Fig. 5. YTHDF1 regulates BMP8B in an m⁶A-dependent manner.

a The mRNA and protein levels of BMP8B in iWAT from mice treated at RT or 4 °C. b The mRNA and protein levels of BMP8B in iWAT from Y1^CTL and Y1^cKO mice treated at 4 °C. c The mRNA level of Ythdf1 and Bmp8b in 3T3-L1 cells with or without YTHDF1 knockdown. d The protein levels of BMP8B expression in 3T3-L1 cells with or without Ythdf1 knockdown. e Polysome profiles of 3T3-L1 cells with or without YTHDF1 knockdown. f The distributions of Gapdh and Bmp8b in polysome fractions. g m⁶A peak distribution within Bmp8b transcripts. * indicates the predicted m⁶A peak. h Schematic of luciferase constructs with the predicted m⁶A sites in the CDS and 3′UTR of Bmp8b mRNA. i Luciferase activity of the Bmp8b reporter in 3T3-L1 cells with or without YTHDF1 knockdown. j Schematic of the mouse treatment regimen. k–m Mice were treated at 4 °C. k Oxygen consumption rates (OCR) of iWAT from Y1^CTL and Y1^cKO mice with or without BMP8B overexpression. Data were presented as mean ± SEM (n = 6 biologically independent mice). ****P < 0.0001. l The expression of BMP8B and UCP1 in iWAT from Y1^CTL and Y1^cKO mice with or without BMP8B expression. m H&E staining of iWAT depots from Y1^CTL and Y1^cKO mice with or without BMP8B expression. Scale bar, 50 μm. The white line indicated the average size. No adjustments. Data in a–c, f, and i were presented as mean ± SEM (n = 3). ns, not significant, *P < 0.05, ****P < 0.0001. All of the P-values are determined by unpaired two-sided t-test. Source data are provided as a Source Data file.