Bishop D L, King R C
J Cell Sci. 1984 Apr;67:87-119. doi: 10.1242/jcs.67.1.87.
Females homozygous for the otu7 allele produce ovarian tumours, as well as egg chambers that reach a relatively late stage of development. Mutant ovarian nurse cells contain giant polytene chromosomes. These are transcriptionally active, and RNA is transported to the oocyte through ring canals, although at reduced rate. Vitellogenic oocytes are endocytotically active. Protein (alpha yolk) spheres are formed, but glycogen (beta yolk) spheres were never seen in the ooplasm. Follicle cells migrate normally and secrete more vitelline membrane and chorion than is required to cover the slowly growing oocyte. Specialized follicle cells also secrete relatively normal dorsal appendages. The micropylar cone is secreted by another cluster of specialized follicle cells called border cells. These are out of phase with the oocyte, and the forming micropylar cone prevents the nurse cells from passing the remainder of their cytoplasm to the oocyte. The result is a morphologically abnormal chamber blocked at the p-12 stage. Sections through the micropylar cone of a p-12 chamber demonstrated that one of the border cells formed a projection containing a bundle of microtubules. Secretions of the border cells were deposited against this tube, which later degenerates or is withdrawn. Normally this results in a canal, the micropyle, through which the sperm enters the egg. The slowed growth of the mutant oocyte presumably results from a defect in the transport of fluids or charged molecules to it, and the otu+ gene is therefore believed to play a vital role in this process.
otu7等位基因纯合的雌性会产生卵巢肿瘤以及发育到相对较晚期的卵室。突变的卵巢滋养细胞含有巨大的多线染色体。这些染色体具有转录活性,RNA通过环管运输到卵母细胞,尽管运输速率降低。卵黄生成期的卵母细胞具有活跃的内吞作用。会形成蛋白质(α卵黄)球,但在卵质中从未见过糖原(β卵黄)球。卵泡细胞正常迁移,分泌的卵黄膜和卵壳比覆盖缓慢生长的卵母细胞所需的更多。特化的卵泡细胞也分泌相对正常的背侧附属物。卵孔锥由另一群称为边缘细胞的特化卵泡细胞分泌。这些细胞与卵母细胞不同步,正在形成的卵孔锥阻止滋养细胞将其剩余的细胞质传递给卵母细胞。结果是在p-12阶段形成了一个形态异常的卵室。对p-12卵室的卵孔锥切片显示,其中一个边缘细胞形成了一个包含一束微管的突起。边缘细胞的分泌物沉积在该管上,该管随后退化或缩回。正常情况下,这会形成一个管道,即卵孔,精子通过它进入卵子。突变卵母细胞生长缓慢可能是由于向其运输液体或带电分子存在缺陷,因此认为otu+基因在这一过程中起着至关重要的作用。