient by 90⁰. In raps^P89 mutant embryos, markers of the basal cortical crescent are mislocalized either as randomly-placed cortical crescents or are localized throughout the cell cortex. raps^P89 mutant embryos show defects in the resolution of alternative sibling cell fate. For example, in the GMC4-2a>RP2/RP2 sib sublineage, RP2sib adopts the fate of its sibling, resulting in duplication of the eve positive RP2 neurons in 60% of the hemisegments. Moreover, a small proportion of GMC4-2a cells are mis-specified, resulting in the loss of eve-expressing RP2 neurons in 15% of hemisegments.

(Yu et al., 2003)

No neuronal fate changes are evident in homozygous embryos. Spindle orientation in neuroblasts and mitotic domain 9 cells is normal. Mutant embryos derived from homozygous or raps^P62/raps^P89 females (lacking maternal and zygotic raps function) have defective mitotic spindle orientation. In cells of mitotic domain 9, the 90^o reorientation which normally occurs in wild-type embryos (which results in the orientation of the spindle along the apical/basal axis) fails to occur. Mitotic spindles of neuroblasts in the segmented central nervous system also often fail to adopt an apical/basal orientation. In approximately 60% of hemisegments, duplicated RP2 neurons are found at the expense of the RP2sib neuron. These two RP2 neurons appear to have indistinguishable nuclear size. In approximately 15% of hemisegments no eve-expressing RP2/RP2sib neurons are produced due to a failure to correctly specify the GMC progenitor of these neurons.

(Yu et al., 2000)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

Pfdn2^Δ10, pins^P89 has abnormal neuroanatomy | third instar larval stage phenotype, suppressible | partially by pins^UAS.cYa/Scer\GAL4^erm.PU

(Zhang et al., 2016)

Pfdn2^Δ10, pins^P89 has increased cell number | third instar larval stage phenotype, suppressible | partially by pins^UAS.cYa/Scer\GAL4^erm.PU

(Zhang et al., 2016)

Pfdn2^Δ10, pins^P89 has abnormal neuroanatomy | third instar larval stage phenotype, suppressible | partially by αTub84B^{Ubi-p63E.GFP(S65C)}

(Zhang et al., 2016)

Pfdn2^Δ10, pins^P89 has increased cell number | third instar larval stage phenotype, suppressible | partially by αTub84B^{Ubi-p63E.GFP(S65C)}

(Zhang et al., 2016)

pins^P89 has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by Pfdn2^Δ10

(Zhang et al., 2016)

pins^P89 has decreased cell number | third instar larval stage phenotype, suppressible by Pfdn2^Δ10

(Zhang et al., 2016)

pins^P89 has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by mgr^G5308

(Zhang et al., 2016)

pins^P89 has decreased cell number | third instar larval stage phenotype, suppressible by mgr^G5308

(Zhang et al., 2016)

pins^P89 has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by Scer\GAL4^insc-Mz1407/αTub67C^GD13885

(Zhang et al., 2016)

pins^P89 has decreased cell number | third instar larval stage phenotype, suppressible by Scer\GAL4^insc-Mz1407/αTub67C^GD13885

(Zhang et al., 2016)

pins^P89 has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by Scer\GAL4^insc-Mz1407/αTub84B^GD17779

(Zhang et al., 2016)

pins^P89 has decreased cell number | third instar larval stage phenotype, suppressible by Scer\GAL4^insc-Mz1407/αTub84B^GD17779

(Zhang et al., 2016)

pins^P89 has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by Scer\GAL4^insc-Mz1407/βTub60D^KK112384

(Zhang et al., 2016)

pins^P89 has decreased cell number | third instar larval stage phenotype, suppressible by Scer\GAL4^insc-Mz1407/βTub60D^KK112384

(Zhang et al., 2016)

pins^P89 has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by Scer\GAL4^insc-Mz1407/βTub56D^GD14171

(Zhang et al., 2016)

pins^P89 has decreased cell number | third instar larval stage phenotype, suppressible by Scer\GAL4^insc-Mz1407/βTub56D^GD14171

(Zhang et al., 2016)

pins^P89 has abnormal mitotic cell cycle | embryonic stage phenotype, suppressible by Mmus\Gpsm2^{hs.2xTag:FLAG}

(Yu et al., 2003)

pins^P89 has abnormal neuroanatomy | embryonic stage phenotype, suppressible by Mmus\Gpsm2^{hs.2xTag:FLAG}

(Yu et al., 2003)

NOT suppressed by

Statement

Reference

pins^P89 has abnormal neuroanatomy | embryonic stage phenotype, non-suppressible by Mmus\Gpsm2^{1-369.hs.2xTag:FLAG}

(Yu et al., 2003)

pins^P89 has abnormal neuroanatomy | embryonic stage phenotype, non-suppressible by Mmus\Gpsm2^{366-672.hs.2xTag:FLAG}

(Yu et al., 2003)

Enhancer of

Statement

Reference

pins^P89 is an enhancer of abnormal neuroanatomy | third instar larval stage phenotype of Pfdn2^Δ10

(Zhang et al., 2016)

pins^P89 is an enhancer of increased cell number | third instar larval stage phenotype of Pfdn2^Δ10

(Zhang et al., 2016)

pins^P89 is an enhancer of abnormal neuroanatomy | third instar larval stage phenotype of αTub84B^GD17779, Scer\GAL4^insc-Mz1407

(Zhang et al., 2016)

pins^P89 is an enhancer of increased cell number | third instar larval stage phenotype of αTub84B^GD17779, Scer\GAL4^insc-Mz1407

(Zhang et al., 2016)

pins^P89 is an enhancer of abnormal neuroanatomy | third instar larval stage phenotype of βTub60D^KK112384, Scer\GAL4^insc-Mz1407

(Zhang et al., 2016)

pins^P89 is an enhancer of increased cell number | third instar larval stage phenotype of βTub60D^KK112384, Scer\GAL4^insc-Mz1407

(Zhang et al., 2016)

pins^P89 is an enhancer of abnormal neuroanatomy | third instar larval stage phenotype of βTub56D^GD14171, Scer\GAL4^insc-Mz1407

(Zhang et al., 2016)

pins^P89 is an enhancer of increased cell number | third instar larval stage phenotype of βTub56D^GD14171, Scer\GAL4^insc-Mz1407

(Zhang et al., 2016)

pins^P89 is an enhancer of abnormal neuroanatomy | third instar larval stage phenotype of mgr^G5308

(Zhang et al., 2016)

pins^P89 is an enhancer of increased cell number | third instar larval stage phenotype of mgr^G5308

(Zhang et al., 2016)

pins^P89 is an enhancer of abnormal neuroanatomy | third instar larval stage phenotype of αTub67C^GD13885, Scer\GAL4^insc-Mz1407

(Zhang et al., 2016)

pins^P89 is an enhancer of increased cell number | third instar larval stage phenotype of αTub67C^GD13885, Scer\GAL4^insc-Mz1407

(Zhang et al., 2016)

Suppressor of

Statement

Reference

pins^P89 is a suppressor | maternal effect | partially of abnormal cell polarity phenotype of Gαi^UAS.cCa, Scer\GAL4^sca-P309

(Cai et al., 2003)

raps[+]/pins^P89 is a suppressor | partially of abnormal cell polarity phenotype of Gαi^UAS.cCa, Scer\GAL4^sca-P309

(Cai et al., 2003)

Other

Statement

Reference

αTub84B^GD17779, Scer\GAL4^erm.PU, pins^P89 has abnormal neuroanatomy | third instar larval stage phenotype

(Zhang et al., 2016)

αTub84B^GD17779, Scer\GAL4^erm.PU, pins^P89 has increased cell number | third instar larval stage phenotype

(Zhang et al., 2016)

βTub56D^GD14171, Scer\GAL4^erm.PU, pins^P89 has abnormal neuroanatomy | third instar larval stage phenotype

(Zhang et al., 2016)

βTub56D^GD14171, Scer\GAL4^erm.PU, pins^P89 has increased cell number | third instar larval stage phenotype

(Zhang et al., 2016)

Phenotype Manifest In

Suppressed by

Statement

Reference

Pfdn2^Δ10, pins^P89 has neuroblast | third instar larval stage phenotype, suppressible | partially by αTub84B^{Ubi-p63E.GFP(S65C)}

(Zhang et al., 2016)

pins^P89 has neuroblast | third instar larval stage phenotype, suppressible by Pfdn2^Δ10

(Zhang et al., 2016)

pins^P89 has neuroblast | third instar larval stage phenotype, suppressible by mgr^G5308

(Zhang et al., 2016)

pins^P89 has larval RP2 motor neuron | ectopic phenotype, suppressible by Mmus\Gpsm2^{hs.2xTag:FLAG}

(Yu et al., 2003)

pins^P89 has RP2sib neuron phenotype, suppressible by Mmus\Gpsm2^{hs.2xTag:FLAG}

(Yu et al., 2003)

NOT suppressed by

Statement

Reference

pins^P89 has larval RP2 motor neuron | ectopic phenotype, non-suppressible by Mmus\Gpsm2^{1-369.hs.2xTag:FLAG}

(Yu et al., 2003)

pins^P89 has larval RP2 motor neuron | ectopic phenotype, non-suppressible by Mmus\Gpsm2^{366-672.hs.2xTag:FLAG}

(Yu et al., 2003)

pins^P89 has RP2sib neuron phenotype, non-suppressible by Mmus\Gpsm2^{1-369.hs.2xTag:FLAG}

(Yu et al., 2003)

pins^P89 has RP2sib neuron phenotype, non-suppressible by Mmus\Gpsm2^{366-672.hs.2xTag:FLAG}

(Yu et al., 2003)

pins^P89 has mitotic domain 9 & spindle phenotype, non-suppressible by Mmus\Gpsm2^{1-369.hs.2xTag:FLAG}

(Yu et al., 2003)

pins^P89 has mitotic domain 9 & spindle phenotype, non-suppressible by Mmus\Gpsm2^{366-672.hs.2xTag:FLAG}

(Yu et al., 2003)

Enhancer of

Statement

Reference

pins^P89 is an enhancer of type I neuroblast | third instar larval stage | increased number phenotype of αTub67C^GD13885, Scer\GAL4^insc-Mz1407

(Zhang et al., 2016)

pins^P89 is an enhancer of type II neuroblast | third instar larval stage | increased number phenotype of αTub67C^GD13885, Scer\GAL4^insc-Mz1407

(Zhang et al., 2016)

pins^P89 is an enhancer of type I neuroblast | third instar larval stage | increased number phenotype of αTub84B^GD17779, Scer\GAL4^insc-Mz1407

(Zhang et al., 2016)

pins^P89 is an enhancer of type II neuroblast | third instar larval stage | increased number phenotype of αTub84B^GD17779, Scer\GAL4^insc-Mz1407

(Zhang et al., 2016)

pins^P89 is an enhancer of type I neuroblast | third instar larval stage | increased number phenotype of βTub60D^KK112384, Scer\GAL4^insc-Mz1407

(Zhang et al., 2016)

pins^P89 is an enhancer of type II neuroblast | third instar larval stage | increased number phenotype of βTub60D^KK112384, Scer\GAL4^insc-Mz1407

(Zhang et al., 2016)

pins^P89 is an enhancer of neuroblast | third instar larval stage phenotype of Pfdn2^Δ10

(Zhang et al., 2016)

pins^P89 is an enhancer of type I neuroblast | third instar larval stage | increased number phenotype of βTub56D^GD14171, Scer\GAL4^insc-Mz1407

(Zhang et al., 2016)

pins^P89 is an enhancer of type II neuroblast | third instar larval stage | increased number phenotype of βTub56D^GD14171, Scer\GAL4^insc-Mz1407

(Zhang et al., 2016)

pins^P89 is an enhancer of neuroblast | third instar larval stage | increased number phenotype of Pfdn2^Δ10

(Zhang et al., 2016)

pins^P89 is an enhancer of mitotic spindle | third instar larval stage phenotype of Pfdn2^Δ10

(Zhang et al., 2016)

pins^P89 is an enhancer of spindle microtubule | third instar larval stage phenotype of Pfdn2^Δ10

(Zhang et al., 2016)

Suppressor of

Statement

Reference

raps[+]/pins^P89 is a suppressor | partially of neuroblast phenotype of Gαi^UAS.cCa, Scer\GAL4^sca-P309

(Cai et al., 2003)

pins^P89 is a suppressor | maternal effect | partially of neuroblast phenotype of Gαi^UAS.cCa, Scer\GAL4^sca-P309

(Cai et al., 2003)

Other

Statement

Reference

Pfdn2^Δ10, pins^P89 has intermediate neuronal progenitor | third instar larval stage phenotype

(Zhang et al., 2016)

Pfdn2^GD13510, Scer\GAL4^erm.PU, pins^P89 has type II neuroblast | third instar larval stage phenotype

(Zhang et al., 2016)

βTub56D^GD14171, Scer\GAL4^erm.PU, pins^P89 has intermediate neuronal progenitor | third instar larval stage phenotype

(Zhang et al., 2016)

Pfdn2^GD13510, Scer\GAL4^erm.PU, pins^P89 has intermediate neuronal progenitor | third instar larval stage phenotype

(Zhang et al., 2016)

Scer\GAL4^erm.PU, mgr^GD12016, pins^P89 has type II neuroblast | third instar larval stage phenotype

(Zhang et al., 2016)

Scer\GAL4^erm.PU, mgr^GD12016, pins^P89 has intermediate neuronal progenitor | third instar larval stage phenotype

(Zhang et al., 2016)

αTub84B^GD17779, Scer\GAL4^erm.PU, pins^P89 has intermediate neuronal progenitor | third instar larval stage phenotype

(Zhang et al., 2016)

Additional Comments

Genetic Interactions

Statement

Reference

Expression of Pfdn2^GD13510 (together with UAS-Dicer2 to enhance RNAi efficiency) under the control of Scer\GAL4^erm.PU in pins^P89 mutant background leads to dedifferentiation of intermediate neural progenitors back into neuroblasts (ectopic type II neuroblasts are observed).

Expression of mgr^GD12016 (together with UAS-Dicer2 to enhance RNAi efficiency) under the control of Scer\GAL4^erm.PU in pins^P89 mutant background leads to dedifferentiation of intermediate neural progenitors back into neuroblasts (ectopic type II neuroblasts are observed).

The increased average number of brain neuroblasts (compared to wild-type) seen in Pfdn2^Δ10 mutant third instar larvae is strongly enhanced by combination with pins^P89 although pins^P89 mutants on their own display decreased number of brain neuroblasts compared to wild-type. The defects in asymmetric protein segregation and mitotic spindle structure in neuroblasts observed both in Pfdn2^Δ10 and pins^P89 single mutants are strongly enhanced in Pfdn2^Δ10;pins^P89 double mutants: all neuroblasts show impaired asymmetric protein segregation and divide symmetrically. Symmetric division is observed also in intermediate neural progenitor cells in the double mutants - a phenotype not detected in either of the single mutants.

The increased number of brain neuroblast as well as the asymmetric protein segregation defects (observed both during metaphase and telophase) characteristic for Pfdn2^Δ10;pins^P89 double mutants are partially rescued by expression of αTub84B^{Ubi-p63E.T:Avic\GFP-S65C} in the double mutant background.

The increased average number of brain neuroblasts (compared to wild-type) seen in mgr^G5308 homozygous third instar larvae is strongly enhanced by combination with pins^P89 although pins^P89 mutants on their own display decreased number of brain neuroblasts compared to wild-type.

The increased number of brain neuroblasts observed in third instar larvae expressing αTub67C^GD13885 under the control of Scer\GAL4^insc-Mz1407 is increased further by combination with pins^P89 (although the pins^P89 mutants on their own display significantly lower number of brain neuroblasts compared to controls) and leads to a dramatic neuroblast overgrowth as well as protein segregation defects in the neuroblasts (aPKC, mira) during metaphase and their mis-segregation in telophase.

The increased number of brain neuroblasts observed in third instar larvae expressing any of the following: αTub84B^GD17779, βTub60D^KK112384 or βTub56D^GD14171 under the control of Scer\GAL4^insc-Mz1407 is increased further by combination with pins^P89 (although the pins^P89 mutants on their own display significantly lower number of brain neuroblasts compared to controls) and leads to a dramatic neuroblast overgrowth.

Expression of either αTub84B^GD17779 or βTub56D^GD14171 under the control of Scer\GAL4^erm.PU in pins^P89 mutant background leads to severely increased number of neuroblast due to dedifferentiation of intermediate neural progenitors. The protein segregation defects observed in pins^P89 mutants during metaphase are enhanced by concomitant βTub56D^GD14171 expression and perdure to telophase leading to protein mis-segregation.

(Zhang et al., 2016)

High frequencies (100%, n = 50) of equal size neuroblast divisions are observed in baz^dsRNA.cCa; raps^P89 mutant embryos. In these equal size divisions both spindle asymmetry and spindle displacement fail to occur. High frequencies of equal size neuroblast divisions occur in raps^P89, aPKC^dsRNA.cCa (80%, n = 46) mutants. In these equal size divisions both spindle asymmetry and spindle displacement fail to occur. The cleavage furrow is equidistant to the centrosomes and both centrosomes lie close to the cortex. A low level of symmetric neuroblast divisions occur in embryos maternally and zygotically homozygous for raps^P89, expressing G-iα65A^Scer\UAS.cCa driven by Scer\GAL4^sca-P309. The number of asymmetric divisions is dramatically higher in otherwise genetically identical embryos, zygotically heterozygous for raps^P89. The frequency of equal size neuroblast division in G-iα65A^dsRNA.cCa embryos is slightly increased by homozygosity for raps^P89 (26%, n = 34).

(Cai et al., 2003)

When baz^dsRNA.cFa is added to raps^P89 mutants neuroblasts form a small symmetric spindle at metaphase, both halves similar to the basal half of the wild-type spindle.

(Fuse et al., 2003)

Xenogenetic Interactions

Statement

Reference

Ectopic expressed Mmus\Gpsm2^{hs.2xT:Zzzz\FLAG} is able to restore 90^o spindle rotation in raps^P89 embryonic neuroblast cells of mitotic domain 9. In contrast, neither Mmus\Gpsm2^{1-369.hs.2xT:Zzzz\FLAG} or Mmus\Gpsm2^{366-672.hs.2xT:Zzzz\FLAG} can restore this spindle rotation. The introduction of Mmus\Gpsm2^{hs.2xT:Zzzz\FLAG} into raps^P89 mutant embryos allows basal proteins to localize as in wild-type cells. Ectopic expression of Mmus\Gpsm2^{hs.2xT:Zzzz\FLAG} in raps^P89 mutant embryos recues defects in the resolution of alternative neuron sibling cell fate. For example, transformation of RP2 sib neurons to RP2 neurons is largely suppressed. Neither Mmus\Gpsm2^{1-369.hs.2xT:Zzzz\FLAG} or Mmus\Gpsm2^{366-672.hs.2xT:Zzzz\FLAG} are able to mediate this rescue.Ectopic expressed Mmus\Gpsm2^{hs.2xT:Zzzz\FLAG} is able to restore 90^o spindle rotation in raps^P89 embryonic neuroblast cells of mitotic domain 9. In contrast, neither Mmus\Gpsm2^{1-369.hs.2xT:Zzzz\FLAG} or Mmus\Gpsm2^{366-672.hs.2xT:Zzzz\FLAG} can restore this spindle rotation. The introduction of Mmus\Gpsm2^{hs.2xT:Zzzz\FLAG} into raps^P89 mutant embryos allows basal proteins to localize as in wild-type cells. Ectopic expression of Mmus\Gpsm2^{hs.2xT:Zzzz\FLAG} in raps^P89 mutant embryos recues defects in the resolution of alternative neuron sibling cell fate. For example, transformation of RP2 sib neurons to RP2 neurons is largely suppressed. Neither Mmus\Gpsm2^{1-369.hs.2xT:Zzzz\FLAG} or Mmus\Gpsm2^{366-672.hs.2xT:Zzzz\FLAG} are able to mediate this rescue.

(Yu et al., 2003)

Complementation and Rescue Data

Rescued by

pins^P89 is rescued by pins^UAS.Tag:FLAG/Scer\GAL4^sca.PU

(Yu et al., 2002)

pins^P89 is rescued by Scer\GAL4^sca.PU/pins^{Δ4.UAS.Tag:FLAG}

(Yu et al., 2002)

pins^P89 is rescued by pins^UAS.cYa/Scer\GAL4^sca-P309

(Yu et al., 2000)

Partially rescued by

pins^P89 is partially rescued by pins^UAS.cYa/Scer\GAL4^erm.PU

(Zhang et al., 2016)

Not rescued by

pins^P89 is not rescued by Scer\GAL4^sca.PU/pins^{Δ2.UAS.Tag:FLAG}

(Yu et al., 2002)

pins^P89 is not rescued by pins^{Δ5.UAS.Tag:FLAG}/Scer\GAL4^sca.PU

(Yu et al., 2002)

Comments

The dramatically increased total average number of brain neuroblast in third instar larvae characteristic for Pfdn2^Δ10;pins^P89 double mutants can be partially rescued by expression of pins^Scer\UAS.cYa under the control of Scer\GAL4^erm.PU in the double mutant background.

(Zhang et al., 2016)

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (5)

Reported As

Symbol Synonym

pins P89

(Fuse et al., 2003)

pins⁸⁹

(Wang et al., 2006, Cai et al., 2003, Yu et al., 2003, Yu et al., 2003)

pins^P89

(Pham et al., 2019, Roubinet et al., 2017, Tsankova et al., 2017, Roth et al., 2015, Janic et al., 2010, Januschke and Gonzalez, 2010, Rebollo et al., 2007, Yu et al., 2005, Yu et al., 2000)

pins^p89

(Zhang et al., 2016, Januschke et al., 2013, Yu et al., 2002)

raps^P89

(Caussinus and Gonzalez, 2005)

Name Synonyms

Secondary FlyBase IDs

References (18)

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