Amino acid replacement: P830L.
C1325293T
P830L | fs(1)N-PA
P830L
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
Embryos derived from homozygous females show a terminal phenotype.
Deletion of anterior and posterior structures.
Failure to differentiate cuticular structures derived from the anterior and posterior regions of the egg.
A hole is seen in the blastoderm layer below the pole cells in embryos. The ventral furrow is extended posteriorly. Segments A8 to the telson are deleted. Segments A5 to A7 are expanded. Some twisting of the germband is seen. Labral and acron-derived structures are deleted. There is cell death in the head and tail region.
Embryos display a tor phenotype.
Eggs are laid but collapse on deposition.
Homozygous fs(1)N12 females produce embryos with defects in anterior and posterior development (Degelmann, Hardy, Perrimon and Mahowald, 1986; Degelmann, Hardy and Mahowald, 1990). Head involution fails; anterior endodermal derivatives are deficient and the absence of pharyngeal musculature causes collapse of the cephalopharyngeal apparatus. Embryos lack all posterior endodermal derivatives as well as structures characteristic of abdominal segments 8 to 10 usually, but have six abdominal denticle belts, and occasionally partial seventh or seventh and eighth. In addition, posterior midgut, hindgut, Malpighian tubules, filzkorper, spiracles, anus, anal pad and anal tuft absent; lateral tracheal trunks end blindly, usually in the sixth segment; posterior disorganization of CNS seen. Pole cells form abnormally and seldom migrate to form the gonad; posterior blastoderm nuclei fail to cellularize and the centrosome position vis a vis the blastoderm nuclei erratic; remarkably free of microtubules. Six rather than seven stripes of ftz transcription seen in blastoderm, with the sixth stripe wider than normal and separated from the fifth by a wider-than-normal space. At gastrulation neither posterior midgut invagination nor proctodeal invagination occur normally.
fs(1)N12 is a suppressor of embryonic segment phenotype of tsltor.PF
Engstrom.