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. Author manuscript; available in PMC: 2013 Sep 21.
Published in final edited form as: Biochem Biophys Res Commun. 2012 Aug 19;426(2):183–189. doi: 10.1016/j.bbrc.2012.08.058

Figure 2. Forced expression of non-canonical microRNAs miR-320 and miR-702 in Dicer- deficient ESCs promotes proliferation.

Figure 2

(A) miR-320 and miR-702 increased the proliferation rate of Dicer-deficient (DcrΔ/Δ) ESCs to that of Dgcr8-deficient (Dgcr8Δ/Δ) ESCs, rescuing the severe proliferation defect. Each value is represented relative to an assigned Dgcr8Δ/Δ value of 1.0. Data are presented as mean +/− SD with N=3. (B) Dgcr8-deficient ESCs accumulated in the G1 phase of the cell cycle compared to wild-type (Wt) ESCs. Dicer-deficient ESCs accumulated in the G1 phase even more than Dgcr8-deficient ESCs. Transducing miR-320 or miR-702 mimic into Dicer-deficient ESCs decreased the proportion of cells in G1. Data are presented as mean +/− SD with N=5. (C, D) Expression levels determined by qRT-PCR (C) and immunoblot analysis (D) of cyclin-dependent kinase inhibitors p21, p27, and p57 demonstrate upregulation in Dicer-deficient ESCs compared to Dgcr8-deficient ESCs. With the introduction of miR-320 or miR-702 into Dicer-deficient ESCs, mRNA levels of all three cyclin-dependent kinase inhibitors showed decreasing trend (C), while only p21 and p57 protein levels were clearly downregulated (D). α-tubulin expression level was used as loading control for the protein blot. For (C), each value is represented relative to an assigned Dgcr8Δ/Δ values of 1.0, and data are presented as mean +/− SD with N=3.