P element insertion at cytological location 5D5--5D6 and accompanying 8bp duplication.
RNase protection experiments demonstrate that the mutant sqh1 transcript is transcribed at about 10% of the level of the wild type transcript.
lethal, with sqhAE.EGFP
lethal, with sqhTA.EGFP
sqh1 germline clone egg chamber exhibit slower and incomplete nurse cell dumping into the oocyte.
In embryos expressing sqhTA.T:Avic\GFP-EGFP in a sqh1 mutant background apical constriction appears more continuous than in wild type, with fewer rapid phases of constriction that are lower in magnitude. Constriction occurs more slowly than in control embryos.
In embryos expressing sqhAE.T:Avic\GFP-EGFP in a sqh1 mutant background apical constriction appears more continuous than in wild type, with fewer rapid phases of constriction that are lower in magnitude. Constriction occurs more slowly than in control embryos.
In the few homozygous sqh1 mutant embryos that complete development, the wound repair response is severely impaired: upon ablation, wounds expand normally but fail to contract.
Germband elongation is strongly reduced in sqh1 mutants.
Homozygous cells in the morphogenetic furrow (in clones that encompass the morphogenetic furrow) fail to undergo apical constriction and apicobasal contraction.
Spiracle cells fail to invaginate and to form a lumen in homozygous embryos derived from homozygous female germline clones. Spiracle cells are seen detached from the main cluster in these mutant embryos, and some of the spiracle cells fail to constrict apically. Spiracle cells invaginate but fail to form a lumen in embryos derived from homozygous female germline clones in which sqh+ function has been rescued paternally.
In sqh1 embryos, the membrane invaginations of cellularization still occur. However, the anterior half of the embryo begins to cellularize before the posterior. The furrows of the anterior half progress almost as wild type. When the furrow front has nearly reached its maximum depth at the anterior half, it is only beginning to invaginate near the posterior pole. At the end of cellularization, myosin II is present at the furrow base, but is severely disorganized. The syncytial divisions of sqh1 embryos are asynchronous and occur in waves that propagate from the posterior to the anterior pole. This asynchrony is due to a defect in nuclear axial expansion. However, metaphase furrow formation during syncytial mitoses is not disrupted and there is no evidence of spindle collision. The first cytokinesis after cellularization is disrupted in sqh1 embryos and a large proportion of cells are unable to divide. These cells are smaller than in wild type, fail to round up fully and do not form cleavage furrows. Such furrows can start to form at the apical side of the cells but do not proceed all around the equator of the cell and disappear deeply in the cell.
Homozygotes die just after pupariation, after a prolonged larval period of several weeks. Imaginal tissues are rudimentary and highly polyploid.
Germ line clones produce small eggs, with the egg chambers showing a dumpless phenotype, even though the actin filaments of stage 10B are intact, suggesting that nurse cell myosin II is the motive force for dumping. These embryos have no axial migration of nuclei to posterior poles of the syncytial blastoderm.
Developing oocytes in homozygous germline clones often fail to attain full size due to a defect in 'dumping', the rapid phase of cytoplasmic transport from nurse cells. Egg chambers do not show ring canal obstructions and the actin network is unchanged. Clonally derived fertilised eggs are smaller than wild type but early in development exhibit a defect in axial migration of cleavage nuclei towards the posterior pole of the embryo.
Cytokinesis is defective. 20--25% cells from hemizygous flies are diploid compared to half from homozygous flies.
Probably a hypomorph. late L3 larval/early pupal lethal extended larval period (10-14 days), normally diploid larval tissues (e.g., brain, imaginal disc and gonad) possess numerous polyploid cells resulting from an intermittent failure of cytokinesis. Repeated rounds of apparently normal mitosis without cytokinesis produce cells containing hundreds of chromosomes, during which the brain grows to enormous size. Imaginal discs are small and poorly formed (Karess).
sqh1 is a suppressor | partially of abnormal neuroanatomy phenotype of Ggal\MLCKct.UAS, Scer\GAL4ftz.ng
sqh1/sqh[+] is a suppressor of aster | embryonic cycle 5 phenotype of CycB+t10
sqh1/sqh[+] is a suppressor of aster | embryonic cycle 6 phenotype of CycB+t10
sqh1/sqh[+] is a suppressor of aster | embryonic cycle 7 phenotype of CycB+t10
sqh1/sqh[+] is a suppressor of mitotic domain 1 | embryonic cycle 14 phenotype of CycB+t10
sqh1 is a suppressor | partially of larval longitudinal connective phenotype of Ggal\MLCKct.UAS, Scer\GAL4ftz.ng
sqh1 shows no interaction with Sbunspecified (assayed in terms of a malformed leg phenotype).
The midline crossover phenotype caused expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng is partially suppressed by sqh1.
sqh1 is partially rescued by sqhE20.E21
sqh1 is not rescued by sqhAA.EGFP
sqh1 is not rescued by sqhTA.EGFP
sqh1 is not rescued by sqhAS.EGFP
sqh1 is not rescued by sqhTE.EGFP
sqh1 is not rescued by sqhAE.EGFP
sqh1 is not rescued by sqhEE.EGFP
Expression of sqhTS.T:Avic\GFP-EGFP rescues the nuclear migration and uneven cellularization seen in sqh1 mutant embryos.
Expression of sqhAA.T:Avic\GFP-EGFP does not rescue the nuclear migration and uneven cellularization seen in sqh1 mutant embryos. No adult flies are observed.
Expression of sqhAE.T:Avic\GFP-EGFP does not rescue the nuclear migration and uneven cellularization seen in sqh1 mutant embryos. No adult flies are observed.
Expression of sqhTE.T:Avic\GFP-EGFP does not rescue the nuclear migration and uneven cellularization seen in sqh1 mutant embryos. No adult flies are observed.
Expression of sqhEE.T:Avic\GFP-EGFP does not rescue the nuclear migration and uneven cellularization seen in sqh1 mutant embryos. No adult flies are observed.
Expression of sqhAS.T:Avic\GFP-EGFP does not rescue the nuclear migration and uneven cellularization seen in sqh1 mutant embryos. No adult flies are observed.
Expression of sqhTA.T:Avic\GFP-EGFP does not rescue the nuclear migration and uneven cellularization seen in sqh1 mutant embryos. No adult flies are observed.
Expressing one copy of the sqhE20.E21 transgene restores axial expansion in sqh1 germline clones.
All phenotypes are completely rescued by sqh+t3.0.
Denell and Johnson.
sqh1 is a leaky allele. Dysgenesis induced wild type revertants have lost the P element at sqh. sqh1 mutant phenotype can be rescued by introduction of a P element insert carrying a wild type copy of sqh.