FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\pimIL
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General Information
Symbol
Dmel\pimIL
Species
D. melanogaster
Name
FlyBase ID
FBal0056312
Feature type
allele
Associated gene
Dmel\pim
Associated Insertion(s)
Carried in Construct
Also Known As
pim1, pimIL97
Key Links
Genomic Maps

Allele class

amorphic allele - genetic evidence

Mutagen
Nature of the Allele
Allele class

amorphic allele - genetic evidence

(Stratmann and Lehner, 1996)
Mutagen
ethyl methanesulfonate
(Tearle and Nusslein-Volhard, 1987)
Progenitor genotype
Cytology
Description

Nucleotide substitution: G550A. Causes a defective splice donor site in intron 2.

(Stratmann and Lehner, 1996)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
point_mutation
2L:10,363,526..10,363,526 [+]
Nucleotide change:

G10363526A

Reported nucleotide change:

G550A

Comment:

splice donor mutation

(Stratmann and Lehner, 1996)
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 ( 0 )
      Disease
      Evidence
      References
      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
      Detailed Description
      Statement
      Reference

      Embryos homozygous for pimIL initially develop normally (due to maternal contribution of pim protein). However, starting with mitosis 15 sister chromatids are not separated. these defects become apparent at the metaphase-to-anaphase transition. The dynamic reorganisation of the mitotic spindle that accompanies wild-type anaphase and telophase occurs in pimIL mutants. The time from anaphase onset until the end of mitosis in pimIL mutants is only 1.2 times higher than in wild-type embryos. After exit from mitosis 15, pimIL mutants progress through interphase 16 and enter mitosis 16 without apparent delays. However, mitosis 16 lasts on average 4 times longer than in wild-type, with bipolar spindles and normal metaphase plates. However, the majority of epidermal cells in thr1 mutants embryos have only two and not four centrosomes at the stage of mitosis 16.

      Mutant pimIL embryos exhibit an increase in apoptosis after mitosis 16 and epithelial disorganisation, displaying an abnormal pseudostratified appearance.

      (Pandey et al., 2005)

      In pimIL/pimIL embryos (from pimIL/+ mothers), sister chromatid separation during mitosis 15 is inhibited.

      (Leismann and Lehner, 2003)

      Lethality resulting from homozygosity of the pim1 chromosome is completely prevented by a pim+ transgene.

      (Leismann et al., 2000)

      Malpighian tubules arrest early in their morphogenesis in homozygous embryos. The tubules are much shorter than normal but are tube shaped. The tip cells are present. The tubules attain a length approximately 1/3 that of wild-type tubules and a width approximately the same as wild-type tubules. The nuclei are very large.

      (Jack and Myette, 1999)

      Chromatid segregation, but not chromatin decondensation is blocked in mitosis 15. Chromosome segregation is also blocked in mitosis 16. pimIL thr1 double mutants resemble pimIL or thrunspecified single mutants. thr1 pimIL double mutants and thr1 fzy3 pimIL triple mutants have a similar phenotype to fzyunspecified single mutants.

      (Philp and Glover, 1997)

      Chromosome distribution in mitosis is defective. Sister chromatid separation in the centromeric region fails.

      (Stratmann and Lehner, 1996)

      Malpighian tubule elongation is incomplete in homozygous embryos.

      (Harbecke and Lengyel, 1995)

      Polyploid nuclei due to failure to complete mitosis.

      (Smith et al., 1993)

      pimIL embryos have poorly differentiated cuticle with necrotic patches. The head is abnormal.

      (Tearle and Nusslein-Volhard, 1987)

      embryonic lethal Cuticle poorly differentiated with necrotic patches. Head abnormal. arrests in cycle 15

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

      pimIL has abnormal cytokinesis phenotype, non-enhanceable by pbl3

      (Pandey et al., 2005)

      pimIL has abnormal mitotic cell cycle phenotype, non-enhanceable by pbl3

      (Pandey et al., 2005)

      pimIL has abnormal cytokinesis phenotype, non-enhanceable by pbl5

      (Pandey et al., 2005)

      pimIL has abnormal mitotic cell cycle phenotype, non-enhanceable by pbl5

      (Pandey et al., 2005)
      Suppressed by
      Statement
      Reference

      pimIL has abnormal cytokinesis phenotype, suppressible by dupa1

      (Pandey et al., 2005)

      pimIL has abnormal mitotic cell cycle phenotype, suppressible by dupa1

      (Pandey et al., 2005)
      NOT Enhancer of
      Statement
      Reference

      pimIL is a non-enhancer of abnormal mitotic cell cycle phenotype of pbl3

      (Pandey et al., 2005)

      pimIL is a non-enhancer of abnormal mitotic cell cycle phenotype of pbl5

      (Pandey et al., 2005)
      Suppressor of
      Statement
      Reference

      pimIL/pim[+] is a suppressor of visible | dominant phenotype of gcmPyx

      (Popkova et al., 2012)

      pimIL/pim[+] is a suppressor of abnormal mitotic cell cycle | maternal effect | embryonic stage phenotype of CycB+t10

      (Ji et al., 2005)

      pimIL is a suppressor of abnormal mitotic cell cycle phenotype of dupa1

      (Pandey et al., 2005)

      pimIL is a suppressor of abnormal cytokinesis phenotype of dupa1

      (Pandey et al., 2005)
      Phenotype Manifest In
      NOT Enhanced by
      Statement
      Reference

      pimIL has centrosome phenotype, non-enhanceable by pbl3

      (Pandey et al., 2005)

      pimIL has centrosome phenotype, non-enhanceable by pbl5

      (Pandey et al., 2005)
      Suppressed by
      Statement
      Reference

      pimIL has metaphase plate phenotype, suppressible by dupa1

      (Pandey et al., 2005)
      NOT Enhancer of
      Statement
      Reference

      pimIL is a non-enhancer of centrosome phenotype of pbl3

      (Pandey et al., 2005)

      pimIL is a non-enhancer of centrosome phenotype of pbl5

      (Pandey et al., 2005)
      Suppressor of
      Statement
      Reference

      pimIL/pim[+] is a suppressor of chaeta | increased number phenotype of gcmPyx

      (Popkova et al., 2012)

      pimIL/pim[+] is a suppressor of embryo | maternal effect | embryonic cycle 10 phenotype of CycB+t10

      (Ji et al., 2005)

      pimIL/pim[+] is a suppressor of embryo | maternal effect | embryonic cycle 14 phenotype of CycB+t10

      (Ji et al., 2005)

      pimIL/pim[+] is a suppressor of microtubule | maternal effect | embryonic cycle 9 phenotype of CycB+t10

      (Ji et al., 2005)

      pimIL is a suppressor of metaphase plate phenotype of dupa1

      (Pandey et al., 2005)
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      The delay in onset of anaphase (measured during cycles 6-11) seen in embryos with two extra copies of the maternal CycB+ gene dose (derived from females carrying copies of CycB+t10) is suppressed by pimIL. Nuclear cortical migration is initiated at telophase of cycle 9 and ends about 1.5 minutes into early interphase of cycle 10 in embryos with two extra copies of the maternal CycB+ gene dose (derived from females carrying copies of CycB+t10) and carrying pimIL, as occurs in wild-type embryos, but the velocity and pattern of nuclear migration are abnormal; nuclear movements are faster than in wild-type embryos and the nuclei move in curved paths and at an angle to the cortex (the nuclei migrate in straight paths perpendicular to the cortex in wild-type embryos). The reduction in the microtubule network (measured during early interphase of cycle 9) seen in embryos with four extra copies of the maternal CycB+ gene dose (derived from females carrying copies of CycB+t10) is suppressed by pimIL/+.

      (Ji et al., 2005)

      In contrast to pimIL and dupa1 single mutants, double mutants do not exhibit an increase in mitotic index. Chromosomes are found to congress into a metaphase plate during embryonic mitosis 16 as in wild-type.

      pimIL pbl3 double mutants exhibit an increase in centrosome number per cell per cycle.

      pimIL pbl5 double mutants exhibit an increase in centrosome number per cell per cycle.

      (Pandey et al., 2005)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Fails to complement

      pimIR46

      (Dej et al., 2004)

      pimIR47

      (Dej et al., 2004)
      Rescued by

      pimIL is rescued by pimg

      (Leismann and Lehner, 2003)
      Not rescued by

      pimIL is not rescued by pimkenadba.g

      (Leismann and Lehner, 2003)

      pimIL is not rescued by pimkenadba.g.Tag:MYC

      (Leismann and Lehner, 2003)

      pimIL is not rescued by pimg.dba.Tag:MYC

      (Leismann et al., 2000)
      Comments

      Inhibition of sister chromatid separation during mitosis 15 in pimIL/pimIL embryos (from pimIL/+ mothers) is rescued by pimg, but not by pimkenadba.g or pimkenadba.g.T:Hsap\MYC.

      (Leismann and Lehner, 2003)

      The addition of pimg.dba.T:Hsap\MYC does not affect sister chromatid separation, however about 10% of metaphase figures had chromatin bridges. The addition of pimg.dba.T:Hsap\MYC does not rescue the lethality seen in pimIL homozygotes.

      (Leismann et al., 2000)
      Images (0)
      Mutant
      Wild-type
      Stocks (2)
      Notes on Origin
      Discoverer
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (3)
      References (18)