Amino acid replacement: Y742N.
T5961512A
Y783N | fs(1)M3-PA
Y742N
Position of mutation on reference sequence inferred by FlyBase curator. Position differs slightly from author statement.
Homozygous mutant mothers produce embryos with a terminal loss-of-function phenotype. The embryo lacks all structures posterior to abdominal segment 8 and the head skeleton is reduced in size.
Embryos derived from homozygous females fail to develop structures posterior to the seventh abdominal segment as well as anterior-most structures, including the head skeleton.
Embryos derived from homozygous females show a terminal phenotype.
Posterior defect is significantly suppressed, in a dose-dependent manner, by Dsor1Su1.
Collapsed egg phenotype. Little or no tll expression is detected in the posterior of syncytial or cellular blastoderm embryos, at the anterior the early tll cap does not appear and an abnormal anterior tll stripe appears by the late syncytial blastoderm.
Failure to differentiate cuticular structures derived from the anterior and posterior regions of the egg. Double homozygous females fs(1)N12, fs(1)M31901 produce embryos with the terminal cuticle phenotype.
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.
Terminal holes in embryo. Embryonic defects detectable at preblastoderm stages. Eggs are laid and some collapse on deposition.
Dsor1Su1, fs(1)M31901 has embryo | posterior phenotype, enhanceable by rl[+]/rl9
Dsor1Su1, fs(1)M31901 has embryonic abdominal segment 8 phenotype, enhanceable by rl[+]/rl9
Dsor1Su1, fs(1)M31901 has embryo | posterior phenotype, enhanceable by rl[+]/rl10a
Dsor1Su1, fs(1)M31901 has embryonic abdominal segment 8 phenotype, enhanceable by rl[+]/rl10a
fs(1)M31901 has cephalopharyngeal skeleton | maternal effect phenotype, non-enhanceable by Scer\GAL4ET3/tslUAS.cSa
fs(1)M31901 has terminalia | maternal effect phenotype, non-enhanceable by Scer\GAL4ET3/tslUAS.cSa
fs(1)M31901 has embryo | posterior phenotype, suppressible by Dsor1Su1
fs(1)M31901 has terminalia | maternal effect phenotype, non-suppressible by Scer\GAL4ET3/tslUAS.cSa
fs(1)M31901 has cephalopharyngeal skeleton | maternal effect phenotype, non-suppressible by Scer\GAL4ET3/tslUAS.cSa
fs(1)M31901 has embryo | posterior phenotype, non-suppressible by rlSu14
fs(1)M31901 has embryo | posterior phenotype, non-suppressible by rlSu23
fs(1)M31901 is a suppressor of embryonic segment phenotype of tsltor.PF
Dsor1Su1, fs(1)M31901 has embryonic abdominal segment 8 phenotype
The addition of tslScer\UAS.cSa driven by Scer\GAL4ET3 has no effect on the terminal phenotype seen in embryos laid by fs(1)M31901 mothers.
The fs(1)M31901 posterior embryo defect is significantly suppressed if the female is also carrying one copy of Dsor1Su1; an eighth abdominal segment is formed. This suppression is significantly reduced if the females are also carrying one copy of rl9, rl10a or Df(2R)rl10b. The posterior defects of embryos derived from homozygous fs(1)M31901 females are not suppressed if the females are also carrying one copy of rlSu23 or one or two copies of rlSu14.
Embryos derived from fs(1)M31901 females carrying tsltor.PF show no rescue of the fs(1)M31901 phenotype and do not show deletions of the middle segments ("splice" phenotype seen in wild-type embryos carrying tsltor.PF).
A strong allele of fs(1)M3.