bk1 << p1:bk1 << p1:bk6 << bk2
Dp(1;f)γ878/Dp(1;f)26C heterozygotes increases y+ expression, to 46% of full Dp(1;f)γ158 trans-suppression - relative suppression. y+ expression is quantitated in triple row bristles.
Transmission rate through females to progeny is 1.4% in the first 5 days of egg lay. Transmission is improved in the presence of increased nod+ dosage, provided by P{flag-nodhsp}.
Acentric mini-chromosomes are lost at a moderate but elevated rate during male germline mitotic divisions and in female mitosis, but appear to be transmitted efficiently through pre-blastoderm mitoses and male meiosis. mit(1)15 can localise to the mini-chromosome. Acentric mini-chromosomes are normally inherited, transmission is achieved by a mechanism similar to normal centromere-containing chromosomes, which utilises nod and mit(1)15 and involves movement to the spindle poles. Newly generated acentric fragments from the tip of the normal X chromosome do not display neocentromere activity in male meiosis I.
Minichromosome is 285kb in length is missing all centric heterochromatin and retaining only euchromatic sequences and subtelomeric heterochromatin.
Acentric terminal deficiency, 285kb in length containing no centric heterochromatin.
Monosome transmission behaviour from both male and female parents is highly unstable, all heterochromatin is deleted.
Deletion removing centromere.