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General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
Additional Notes
Nucleotide change:


Amino acid change:

Q83term | insc-PA

Reported amino acid change:



Site of nucleotide substitution in mutant inferred by FlyBase based on reported position of amino acid change.

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

Amino acid replacement: Q83term.

Nucleotide substitution: C250T.

A premature translational termination codon is introduced near the amino terminus of the insc coding region.

Expression Data
Reporter Expression
Additional Information
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Modifiers Based on Experimental Evidence ( 0 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
Disease-implicated variant(s)
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

abdominal ventral sensillum campaniformium vc1 & thecogen cell

abdominal ventral sensillum campaniformium vc2 & thecogen cell

abdominal ventral sensillum campaniformium vc3 & thecogen cell

abdominal ventral sensillum campaniformium vc4a & thecogen cell

abdominal ventral sensillum campaniformium vc4b & thecogen cell

mitotic domain 9 & spindle

Detailed Description

The GMC-1 cells in insc22 mutant embryos symmetrically divide into two RP2 cells rather than an RP2 and a sib cell.

In insc22 mutants, the GMC-1 of the RP2/sib lineage symmetrically divides into two RP2s instead of an RP2 and a sib.

In insc22 mutant NB1-1 lineages, the early born pCC neuron is transformed into an aCC neuron. Approximately one fifth of these lineages contain at least one subperineural glia.

insc22 mutant NB4-2 clones show a duplication of the RP2 fate at the expense of the RP2sib neuron. However, the motor neurons in this cluster are present and exhibit wild-type morphology.

insc22 mutant NB7-1 clones contain wild-type motor-neuronal fascicles comprising of the U-neurons. In some clones the U-neuron fascicle appears thinner, possibly indicating fewer U-neurons are present. There is a reduction in the number of eve-positive U-neurons to an average of 3.9 per hemineuromere compared to 4.9 in wild-type controls.

12% of anaphase and telophase neuroblast mitoses are more than 45o off-axis in homozygous embryos (in contrast to wild type where all neuroblast divisions are oriented within 45o of the apicobasal axis). The average length of metaphase spindles in homozygous and heterozygous neuroblasts is significantly less than normal.

Mutant neuroblasts have defects in spindle orientation.

neuroblast divisions that produce equal-sized daughter cells are not seen in insc22 mutant embryos.

In insc22 mutant embryos a duplication of the abdominal ventral multidendritic neuron 1a is seen in 13% of segments (N=77).

insc22 mutant NB1-1, NB4-2 and NB7-1 show deviations from wild-type morphology. In all three lineages, insc appears to be required specifically for the cell-fate resolution of the earliest born neurons, later born components of these lineages appear not to require or can partially bypass insc.

All insc22 clones associated with NB1-2, NB3-2, NB4-1, NB5-2, NB7-2 and MP2 are morphologically wild-type in terms of cell numbers, positions and axonal projections.

insc22 mutant MP2 clones display wild-type morphology and development.

In insc22 mutant embryos, about 10% of neuroblast spindles are misoriented as compared to wild-type.

The vp1-vp4a external sensory organ pI divisions occur within the plane of the epithelium in mutant embryos (as occurs in wild type). The loss of insc activity has no effect on the polarity and orientation of the pI division. The socket and shaft cells are always present at all vp4a positions in mutant embryos. However, in some segments, the vdaa md neuron is duplicated and the vp4a es neuron and sheath cell are missing. The socket and shaft cells are always detected, while the neuron and sheath form properly in only 66% of the vp1-vp4 organs. In 6% of these es organs, the es neuron and sheath cell are both missing. This defect is always associated with the presence of an additional md neurone at the vdaA-D/vbp position. In some segments, the presence of one additional md neuron at the vdaA-D/vbp position cannot be correlated with a defect in the number of the vp1-vp4 organ cells.

Cells of mitotic domain 9 and most neuroblasts fail to reorient their mitotic spindles perpendicular to the apical surface.

Ganglion mother cell (GMC) 1-1a and GMC4-2a are formed correctly. However GMC1-1a divides to form two sibling neurons that both adopt the aCC fate with respect to marker gene expression, and GMC4-2a divides to form two sibling neurons that both adopt the RP2 fate with respect to marker gene expression. The duplicated RP2 cells are equal with respect to their cell and nuclear size. The orientation of GMC division is altered; in 74% of cases the metaphase plate is oriented perpendicular or close to perpendicular to the apical surface. numb1 insc22 double mutant embryos lack an eve-positive cell in the RP2 position in 98% of hemisegments.

Embryonic muscle loss is due to defects in early somatic differentiation. Severe abnormalities are observed in a subset of pericardial cells.

Fusion defects of myoblasts.

Embryos exhibit large gaps in the ventral, pleural and dorsal musculature. A lot of myoblasts are present which suggests the fusion of myoblasts to myotubes is not complete. Lateral and pleural muscle pattern is reduced, dorsal muscles are less affected. Dorsal vessel is normal. Pattern formation of the cuticle is normal suggesting the observed muscle phenotype is not a consequence of epidermis defects.

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Enhancer of

insc22 is an enhancer of neuroblast phenotype of pinsP62

insc22 is an enhancer of neuroblast phenotype of GαidsRNA.cCa

insc22 is an enhancer of spindle & neuroblast phenotype of GαiP8


bazunspecified, insc22 has spindle pole centrosome & astral microtubule phenotype

insc22, pinsunspecified has spindle pole centrosome & astral microtubule phenotype

Additional Comments
Genetic Interactions

Embryos double mutant for insc22 and HemJ4-48 display hemisegments containing 4 RP2 neurons and no sib cells. No RP2 or sib cells are found in the contralateral hemisegment.

In midlos1, insc22 mutants, two ectopic RP2s are observed.

Heat-shocked, stage 14 pdm2hs.P; insc22/insc22 embryos have extra RP2 neurons, but not extra RP2 sibs.

Equal size neuroblast divisions are not seen in insc22; bazdsRNA.cCa mutant neuroblasts (n = 72), or in insc22; aPKCdsRNA.cCa mutant neuroblasts (n = 65). In G-iα65AdsRNA.cCa; insc22 embryos the majority of neuroblasts undergo equal size divisions (76%, n = 39) Being mutant for insc22 enhances the penetrance of the symmetric division (9% to 31%), and reverse orientation division (2% to 11%) phenotypes seen in pon::rapsc-pon.Scer\UAS; Scer\GAL4sca-P309 embryos (n=63). In insc22, rapsP62 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.

In rapsunspecified insc22 or bazunspecified insc22 double mutant neuroblasts, both centrosomes are associated with astral microtubules, with a cap structure forming over each centrosome from metaphase onwards. This phenotype is not observed in single mutants for these genes. Equal size division between daughter cells is observed in 100% of G-iα65AP8 insc22 double mutants. In G-iα65AP8 insc22 mutant neuroblasts, the spindle geometry remains symmetric even at telophase with the cleavage plane being equidistant to both centrosomes. The spindle is positioned symmetrically with both centrosomes lying in close proximity to the cell cortex.

Xenogenetic Interactions
Complementation and Rescue Data
Partially rescued by

The neuroblasts phenotype is rescued by the expression of inscA2-A3.hs.T:Zzzz\FLAG. 49% of hemisegments show duplication of the RP2 neuron at the expense of the RP2sib neuron. The RP2 neuron duplication phenotype of insc22 embryos is largely rescued by inschs.PK, insc3'RI.hs.T:Hsap\MYC, insc3'DraIII.hs.T:Hsap\MYC or insc5'NheI.hs.T:Zzzz\FLAG. The RP2 neuron duplication phenotype of insc22 embryos is not rescued by insc3'NheI.hs.T:Hsap\MYC, insc5'BsrBI.hs.T:Zzzz\FLAG or insc5'BsrBI.hs.T:Zzzz\FLAG. The RP2 neuron duplication phenotype of insc22 embryos is partially rescued by insc3'BsrBI.hs.T:Hsap\MYC, insc3'NarI.hs.T:Hsap\MYC, inscBcII.hs.T:Hsap\MYC or inscA1-A5.hs.T:Zzzz\FLAG.

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Notes on Origin
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (28)