Amino acid replacement: A777T.
Nucleotide substitution: G2424A.
G7923311A
G2424A
A777T | lds-PA
A777T
female sterile (with lds3)
The rate of Y chromosome loss in the developing wing imaginal disc in heterozygous males is significantly higher than that seen in wild type.
Heterozygous females deposit normal numbers of normal-looking eggs. However, cleavage divisions do not occur in more than 90% of the eggs. In those eggs in which cleavage divisions are seen, only approximately 12 scattered chromosomes appear, along with unusual microtubule bundles. Abnormal segregation of the chromosomes is already apparent during both the first and second meiotic divisions.
Cytoplasm from newly deposited eggs laid by heterozygous females induces defects during division when injected into lds[+] embryos, producing chromosome tangling during anaphase and telophase, the formation of chromatin bridges, abnormally shaped and positioned nuclei and free centrosomes.
9.1% of the offspring of heterozygous males are XX//X0 mosaics.
Hemizygous flies are viable and emerge with the expected frequency. The females deposit normal numbers of normal-looking eggs which are fertilised, but embryogenesis never commences in these eggs. Fertility of hemizygous males is also strongly reduced. 6.7% of the offspring of ldsHor-D/Df(3R)dsx15 males are XX//X0 mosaics.
XX//X0 mosaics are seen in the progeny of ldsHor-D/lds3 males at a low frequency.
Analysis of germ-line chimeras indicates that the ldsHor-D defects are due to an effect in germ-line cells and not in somatic cells.
Gynandromorph formation is a consequence of the mutation. The gynandromorphs originate through loss and not nondisjunction of the paternally derived X chromosome. Unknown genetic factors contributed by both parents can alter the frequency of X chromosome loss in the zygote. The presence of factors renders the fourth chromosome highly or moderately sensitive to chromosome loss causing haplo-4 mosaics. The second and third chromosomes can also be rendered unstable, Y chromosome remain stable. Derived XO males originate through the fertilization of X eggs by nullo-X sperm, mutation induces mostly equational nondisjunction during spermatogenesis. Males showing abnormal cysts have sperm bundles in which the spermatid heads are not attached to the sperm tails and are abnormally distributed.
Female viability and male fertility are not reduced. The female and male pronuclei approach each other and almost fuse, however that do not divide. Phenotype is not fully penetrant so some embryos develop to the blastoderm stage.
