|Feature type||allele||Associated gene||Dmel\fog|
|Also Known As||fog4a6|
|Allele class||amorphic allele - genetic evidence, loss of function allele|
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|
|Phenotype Manifest In|
The salivary gland cells fail to internalised in mutant embryos.
Mutant embryos show defects in the apical constriction of cells seen during mesoderm invagination. They lack the normal two constriction phases seen in wild-type embryos and instead show weak, asynchronous cell shape changes.
Embryos injected with cholera toxin exhibit apical flattening. Heat induced ectopic expression of foghs.PM causes a widened ventral furrow.
Mutant embryos lack posterior midgut, Malpighian tubules and hindgut. None of the posterior gut primordia invaginate.
Ventral furrow and posterior midgut invaginations fail to form normally. The posterior midgut primordium fails to invaginate. While the first phase of constrictions near the ventral midline proceeds fairly normally, cells in more lateral regions show variable defects. Constrictions fail or are delayed, and although ventral furrow formation is on average delayed by about 4 minutes, almost all of the mesodermal precursors are eventually internalized.
Defective in gonad assembly.
Muscle pattern wild type within constraints imposed by alterations in body plan. Muscles contractile and vigorous.
Embryos fail to form a posterior midgut.
Cellular blastoderm and gastrulation initiation are normal. Normal expression of twi suggesting no abnormalities in dorsal-ventral patterning. Rapid phase of constriction is absent: many cells in midventral domain never constrict and twi expressing cells are brought into the invagination whether or not they constrict. No invagination of the posterior midgut.
fog4 mutant embryos are normal at the cellular blastoderm stage, and gastrulation starts normally. The posterior midgut does not form, and the germband does not elongate but forms a series of transverse ventral folds. Homozygous germline clones give viable embryos.
|Phenotype Manifest In|
|Complementation & Rescue Data|
Ubiquitous foghs.PM expression during the late blastoderm and early gastrula stages rescues the final cuticle phenotype of embryos. Heat shocking during stages 6 and 7 provided the greatest degree of rescue.
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 5 )|
folded gastrulation 4A6
|Secondary FlyBase IDs|
|References ( 17 )|