Skip to main content
Figure 4 | Genome Biology

Figure 4

From: PDGF/VEGF signaling controls cell size in Drosophila

Figure 4

Pvf/Pvr signaling activates a network of signaling modules upstream of the Tor pathway. (a) Gap1 RNAi epistasis. Ras1, Rheb, Tor and S6k dominate in their effect on cell size, ERK suppresses the Gap1 RNAi phenotype, whereas Raf, p110 and Akt only partially ameliorate the large increase in cell size seen following Gap1 RNAi. The insulin receptor has little effect in this assay. (b) Tsc2 RNAi epistasis. Rheb and S6k dominate, placing them genetically downstream of Tsc2. Pvr, Ras1 and members of the MAPK and PI3K pathways fail to have a dramatic impact on the Tsc2 RNAi phenotype. (c) Raf (pole hole) RNAi epistasis. Silencing of Raf leads to a minor reduction in cell size. However, silencing of Raf in conjuction with p110 or Akt1 causes a large reduction in cell size, like that seen in Pvr, Ras, Tor, Rheb, and S6K RNAi experiments. (d) MAPK and PI3K pathway genetic interactions. Raf, ERK and Ksr all show additive or synergistic genetic interactions with p110 and Akt1, but not with InR. Furthermore, these genetic interactions are stronger than those seen when combining p110 or Akt1 dsRNA with dsRNA targeting upstream or downstream pathway components of this putative growth signaling network (Pvr/Ras1 and Tor/S6k, respectively). Error bars indicate the standard error of the mean.

Back to article page