Johnson E, Wayne S, Nagoshi R
Genetics Program, University of Iowa, Iowa City 52242, USA.
Genetics. 1995 May;140(1):207-17. doi: 10.1093/genetics/140.1.207.
Phenotypic and genetic analyses demonstrate that fs (1) Yb activity is required in the soma for the development of a subset of ovarian follicle cells and to support later stages of egg maturation. Mutations in fs (1) Yb cause a range of ovarian phenotypes, from the improper segregation of egg chambers to abnormal dorsal appendage formation. The mutant phenotypes associated with fs (1) Yb are very similar to the ovarian aberrations produced by temperature-sensitive alleles of Notch and Delta. Possible functional or regulatory interactions between fs (1) Yb and Notch are suggested by genetic studies. A duplication of the Notch locus partially suppresses the female-sterility caused by fs (1) Yb mutations, while reducing Notch dosage makes the fs (1) Yb mutant phenotype more severe. In addition, fs (1) Yb alleles also interact with genes that are known to act with or regulate Notch activity, including Delta, daughterless, and mastermind. However, differences between the mutant ovarian phenotype of fs (1) Yb and that of Notch or Delta indicate that the genes do not have completely overlapping functions in the ovary. We propose that fs (1) Yb acts as an ovary-specific factor that determines follicle cell fate.
表型和遗传分析表明,fs(1)Yb活性在体细胞中是卵巢卵泡细胞亚群发育以及支持卵成熟后期所必需的。fs(1)Yb的突变会导致一系列卵巢表型,从卵室的不正确分离到异常的背附肢形成。与fs(1)Yb相关的突变表型与Notch和Delta的温度敏感等位基因产生的卵巢畸变非常相似。遗传研究表明fs(1)Yb与Notch之间可能存在功能或调控相互作用。Notch基因座的重复部分抑制了由fs(1)Yb突变引起的雌性不育,而降低Notch剂量会使fs(1)Yb突变体表型更严重。此外,fs(1)Yb等位基因还与已知与Notch活性相互作用或调控Notch活性的基因相互作用,包括Delta、无女儿基因和主谋基因。然而,fs(1)Yb的突变卵巢表型与Notch或Delta的突变卵巢表型之间的差异表明,这些基因在卵巢中并不具有完全重叠的功能。我们提出,fs(1)Yb作为一种卵巢特异性因子,决定卵泡细胞命运。