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. Author manuscript; available in PMC: 2014 Jul 15.
Published in final edited form as: Cell Rep. 2014 Feb 27;6(5):818–826. doi: 10.1016/j.celrep.2014.01.045

Figure 3. mTOR signaling is required for up regulation of Fgf10.

Figure 3

(A) Alignment of RefSeq gene sequences with mouse genome shows that Fgf10 mRNA has a TOP-like sequence motif, defined as containing at least five pyrimidines within four nucleotides of the transcription start site. The Fgf10 5’UTR sequences carrying either wild type TOP-like sequence (wtTOP) or 6 bp transversion mutations (mutTOP) were cloned into GFP reporter vectors. (B) In transfected NIH-3T3 cells, Torin suppresses phosphorylation of S6 and 4EBP1, and expression of GFP in wild type but not mutant Fgf10 reporters. Rapamycin (rap) treatment, however, abolished S6 phosphorylation, but left 4EBP1 phosphorylation partially reduced and GFP expressions unchanged. (C) A reduction in levels of mTORC1 downstream effectors (p4EBP1 and pS6) and Fgf10 was seen in lysates from PtenCKO;RaptorCKO mice. (D-P) Phenotypic comparison of facial skin in wild type (n=9), PtenCKO (n=9), PtenCKO;RictorCKO (n=9) and PtenCKO;RaptorCKO (n=3) mice; Rescue of the hyperkeratosis (L) and loss of Fgf10 (P) were observed in PtenCKO;RaptorCKO mice. One-way ANOVA test: * P < 0.001; N.S., not significant. Data are presented as mean ± s.e.m. White and black arrows point to facial skin (E-H) and epidermis (I-P), respectively.