Open Close
General Information
D. melanogaster
from X irradiation
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
Associated Sequence Data
DNA sequence
Protein sequence
Progenitor genotype
Nature of the lesion

Insertion of an F-element in the second coding exon of sn.

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.

Insertion components
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
Detailed Description

In snX2/snX2 and snX2/+ nurse cells, the nucleolus has a dispersed phenotype and fewer interconnected tubules than controls. The severity of the phenotype is lower at oogenesis stages 8, 9 and 10A compared to 10B, and in anterior nurse cells.

snX2/Df(1)C128 mutant terminal cells are morphologically indistinguishable from wild type. No apparent alteration of actin organisation in terminal cells is seen.

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.

neurons cultured from snX2/sn3 brains have a distinctive abnormal morphology. Axons curl, creating a filagree pattern. Filamentous axon distribution within these neurons is abnormal.

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.

Repression potential of a P-element repressor protein in a singed sterility assay of snw/snX2 heterozygotes shows partial correspondence with gonadal dysgenic sterility in that strong repression of gonadal dysgenic sterility shows some effect in the singed sterility assay.

Extreme bristle phenotype.

Extreme bristle phenotype, female sterile.

snX2/snMR39B1 flies are sterile.

class 1 - female sterile with gnarled macrochaetae and kinky microchaetae

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
NOT Enhanced by

snX2 has actin filament & egg chamber phenotype, non-enhanceable by ActnΔ233

NOT suppressed by

snX2 has actin filament & egg chamber phenotype, non-suppressible by ActnΔ233

NOT Suppressor of
Additional Comments
Genetic Interactions

The short actin bundles seen in the egg chambers of snX2 single mutants are also seen in ActnΔ233 snX2/ActnΔ233 snX2 double mutant egg chambers.

Xenogenetic Interactions
Complementation and Rescue Data
Partially rescued by

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.

Images (0)
Stocks (24)
Notes on Origin


External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
References (27)