FlyBase Allele Report: Dmel\pins[P62]

General Information

Symbol

Dmel\pins^P62

Species

D. melanogaster

Name

FlyBase ID

FBal0104445

Feature type

allele

Associated gene

Dmel\pins

Associated Insertion(s)

Carried in Construct

Also Known As

pins⁶²

Key Links

Allele class

amorphic allele - genetic evidence

loss of function allele

Mutagen

Delta2-3 transposase

Nature of the Allele

Allele class

amorphic allele - genetic evidence

(Le Borgne and Schweisguth, 2003)

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

The deletion extends from -898 to +1210 from the translation start site.

(Le Borgne and Schweisguth, 2003)

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^P89

(Caussinus and Gonzalez, 2005)

model of cancer

CEA with pins^P89

(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

aster

(Bonaccorsi et al., 2007)

centrosome (with pins^P89)

(Rebollo et al., 2007)

embryonic neuroblast

(Yoshiura et al., 2012)

embryonic neuroblast & spindle

(Yu et al., 2000)

larval brain & neuroblast

(Lee et al., 2006)

larval neuroblast

(Bonaccorsi et al., 2007)

larval RP2 motor neuron

(Yu et al., 2000)

larval RP2 motor neuron | ectopic

(Yu et al., 2000)

mitotic cell cycle & spindle

(Yu et al., 2000)

mitotic domain 9 & epithelial cell

(Izumi et al., 2004)

mitotic domain 9 & spindle

(Yu et al., 2000)

RP2sib neuron

(Yu et al., 2000)

sensory mother cell | P-stage

(Ségalen et al., 2010)

spindle

(Smith and Prehoda, 2011, Izumi et al., 2004)

spindle & external sensory organ precursor cell I

(David et al., 2005)

spindle & larval neuroblast

(Bonaccorsi et al., 2007)

spindle | P-stage

(Ségalen et al., 2010)

Detailed Description

Statement

Reference

pins^P62 mutant embryos do not exhibit significant defects in axon guidance.

(Cate et al., 2016)

Centrosome asymmetry during cytokinesis in mutant pI (sensory organ precursor) cells in the notum is identical to that seen in wild-type pI cells.

(Jauffred et al., 2013)

Mutant embryos show defects in the orientation of neuroblast cell polarity, with the crescent of the Par-complex being variably oriented. The orientation of the spindle with the orientation of cell polarity is defective in the mutant neuroblasts.

(Yoshiura et al., 2012)

raps^P62 mutant larval brain cells exhibit misaligned spindles.

(Smith and Prehoda, 2011)

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)

In pins^P62/pins^P62 pupal sensory mother cells, mitotic spindle orientation is not parallel to the plane of the epithelium.

(Ségalen et al., 2010)

Most neuroblast prometaphases and metaphases show normal asters in raps^P62 larval brains, but most ana-telophases are characterised by an abnormally small apical aster. The density of the spindle microtubules in the mutant neuroblasts is comparable to that of wild type. The spindles of mutant ganglion mother cells are indistinguishable from wild type.

The average length of neuroblast spindles is shorter in homozygous larval brains compared to wild type. The average length of ganglion mother cell spindles in homozygous larval brains is similar to that of wild type.

Homozygous larval brain neuroblasts divide more symmetrically than wild-type neuroblasts.

Only 39% of homozygous larval brain neuroblasts have centrosomes of different sizes at their poles (compared to 88% of wild-type neuroblasts).

(Bonaccorsi et al., 2007)

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)

Mutants show a decreased number of brain neuroblasts at 96 hours after larval hatching (ALH) compared to controls. This is not due to a subset of neuroblasts remaining quiescent, because from 24 to 96 hours ALH the neuroblast numbers peak and then decline over time, and it is not due to neuroblast cell death. 72.8% of mutant neuroblast clones in the larval brain contain no neuroblasts, and the remainder have a single neuroblast (control clones contain a single neuroblast).

(Lee et al., 2006)

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)

In raps^P62 mutant pI sensory organ precursor cells, the spindle appears more tilted along the apico-basal axis than normal, although it is correctly oriented along the anterior-posterior axis in these cells. In raps^P62 epithelial cells, division takes place in the plane of the epithelium, as occurs in wild type.

(David et al., 2005)

raps^P62 mutant mitotic domain 9 epithelial cells divide not only perpendicular to the surface (as occurs in wild type) but also parallel or at an oblique angle to the surface.

(Izumi et al., 2004)

Embryos lacking both maternal and zygotic raps^P62 are antigen minus and are phenotypically indistinguishable from germline clones derived from alleles raps^P120 and raps^P17.

(Cai 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

Enhanced by

Statement

Reference

pins^P62 has abnormal cell polarity phenotype, enhanceable by Sgt1^s2383

(Andersen et al., 2012)

Enhancer of

Statement

Reference

pins^P62 is an enhancer of abnormal cell polarity phenotype of Sgt1^s2383

(Andersen et al., 2012)

NOT Enhancer of

Statement

Reference

pins^P62 is a non-enhancer of abnormal neuroanatomy | embryonic stage phenotype of mud³

(Cate et al., 2016)

pins^P62 is a non-enhancer of abnormal neuroanatomy | embryonic stage phenotype of fra⁹⁵⁷

(Cate et al., 2016)

Phenotype Manifest In

Enhanced by

Statement

Reference

pins^P62 has neuroblast phenotype, enhanceable by insc²²

(Cai et al., 2003)

Suppressed by

Statement

Reference

pins^P62 has neuroblast phenotype, suppressible by Sgt1^s2383

(Andersen et al., 2012)

NOT Enhancer of

Statement

Reference

pins^P62 is a non-enhancer of larval ventral nerve cord | embryonic stage phenotype of mud³

(Cate et al., 2016)

pins^P62 is a non-enhancer of larval ventral nerve cord commissure | embryonic stage phenotype of mud³

(Cate et al., 2016)

pins^P62 is a non-enhancer of larval ventral nerve cord | embryonic stage phenotype of fra⁹⁵⁷

(Cate et al., 2016)

pins^P62 is a non-enhancer of larval ventral nerve cord commissure | embryonic stage phenotype of fra⁹⁵⁷

(Cate et al., 2016)

Suppressor of

Statement

Reference

pins^P62 is a suppressor of neuroblast phenotype of Sgt1^s2383

(Andersen et al., 2012)

Other

Statement

Reference

Sgt1^s2383, pins^P62 has neuroblast | increased number phenotype

(Andersen et al., 2012)

insc²², pins^P62 has neuroblast phenotype

(Cai et al., 2003)

Df(2L)TE35BC-3, pins^P62 has neuroblast phenotype

(Cai et al., 2003)

Additional Comments

Genetic Interactions

Statement

Reference

pins^P62 does not enhance the midline crossing defects of mud³ mutant embryos.

pins^P62 does not modify the ventral nerve cord phenotype of fra⁹⁵⁷ mutant embryos.

(Cate et al., 2016)

Sgt1^s2383 raps^P62 double mutant neuroblasts establish little or no apical or basal cortical polarity. The developmental consequences of this loss of polarity are the formation of ectopic neuroblasts throughout the brain. This is in striking contrast to either single mutant, where the brains are smaller with reduced neuroblast numbers.

(Andersen et al., 2012)

The spindles of both neuroblasts and ganglion mother cells are much more defective in lkb1³¹⁵ raps^P62 double mutant brains compared to those of either single mutant. In addition to cells with severely defective spindles, approximately 50% of mitotic figures have barely recognisable spindles. In double mutant metaphases, the microtubule density is extremely low, the spindle poles have a characteristic pointed appearance and the asters are completely absent. Double mutant ana-telophases are also completely devoid of asters and have few and sparse central spindle microtubules, which are never pinched in the middle. The double mutant neuroblast spindles are smaller than in wild type. 90% of the large metaphase figures (likely to be neuroblasts) have equally sized centrosomes in the double mutants.

(Bonaccorsi et al., 2007)

The brains of l(2)gl³³⁴ raps^P62 double mutant larvae contain large numbers of ectopic, proliferating, self-renewing neuroblasts.

(Lee et al., 2006)

In Df(2L)TE35BC-3; raps^P62 mutant embryos, all neuroblasts divide symmetrically and produce two equal-sized daughter cells (100%, n = 85). The cleavage furrow is equidistant from the two centrosomes (R = long arm/short arm = 1.04 plus or minus 0.07, n = 30), indicating that the telophase mitotic spindle is symmetric; moreover, both centrosomes lie in close proximity of the cortex and the spindle is not displaced to one side of the neuroblast. In insc²², raps^P62 double mutant embryos, all neuroblasts (100%, n = 98) give rise to equal-sized daughters (R = 1.02 plus or minus 0.08, n = 30). These equal size divisions are characterized by a symmetric undisplaced mitotic spindle.

(Cai et al., 2003)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

pins^P62 is rescued by Scer\GAL4^wor.PA/pins^UAS.cYa

(Smith and Prehoda, 2011)

pins^P62 is rescued by pins^UAS.cYa/Scer\GAL4^sca-P309

(Yu et al., 2000)

Partially rescued by

pins^P62 is partially rescued by pins^{ΔGL1,2.UAS.Tag:HA}/Scer\GAL4^wor.PA

(Smith and Prehoda, 2011)

Comments

Expression of raps^Scer\UAS.cYa via the neuroblast-specific Scer\GAL4^wor.PA driver rescues the mitotic spindle orientation defect in raps^P62 mutants cells.

Expression of raps^{ΔGL1,2.Scer\UAS.T:Ivir\HA1} via the neuroblast-specific Scer\GAL4^wor.PA driver partially rescues the mitotic spindle orientation defect in raps^P62 mutants cells.

(Smith and Prehoda, 2011)

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (7)

Reported As

Symbol Synonym

Pins^P62

(Wang et al., 2005)

pins⁶²

(Khan and Rusan, 2025, Bosveld et al., 2016, Wang et al., 2011, Ségalen et al., 2010, Lee et al., 2006, David et al., 2005, Langevin et al., 2005, Yu et al., 2005, Yu et al., 2003)

pins^P62

(Pham et al., 2019, Tsankova et al., 2017, Cate et al., 2016, Jauffred et al., 2013, Smith and Prehoda, 2011, Janic et al., 2010, Januschke and Gonzalez, 2010, Bonaccorsi et al., 2007, Rebollo et al., 2007, Izumi et al., 2004, Yu et al., 2000)

pins^p62

(Finegan et al., 2025, Neville et al., 2023, Chanet et al., 2017, Bergstralh et al., 2016, Bell et al., 2015, Januschke et al., 2013, Andersen et al., 2012, Yoshiura et al., 2012)

raps⁶²

(Cai et al., 2003)

raps^P62

(Caussinus and Gonzalez, 2005)

raps^Δ62

(Le Borgne and Schweisguth, 2003)

Name Synonyms

Secondary FlyBase IDs

References (32)

Report Sections

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