Skip to main content
. 2016 Sep 7;36(36):9454–9471. doi: 10.1523/JNEUROSCI.0936-16.2016

Figure 5.

Figure 5.

Tgfβ signaling is promoted by Akt and acts cell autonomously to block amacrine cell differentiation. A–C, E18.5 retinas electroporated with pCIG2 control (A), TgfβRII-CA (B) or TgfβRII-DN (C) and cultured for 8 DIV. GFP+ (green) electroporated amacrine cells were identified by Pax6 immunolabeling (red). Blue is a DAPI counterstain. D, Percentages of GFP+ amacrine cells (GFP+Pax6+) after electroporation of pCIG2, TgfβRII-CA, or TgfβRII-DN. E, qPCR to assess Pax6 transcript levels in GFP+ cells sorted by FACS after electroporation of pCIG2, TgfβRII-CA, or TgfβRII-DN. F, GFP+ HEK cells 24 h after transfection. G–I, Western blot analysis and densitometry of pSmad2 after transfection of TgfβRII-CA (G), TgfβRII-DN (H), and Akt-CA (I). J, Schematic model of how amacrine cell differentiation is regulated by both Tgfβ and Pten signaling pathways. Note that pAkt could regulate pSmad2 via directly influencing phosphorylation of Smad2 or the upstream receptor TgfβRII. *p < 0.05; **p < 0.01; ***p < 0.001.