Role of Notch pathway in terminal follicle cell differentiation during Drosophila oogenesis

Abstract

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.

Delta signaling from the germ line controls the proliferation and differentiation of the somatic follicle cells during Drosophila oogenesis

“…The up-regulation of FasIII in Notch mutants has previously been interpreted as transformation to polar follicle cell fate (Ruohola et al 1991;Goode et al 1996b;Larkin et al 1999). As pointed out by Zhang and Kalderon (2000), however, FasIII is also expressed by all follicle cells earlier in oogenesis, and an alternative explanation for this phenotype is that the mutant cells are arrested in an immature state.…”

“…It has previously been reported that temperature-sensitive alleles of the DSL ligand, Delta, cause many of the same phenotypes as Notch ts , whereas germ line clones of Delta do not, suggesting that Delta is required in the somatic follicle cell layer for the activation of Notch (Ruohola et al 1991;Larkin et al 1999). We therefore generated follicle cell clones of a strong loss of function allele, Dl…”

“…Furthermore, Delta germ line clones have also been reported to have no effect on axis formation, and several studies have supported the conclusion that Delta is required in the follicle cells as well (Ruohola et al 1991;Bender et al 1993;Larkin et al 1999). Thus, Delta and Notch must act upstream of the signaling to the oocyte and presumably play a role in the patterning of the follicle cells.…”

“…This has led to the suggestion that the defects in A-P axis formation may be a consequence of forming too many posterior polar cells at the expense of the stalk cells . However, these egg chambers also show defects in the specification and patterning of the anterior and posterior terminal populations of epithelial follicle cells (González-Reyes and St. Johnston 1998;Larkin et al 1999). Thus, an alternative model is that Notch signaling is required for the formation of the terminal follicle cells, which, unlike the main-body cells, are competent to respond to Gurken by becoming posterior.…”

Lethal(2)giant larvae is required in the follicle cells for formation of the initial AP asymmetry and the oocyte polarity during Drosophila oogenesis

“…A number of mutants have been identified that abolish this signal. Among those mutants, many disrupt the specification of the posterior follicle cell fate, rather than the signaling pathway itself [16,17,[51][52][53]. As presented above, Lgl is required in the posterior follicle cells for both the restricted localization of the polarity determinants and the reorganization of the MT cytoskeleton in the oocyte.…”