Amino acid replacement: V215M.
G21778771A
V215M | tsl-PA; V215M | tsl-PB; V215M | tsl-PC
V215M
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
Posterior defect is significantly suppressed, in a dose-dependent manner, by Dsor1Su1.
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. Cephalic furrow and anterior midgut invagination are shifted anteriorly.
maternal-effect lethal Anterior- and posteriormost structures (labrum, dorsal bridge, telson, eighth and part of seventh abdominal segments) deleted in embryos produced by homozygous mothers. tsl pole cells transplanted into wild-type hosts produce normal progeny, whereas the reciprocal transplant produces tsl embryos.
bcd6, tsl1 has embryonic/first instar larval cuticle phenotype
The addition of bcdΔA to tsl1, bcd6 embryos rescues the anterior part of the tsl1 mutant phenotype (rescuing the labrum and dorsal bridge) as well as rescuing the bcd6 mutant phenotype. This results in embryos with a posterior terminal mutant phenotype only.
The addition of tsl1 does not effect the ability of bcdΔQAC to rescue the bcd6 phenotype. The addition of bcdΔA to tsl1, bcd6 embryos rescues the terminal system phenotype seen in these animals.
Mutant phenotype of bcd, tsl double mutants is partially rescued by hbbcd.3UTR.
Allelic series: tsl5 = tsl4 > tsl3 > tsl1 > tsl2