Nucleotide substitution: G?A.
Amino acid replacement: W53term.
G20065440A
G?A
W53term | vls-PA
W53term
TGG to TGA
Prevents the posterior accumulation of G-iα65A protein.
Strong abdominal defect.
Absence of posterior pole plasm, polar granules and pole cells.
Embryos lack pole cells. Large amounts of vas protein are expressed in early stages of oogenesis. vas protein localizes to the posterior pole at the same stage of egg development as wild type, the protein disappears by early gastrulation.
Hemizygous vls2embryos derived from homozygous females have no polar granules, fail to form pole cells and have deletions of abdominal structures. vas and CycB transcripts are localized at the posterior.
Eggs derived from homozygous females form a syncytial blastoderm but 80-90% of the embryos fail to cellularise. Those that do cellularise show variable cellularisation defects. The embryos show a "grandchildless-knirps" phenotype; they lack polar granules and pole cells and show typical maternal kni-like abdominal segment deletions.
Homozygous females produce embryos that fail to form pole cells, lack polar granules normally found at the posterior pole, and have deletions of abdominal segments. There are also frequent defects in cellularisation at the blastoderm stage.
Embryos derived from mutant females completely lack pole cells and show deletions in the abdominal segments. The same phenotype is seen in embryos derived from homozygous or hemizygous females.
Stated to be lost.
Germline mosaic analysis shows that vls is required in the germline.
Cytoplasmic transplantation of wild type plasm into the abdominal region restores normal abdominal development.
Although tud protein is present in mutant embryo extracts, its localization in the embryo is altered.