Hippo promotion of mouse adipocyte differentiation via RNA‐binding protein phosphorylation. (A) Phase contrast images (left) and total DAG levels (right) of primary mouse adipocytes on days 0, 2, 6, and 8 after differentiation and co‐treatment with the Mst1 inhibitor Xmu‐mp‐1 (5 μM) or vehicle (DMSO) beginning on day 0. N = 3, ***p < 0.001, from Student's t‐test. (B) mRNA (RT‐qPCR, right) and protein (Western blot, left) levels of Lep, Fabp4, Adipoq, and Gcg mRNAs and proteins from pre‐adipocytes (Day 0) and mature adipocytes (Day 8) after treatment with the Mst1 inhibitor or vehicle. Values are expressed as mean ± SD of three independent experiments (p < 0.001, Student's t‐test). N = 3, ***p < 0.001, **p < 0.01, *p < 0.05, NS, not significant from Student's t‐test. (C) mRNA (RT‐qPCR, right) and protein (Western blot, left) levels of p16, p21, and Actb mRNAs and proteins from pre‐adipocytes (Day 0) and mature adipocytes (Day 8) after treatment with the Mst1 inhibitor or vehicle. Values are expressed as mean ± SD of three independent experiments (p < 0.001, Student's t‐test). N = 3, *p < 0.05, NS, not significant from Student's t‐test. (D) Gcg and Fabp4 mRNA stabilities were measured after inhibiting transcription with Actinomycin D in mouse 3 T3‐L1 cells before and after differentiation and with or without treatment with the Mst1 inhibitor. Data were normalized to 18S rRNA.