Nucleotide substitution: TTC to ATC Amino acid replacement: F684I.
T17462435A
T?A
F684I | BicD-PA; F684I | BicD-PB; F684I | BicD-PC; F684I | BicD-PD
F684I
Heterozygous BicD1 females produce 16% wild-type embryos and 84% embryos with various defects, including reduced mouthparts and bicaudal phenotypes.
Embryos derived from BicD1/BicD2 mothers show a duplication of posterior structures and a lack of anterior structures. These embryos lack macrophages. Apoptotic cells accumulate at the ventral surface of the central nervous system (CNS), and subperineural glia contain an abundance of apoptotic cells. Single unengulfed apoptotic cells are also seen inside the CNS. The number of subperineural glia per abdominal segment is not significantly different from wild-type in stage 16 embryos.
Does not prevent the posterior localization of G-iα65A protein.
Embryos from mutant females are bicaudal.
Hemocytes cannot be detected, suggesting that in the absence of head mesoderm the trunk population of mesoderm cannot produce hemocytes. Cellular debris becomes located in the extracellular space.
Lack of head and thoracic anlagen is caused by the lack of bcd protein.
BicD1 has embryo phenotype, suppressible by pAbp[+]/pAbpk10109
BicD1, pAbp[+]/pAbpk10109 has embryo phenotype, suppressible by pAbp+t7.8
The BicD1/+ mutant embryonic phenotypes are suppressed by pAbpk10109/+.
The BicD1/+ mutant embryonic phenotypes are suppressed by pAbp37-2/+.
The suppression of the BicD1/+ embryonic phenotypes by pAbpk10109/+ is partially reverted by one copy of pAbp+t7.8.
The suppression of the BicD1/+ embryonic phenotypes by pAbp37-2/+ is partially reverted by one copy of pAbp+t7.8.