In wild type females, BicD RNA is detected very early in oogenesis in the 16 cystocyte cluster and progressively accumulates in a single cell, the oocyte. In BicDR26 mutants, BicD RNA does not localized to a single cystocyte, but is found in all of the pro-nurse cells.
13% of neuroblast mitoses are more than 45o off-axis in embryos derived from BicDHA40.T:Ivir\HA1 ; BicDR26/Df(2L)TW119 females mated to BicDR26/+ males (in contrast to wild type where all neuroblast divisions are oriented within 45o of the apicobasal axis). The average length of metaphase spindles in these mutant neuroblasts is significantly less than normal.
More than 4 cells per germline cyst enter meiosis in homozygous females, but the cysts still retain a graded distribution of the synaptonemal complex (SC), with the highest levels in the two pro-oocytes. The SC sometimes becomes restricted to these 2 cells in region 2b/3, but eventually disappears in region 3. The 2 cells eventually adopt the nurse cell fate.
When in combination with BicDH2, BicDH3 or BicDHA40.T:Ivir\HA1 over null or loss of function BicD, BicDR26 increases the proportion of ventralised eggs to 100%. When transheterozygous with a wild type allele, female fertility is normal.