Keller Larkin M, Deng W M, Holder K, Tworoger M, Clegg N, Ruohola-Baker H
Department of Biochemistry, J-581 Health Science Building, Box 357350, University of Washington, Seattle, WA 98195-7350, USA.
Dev Genes Evol. 1999 May;209(5):301-11. doi: 10.1007/s004270050256.
During Drosophila oogenesis the body axes are determined by signaling between the oocyte and the somatic follicle cells that surround the egg chamber. A key event in the establishment of oocyte anterior-posterior polarity is the differential patterning of the follicle cell epithelium along the anterior-posterior axis. Both the Notch and epithelial growth factor (EGF) receptor pathways are required for this patterning. To understand how these pathways act in the process we have analyzed markers for anterior and posterior follicle cells accompanying constitutive activation of the EGF receptor, loss of Notch function, and ectopic expression of Delta. We find that a constitutively active EGF receptor can induce posterior fate in anterior but not in lateral follicle cells, showing that the EGF receptor pathway can act only on predetermined terminal cells. Furthermore, Notch function is required at both termini for appropriate expression of anterior and posterior markers, while loss of both the EGF receptor and Notch pathways mimic the Notch loss-of-function phenotype. Ectopic expression of the Notch ligand, Delta, disturbs EGF receptor dependent posterior follicle cell differentiation and anterior-posterior polarity of the oocyte. Our data are consistent with a model in which the Notch pathway is required for early follicle cell differentiation at both termini, but is then repressed at the posterior for proper determination of the posterior follicle cells by the EGF receptor pathway.
在果蝇卵子发生过程中，体轴由卵母细胞与围绕卵室的体细胞滤泡细胞之间的信号传导决定。卵母细胞前后极性建立过程中的一个关键事件是滤泡细胞上皮沿前后轴的差异模式形成。Notch和上皮生长因子（EGF）受体途径对于这种模式形成都是必需的。为了了解这些途径在该过程中的作用方式，我们分析了伴随EGF受体组成型激活、Notch功能丧失和Delta异位表达时前后滤泡细胞的标志物。我们发现，组成型激活的EGF受体可诱导前滤泡细胞而非侧滤泡细胞产生后部命运，这表明EGF受体途径仅能作用于预先确定的终末细胞。此外，Notch功能在两端对于前后标志物的适当表达都是必需的，而EGF受体和Notch途径的缺失均模拟了Notch功能丧失的表型。Notch配体Delta的异位表达会干扰EGF受体依赖性的后滤泡细胞分化以及卵母细胞的前后极性。我们的数据与这样一种模型一致，即Notch途径在两端早期滤泡细胞分化中是必需的，但随后在后部被抑制，以便EGF受体途径正确确定后滤泡细胞。
