Approximately 3.5kb deletion that removes most of the coding sequence of all isoforms of Bsg25D. Generated by imprecise excision of P{EP}Bsg25DG13518; a portion of the original insertion, including the w+mC marker, is still present.
Approximate boundaries of a ~3.5 kb deletion resulting from the imprecise excision of P{EP}Bsg25DG13518 that removes most of the coding sequence of Bsg25D. A portion of the transposon including the w minigene remain at the site of the excision. The 3' boundary of the deletion was only approximately mapped to within a 300 bp region.
Bsg25D1/Bsg25D1 embryos only have a slightly reduced (non significant) embryo hatching rate compared to wild type and cleavage furrows and other aspects of cleavage (spindle morphology, nuclear positioning) appear normal. Bsg25D1/Bsg25D1 flies develop and survive similar to wild type in response to DNA damage (hydroxyurea or methyl methanesulfonate exposure). Bsg25D1/Bsg25D1 flies show similar climbing ability to controls and third instar larvae have similar central brain neuroblast numbers (with no overt effects on asymmetric cell division) as controls.
Nin1 is an enhancer of some die during embryonic stage phenotype of Rab1193Bi
Nin1 is an enhancer of majority die during embryonic stage phenotype of Rab1193Bi/Rab11j2D1
Bsg25D1 leads to a small but significant enhancements of reduced embryo hatching rates in Rab1193Bi/Rab1193Bi or Rab1193Bi/Rab11j2D1 mutants.
Bsg25D1 Cep135f01951 or Bsg25D1 Cep135c04199 double mutants do not overtly modify phenotypes (adult morphology, viability, female fertility) of Cep135f01951 or Cep135c04199 alone.
Bsg25D1 cnn25cn1 or Bsg25D1 cnnHK21 double mutants do not overtly modify phenotypes (adult morphological features, viability) of cnn25cn1 or cnnHK21 alone.
