TGF-β Controls miR-181/ERK Regulatory Network during Retinal Axon Specification and Growth
Fig 5
TGF-β signaling regulates RhoA levels via two independent and synergistic cascades.
(a) qRT-PCR analysis of erk2 transcripts in total eye RNA derived from St32 control-MOs, miR-181a/b morphants and TGF-β-treated miR-181a/b morphants. The TGF-β-mediated increase of miR-181a/b caused a rescue of miR-181a/b target transcripts, such as prox1 and erk2, in miR-181a/b morphants. (b, c) Representative Western blotting on protein from St32 eyes (b) and corresponding quantification (c) show that administration of TGF-β to MO-miR-181a/b embryos leads to restoration of total-, phospho-Erk2 and RhoA protein levels. When MO-miR-181a/b embryos were treated with both TGF-β and the proteasomal inhibitor MG132, total- and phospho-Erk2 protein levels were still rescued, whereas RhoA levels were only partially rescued. Data are means +SEM.* P <0.05; **P <0.01; *** P <0.001 (two-way ANOVA).