Tworoger M, Larkin M K, Bryant Z, Ruohola-Baker H
Department of Biochemistry, University of Washington, Seattle, Washington 98195-7350, USA.
Genetics. 1999 Feb;151(2):739-48. doi: 10.1093/genetics/151.2.739.
The fates of two small subgroups of the ovarian follicle cells appear to be linked: mutations in Notch, Delta, fs(1)Yb, or hedgehog cause simultaneous defects in the specification of stalk cells and polar cells. Both of these subgroups are determined in the germarium, and both cease division early in oogenesis. To test the possibility that these subgroups are related by lineage, we generated dominantly marked mitotic clones in ovaries. Small, restricted clones in stalk cells and polar cells were found adjacent to each other at a frequency much too high to be explained by independent induction. We therefore propose a model in which stalk cells and polar cells are derived from a precursor population that is distinct from the precursors for other follicle cells. We support and extend this model by characterization of mutants that affect stalk and polar cell formation. We find that ectopic expression of Hedgehog can induce both polar and stalk cell fate, presumably by acting on the precursor stage. In contrast, we find that stall affects neither the induction of the precursors nor the decision between the stalk cell and polar cell fate but, rather, some later differentiation step of stalk cells. In addition, we show that ectopic polar and stalk cells disturb the anterior-posterior polarity of the underlying oocyte.
Notch、Delta、fs(1)Yb或刺猬蛋白（hedgehog）的突变会导致柄细胞和极细胞特化同时出现缺陷。这两个亚群均在卵巢原基中被确定，并且在卵子发生早期都停止分裂。为了测试这些亚群是否通过谱系相关联，我们在卵巢中生成了显性标记的有丝分裂克隆。在柄细胞和极细胞中发现的小的、局限的克隆彼此相邻，其频率过高，无法用独立诱导来解释。因此，我们提出了一个模型，其中柄细胞和极细胞源自一个不同于其他卵泡细胞前体的前体群体。我们通过对影响柄细胞和极细胞形成的突变体进行表征来支持并扩展这一模型。我们发现刺猬蛋白的异位表达可以诱导极细胞和柄细胞命运，大概是通过作用于前体阶段。相比之下，我们发现stall既不影响前体的诱导，也不影响柄细胞和极细胞命运之间的决定，而是影响柄细胞的一些后期分化步骤。此外，我们表明异位的极细胞和柄细胞会扰乱其下方卵母细胞的前后极性。
