FlyBase Allele Report: Dmel\insc[22]

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.

(Udolph et al., 2009)

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

(Hughes et al., 2004)

Mutant neuroblasts have defects in spindle orientation.

(Albertson and Doe, 2003)

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

(Cai et al., 2003)

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

(Orgogozo et al., 2002)

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.

(Rath et al., 2002)

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

(Cai et al., 2001)

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 vda_A-D/vbp position. In some segments, the presence of one additional md neuron at the vda_A-D/vbp position cannot be correlated with a defect in the number of the vp1-vp4 organ cells.

(Orgogozo et al., 2001)

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

(Tio et al., 1999)

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.

(Buescher et al., 1998)

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

(Knirr et al., 1997)

Fusion defects of myoblasts.

(Knirr et al., 1996)

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.

(Burchard et al., 1995)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhancer of

Statement

Reference

insc²² is an enhancer of abnormal cell polarity phenotype of Scer\GAL4^hs.PB, pon::pins^c-pon.UAS

(Cai et al., 2003)

Other

Statement

Reference

Hem^J4-48, insc²² has abnormal neuroanatomy | embryonic stage phenotype

(Zhu and Bhat, 2011)

Hem^J4-48, insc²² has abnormal cell migration | embryonic stage phenotype

(Zhu and Bhat, 2011)

insc²², mid^los1 has abnormal neuroanatomy | embryonic stage phenotype

(Gaziova and Bhat, 2009)

Phenotype Manifest In

Enhancer of

Statement

Reference

insc²²/insc²² is an enhancer of larval RP2 motor neuron | ectopic phenotype of pdm2^hs.P

(Bhat and Apsel, 2004)

insc²² is an enhancer of neuroblast phenotype of pins^P62

(Cai et al., 2003)

insc²² is an enhancer of neuroblast phenotype of Scer\GAL4^hs.PB, pon::pins^c-pon.UAS

(Cai et al., 2003)

insc²² is an enhancer of spindle & neuroblast phenotype of Gαi^P8

(Yu et al., 2003)

Other

Statement

Reference

Hem^J4-48, insc²² has larval RP2 motor neuron | embryonic stage phenotype

(Zhu and Bhat, 2011)

Hem^J4-48, insc²² has RP2sib neuron | embryonic stage phenotype

(Zhu and Bhat, 2011)

insc²², mid^los1 has larval RP2 motor neuron | increased number phenotype

(Gaziova and Bhat, 2009)

insc²², pins^P62 has neuroblast phenotype

(Cai et al., 2003)

baz^unspecified, insc²² has spindle pole centrosome & astral microtubule phenotype

(Yu et al., 2003)

insc²², pins^unspecified has spindle pole centrosome & astral microtubule phenotype

(Yu et al., 2003)

Additional Comments

Genetic Interactions

Statement

Reference

Embryos double mutant for insc²² and Hem^J4-48 display hemisegments containing 4 RP2 neurons and no sib cells. No RP2 or sib cells are found in the contralateral hemisegment.

(Zhu and Bhat, 2011)

In mid^los1, insc²² mutants, two ectopic RP2s are observed.

(Gaziova and Bhat, 2009)

Heat-shocked, stage 14 pdm2^hs.P; insc²²/insc²² embryos have extra RP2 neurons, but not extra RP2 sibs.

(Bhat and Apsel, 2004)

Equal size neuroblast divisions are not seen in insc²²; baz^dsRNA.cCa mutant neuroblasts (n = 72), or in insc²²; aPKC^dsRNA.cCa mutant neuroblasts (n = 65). In G-iα65A^dsRNA.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::raps^{c-pon.Scer\UAS}; Scer\GAL4^sca-P309 embryos (n=63). 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)

In raps^unspecified insc²² or baz^unspecified 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-iα65A^P8 insc²² double mutants. In G-iα65A^P8 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.

(Yu et al., 2003)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

insc^k07505

(Hassan et al., 1998)

insc^Δ13

(Hassan et al., 1998)

insc^P8

(Knirr et al., 1997)

insc^P49

(Knirr et al., 1997)

insc^Δ13

(Knirr et al., 1997)

Rescued by

insc²² is rescued by insc^{A2-A3.hs.Tag:FLAG}

(Tio et al., 1999)

insc²² is rescued by insc^{3'RI.hs.Tag:MYC}

(Tio et al., 1999)

insc²² is rescued by insc^{5'NheI.hs.Tag:FLAG}

(Tio et al., 1999)

insc²² is rescued by insc^hs.PK

(Tio et al., 1999)

insc²² is rescued by insc^{3'DraIII.hs.Tag:MYC}

(Tio et al., 1999)

Partially rescued by

insc²² is partially rescued by insc^{3'NarI.hs.Tag:MYC}

(Tio et al., 1999)

insc²² is partially rescued by insc^{A1-A5.hs.Tag:FLAG}

(Tio et al., 1999)

insc²² is partially rescued by insc^{3'BsrBI.hs.Tag:MYC}

(Tio et al., 1999)

insc²² is partially rescued by insc^{BcII.hs.Tag:MYC}

(Tio et al., 1999)

Not rescued by

insc²² is not rescued by insc^{5'RI.hs.Tag:FLAG}

(Tio et al., 1999)

insc²² is not rescued by insc^{3'NheI.hs.Tag:MYC}

(Tio et al., 1999)

insc²² is not rescued by insc^{5'BsrBI.hs.Tag:FLAG}

(Tio et al., 1999)

Comments

The neuroblasts phenotype is rescued by the expression of insc^{A2-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 insc^hs.PK, insc^{3'RI.hs.T:Hsap\MYC}, insc^{3'DraIII.hs.T:Hsap\MYC} or insc^{5'NheI.hs.T:Zzzz\FLAG}. The RP2 neuron duplication phenotype of insc²² embryos is not rescued by insc^{3'NheI.hs.T:Hsap\MYC}, insc^{5'BsrBI.hs.T:Zzzz\FLAG} or insc^{5'BsrBI.hs.T:Zzzz\FLAG}. The RP2 neuron duplication phenotype of insc²² embryos is partially rescued by insc^{3'BsrBI.hs.T:Hsap\MYC}, insc^{3'NarI.hs.T:Hsap\MYC}, insc^{BcII.hs.T:Hsap\MYC} or insc^{A1-A5.hs.T:Zzzz\FLAG}.

(Tio et al., 1999)

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

39678

insc²²/CyO

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (3)

Reported As

Symbol Synonym

insc22

(Yu et al., 2002)

insc²²

(Ruan et al., 2013, Tio et al., 2011, Zhu and Bhat, 2011, Gaziova and Bhat, 2009, Udolph et al., 2009, Wang et al., 2006, Siegrist and Doe, 2005, Rath et al., 2002)

nem²²

Name Synonyms

Secondary FlyBase IDs

References (28)

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