19bp deletion in the second obe exon and a C173T point mutation. These changes introduce a frameshift after amino acid 48 and a stop codon at amino acid 52.
19 base deletion in the second exon of obe which causes a frameshift. One of two lesions in mutant.
C15486369T
C173T
P58L | obe-PA
A single base change causing a stop codon in the mutant (in the context of the 19 bp frameshift-inducing deletion just upstream also found in the @obe[2] mutant). There is also a C to T polymorphism between the reported sequence and the reference genome sequence 8 bases upstream of this point mutation.
adherens junction (with obe1)
centrosome (with obe1)
Embryos derived from obe1/obe2 females show significantly reduced axis elongation during germband extension compared to wild type (the severity of the defect is unaffected by the paternal obe contribution).
obe2/Df(3R)Exel6174 embryos derived from obe2/Df(3R)Exel6174 females crossed to obe2/+ males show significantly reduced axis elongation during germband extension compared to wild type.
obe2/Df(3R)Exel6174 embryos derived from obe2/Df(3R)Exel6174 females crossed to obe2/+ males and obe1/obe2 embryos derived from obe1/obe2 females crossed to obe2/+ males show an abnormal aggregation of adherens junction proteins at stage 7.
In contrast to wild type, most of the centrosomes in epithelial cells fail to dissociate from microtubules and remain in close proximity to adherens junctions throughout axis elongation (stages 6 and 7) in obe1/obe2 embryos derived from obe1/obe2 females crossed to obe2/+ males. This results in a failure of the centrosomes to relocalise laterally. The mis-positioned centrosomes are often associated with adherens junction aggregates.
The adherens junction and centrosome defects seen in stage 7 obe1/obe2 embryos derived from obe1/obe2 females crossed to obe2/+ males are rescued by nocodazole treatment (which inhibits microtubule polymerisation).
obe1/obe2 is rescued by obeCH322-15H13
Separable mutation isolated in the P{XP}Surf4d04274 insertion line.