Open Close
General Information
Symbol
Dmel\pimIL
Species
D. melanogaster
Name
FlyBase ID
FBal0056312
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
pim1, pimIL97
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

G10363526A

Reported nucleotide change:

G550A

Comment:

splice donor mutation

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

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

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
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.

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

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

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.

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.

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

Malpighian tubule elongation is incomplete in homozygous embryos.

Polyploid nuclei due to failure to complete mitosis.

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

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 cytokinesis defective phenotype, non-enhanceable by pbl3

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

pimIL has cytokinesis defective phenotype, non-enhanceable by pbl5

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

Suppressed by
Statement
Reference

pimIL has cytokinesis defective phenotype, suppressible by dupa1

NOT Enhancer of
Statement
Reference

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

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

Suppressor of
Statement
Reference

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

pimIL is a suppressor of cytokinesis defective phenotype of dupa1

Phenotype Manifest In
NOT Enhanced by
Statement
Reference

pimIL has centrosome phenotype, non-enhanceable by pbl3

pimIL has centrosome phenotype, non-enhanceable by pbl5

Suppressed by
Statement
Reference

pimIL has metaphase plate phenotype, suppressible by dupa1

NOT Enhancer of
Statement
Reference

pimIL is a non-enhancer of centrosome phenotype of pbl3

pimIL is a non-enhancer of centrosome phenotype of pbl5

Suppressor of
Statement
Reference

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

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

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

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

pimIL is a suppressor of metaphase plate phenotype of dupa1

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/+.

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.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Rescued by
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.

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.

Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (17)