T to A mutation in the last nucleotide of the intron within dsRNA-binding domain 5 (dsRBD5). Failure to splice this intron is predicted to produce a protein that lacks dsRBD5, and instead has coding sequence from the intron followed by a premature stop codon.
No molecular modification is detectable in Southern blots.
stau1 mutants show supernumerary boutons (total and satellite) in the third instar larval neuromuscular junction; ventral longitudinal muscles exhibit increased evoked EJC amplitude and increased spontaneous EJC frequency.
stau1/Df(2R)Pcl7B larvae have a significantly reduced number of type Ib boutons compared to wild type.
Heterozygous females with mama1 are fertile.
Shallow gradient of bcd protein with reduced amounts in anterior regions. The gt posterior domain is abolished and the anterior domain is shifted anteriorly.
Absence of posterior pole plasm, polar granules and pole cells.
Does not interact with RpII140wimp maternal effect.
Embryos lack pole cells. Large amounts of vas protein are expressed in early stages of oogenesis. Perinuclear localization is reduced in favour of additional protein in the cytoplasm: vas protein fails to distribute asymmetrically. Cleavage embryos have uniform vas protein distribution, the protein disappears by early gastrulation.
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. The embryos also show a tor-like head deletion.
Cellularisation is always normal in embryos derived from homozygous females. During gastrulation, the cephalic fold, anterior midgut and dorsal head clusters are formed by cells in more anterior positions than in a wild-type embryo. The embryos completely lack pole cells. Variable deletion of the abdominal segments is seen and chitinous head structures corresponding to the embryonic labral segment are reduced. The severity of the abdominal segment deletion and the head defect phenotype is more severe in stau1/Df(2R)PC4 embryos.
weak allele maternal-effect lethal Embryos from homozygous mothers exhibit a so-called 'grandchildless-knirps' phenotype; all eggs lack polar granules and no pole cells are formed; most embryos show variable deletions of abdominal segments, whereby segment A4 is deleted most frequently; larger deletions may delete segments A2 through A7; in extreme cases, anterior parts of segment A1 become fused to posterior parts of segment A8, but telson elements are always present and relatively normal. In addition, embryos show deletions of the anterior-most head structures and the cephalic furrow is shifted anteriorly at gastrulation. Analysis of germ-line clones indicates that the mutation is germ-line autonomous (Schupbach and Wieschaus, 1986).
stau1 is an enhancer of abnormal neuroanatomy phenotype of Hsap\ATXN8OSCTG112.UAS, Scer\GAL4GMR.PF
Fmr1Δ50M/Fmr1[+], stau1 has abnormal neuroanatomy | third instar larval stage phenotype
Fmr1Δ50M, stau1 has lethal - all die before end of larval stage phenotype
Fmr1Δ50M/Fmr1[+], stau1 has embryonic/larval neuromuscular junction | third instar larval stage phenotype
Fmr1Δ50M/Fmr1[+], stau1 has NMJ bouton | increased number | third instar larval stage phenotype
stau1 is rescued by Scer\GAL4how-24B/stauUAS.GFP
Germline mosaic analysis shows that stau is required in the germline.
Cytoplasmic transplantation of wild type plasm into the abdominal region restores normal abdominal development.