|Feature type||allele||Associated gene||Dmel\stau|
|Also Known As||stauHL, stauHL54|
|Allele class||hypomorphic allele - genetic evidence|
What does this section display?
This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms).
What does this section not display?
This section does not currently display links that were removed or gene model changes.
Click the icon below to subscribe to this FlyBase record and receive updates automatically through your feed reader.
|All updates||Click here to see a list of all updates to this record from FB2010_08 and on.|
|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
No molecular modification is detectable in Southern blots.
|Phenotype Manifest In|
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.
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.
Embryos from homozygous stau1 mothers have normal abdomen, hatch and survive to adulthood. Embryos from mothers transheterozygous for stau1 over a deletion of stau have severe abdominal deletions.
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).
|Phenotype Manifest In|
|Complementation & Rescue Data|
|Stocks ( 2 )|
|Notes on Origin|
Cytoplasmic transplantation of wild type plasm into the abdominal region restores normal abdominal development.
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 4 )|
(Crauk and Dostatni, 2005, Houchmandzadeh et al., 2002, Gao et al., 1996, Liang et al., 1994, Ding et al., 1994, Lehmann and Nusslein-Volhard, 1991, St. Johnston et al., 1991, Lasko and Ashburner, 1990, Tearle and Nusslein-Volhard, 1987, Schupbach and Wieschaus, 1986, Schupbach and Wieschaus, 1986, He et al., 2008)
|Secondary FlyBase IDs|
|References ( 24 )|
|Generate a list of|
|List References by type|
|Recent research papers (0)|
|All research papers listed in FlyBase were published before 2011|
|Recent reviews (0)|
|All reviews listed in FlyBase were published before 2011|