The 0.1kb insertion between -1.2 and -1.9 (coordinates as in FBrf0048245) is present in the parental In(1)dl-49 chromosome and is a polymorphism rather than the cause of the mutant phenotype.
Insertion of 0.1kb DNA, at coordinates -1.9 to -1.2.
Stage 14 snX2 embryos show a substantial delay in the migration of plasmatocytes along the ventral midline. 31% of these embryos show "strong" migration defects. These defects persist at later stages - plasmatocytes remain aggregated in the ventral part of the embryo and are unable to reach the posterior region.
The number of plasmatocytes recruited to a laser-induced wound is significantly reduced in snX2 mutants compared to controls. The migratory speed of snX2 plasmatocytes is also reduced.
snX2 mutant bristles lack fascin crossbridges but still form microvilli. Pimple and microvilli in this mutant appear not only along the epithelial cells between the bristle shafts but are also prominent on the new emerging bristle. A linear array of tiny actin bundles is found attached to the plasma membrane. Each of these contains approximately the same number of filaments as those in the microvilli on the bristle tip or to those in longitudinal section.
Homozygous egg chambers contain short actin bundles compared to wild-type.
Apoptotic nuclei are seen in snX2 egg chambers, although the pattern of apoptosis appears somewhat different to wild-type.
Strong bristle phenotype.
Tiny bundles of actin appear near the plasma membrane at the tip of elongating snX2 bristles, as in the wild-type. These bundles aggregate into ribbon-shaped aggregations of filaments adjacent to the plasma membrane.
Mutation causes a severe denticle phenotype. Denticles tend to be smaller and have thinner hooks than wild-type denticles. They are also less orderly along each row and sometimes have a floppy appearance. Some hairs are shorter and thicker than normal.
Homozygous females produce sterile eggs. Ring canal morphology in the egg chambers of homozygous females ranges from nearly wild-type to very disorganised. The nurse cell nuclei of late stage follicles are lobed and almost wild-type in morphology. Individual lobes of these nuclei are seen to block the ring canals in these follicles.
Does not show premature cytoplasmic streaming in stage 8 egg chambers.
Bristles are gnarled due to disrupted actin filament bundles. Nurse cell cytoplasmic actin filaments are absent.
Extreme bristle phenotype.
Extreme bristle phenotype, female sterile.
class 1 - female sterile with gnarled macrochaetae and kinky microchaetae
snX2/sn[+] is a non-suppressor of terminal tracheal cell phenotype of wkdMB04624
snX2/Df(1)C128 is a non-suppressor of terminal tracheal cell phenotype of wkdMB04624
snX2 is partially rescued by snUASp.EGFP/Scer\GAL4srp.Hemo
snX2 is partially rescued by snS52A.UASp.EGFP/Scer\GAL4srp.Hemo
snX2 is partially rescued by snS52E.UASp.EGFP/Scer\GAL4srp.Hemo
Scer\GAL4srp.Hemo-driven expression of snScer\UAS.P\T.T:Avic\GFP-EGFP provides significant rescue of the reduced plasmatocyte recruitment seen in snX2 embryos after laser-induced wounding.
Scer\GAL4srp.Hemo-driven expression of snS52A.Scer\UAS.P\T.T:Avic\GFP-EGFP provides significant rescue of the reduced plasmatocyte recruitment seen in snX2 embryos after laser-induced wounding.
Scer\GAL4srp.Hemo-driven expression of snS52D.Scer\UAS.P\T.T:Avic\GFP-EGFP provides significant rescue of the reduced plasmatocyte recruitment seen in snX2 embryos after laser-induced wounding.
Muller.