Szabad J, Hoffmann G
Institute of Genetics, Biological Research Center, Hungarian Academy of Sciences, Szeged.
Dev Biol. 1989 Jan;131(1):1-10. doi: 10.1016/s0012-1606(89)80033-8.
Fs(3)Apc is a dominant female-sterile mutation of Drosophila melanogaster which causes an incomplete migration of follicle cells between the oocyte and the nurse cells. This leads to leakage of anterior egg cytoplasm followed by degeneration of the egg primordium or deposition of flaccid eggs with reduced anterior egg coverings including the dorsal appendages. Analysis of ovarian and germ-line chimeras revealed that the focus of the Apc phenotype is located in the ovarian soma. Apc+ clones, induced by mitotic recombination, lead to the formation of "exceptional" eggs with (often partial) rescue of the mutant phenotype. Analysis of Apc+ mosaics shows that the Apc mutant phenotype depends on the genotype of the anterior follicle cells. The patterns of apparent Apc+ clones suggest that there is no lineage restriction between the follicle cells that form the anterior egg coverings and those that form the dorsal appendages at the follicle envelope stage.
Fs(3)Apc是黑腹果蝇的一种显性雌性不育突变，它会导致卵泡细胞在卵母细胞和滋养细胞之间的迁移不完全。这会导致前极卵细胞质泄漏，随后卵原基退化或产出松弛的卵，其前极卵覆盖物（包括背附器）减少。对卵巢和生殖系嵌合体的分析表明，Apc表型的焦点位于卵巢体细胞中。通过有丝分裂重组诱导产生的Apc+克隆会导致形成“异常”卵，突变表型（通常是部分）得到挽救。对Apc+嵌合体的分析表明，Apc突变表型取决于前卵泡细胞的基因型。明显的Apc+克隆模式表明，在卵泡包膜阶段形成前极卵覆盖物的卵泡细胞与形成背附器的卵泡细胞之间不存在谱系限制。
