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. Author manuscript; available in PMC: 2013 Aug 10.
Published in final edited form as: Mol Cell. 2012 Jun 21;47(3):422–433. doi: 10.1016/j.molcel.2012.05.014

Figure 2.

Figure 2

SRPKs are the major branch in the EGF pathway for global regulation of alternative splicing. (A) EGF induced widespread splicing changes from a global scale, which was largely diminished in SRPK1/2 knockdown cells (p<2.2e-16 according to KS-test). Red dots in the left panel represent splicing ratio changes ≥ 2. Although some changes were detectable in response to double knockdown of SRPK1 and SRPK2 (green dots in the right panel), the magnitude of ratio changes in those cases was much lower. (B) EGF-induced alterative splicing before and after knocking down SRPK1/2. (C) EGF activated multiple signaling branches, including the JAK/STAT, PI3K/Akt, ERK/MAPK and mTOR pathways, each of which could be blocked by a specific inhibitor. (D) Wortmannin effectively blocked EGF-induced splicing, while inhibition of all other pathways had much less effects (see the degree of individual responses in Table S1). (E) A selective panel of splicing events induced by EGF was examined by RT-PCR under different treatment conditions. SRPK knockdown and Wortmannin treatment showed a similar effect in each case, while other inhibitors had minor, if any, effects. The efficiency of SRPK knockdown was shown at bottom.