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. Author manuscript; available in PMC: 2021 Sep 17.
Published in final edited form as: Mol Cell. 2020 Aug 20;79(6):934–949.e14. doi: 10.1016/j.molcel.2020.08.002

Figure 7. NMNAT-1-dependent physiological ADPRylation by PARP-1 inhibits H2B-Ser36 phosphorylation and adipogenesis.

Figure 7.

(A) Eight-week old Dox-inducible Mural Chaser Parp1+/+ or Parp1loxp/loxp mice were treated with Dox for 9 days, followed by 8 weeks on a high-fat/high sucrose diet. Body weights of the mice were measured weekly following the start of the high-fat/high sucrose diet. Each point represents the mean + SEM (n = 7 in Parp1+/+ group, and n = 10 in Parp1loxp/loxp group). Asterisks indicate significant differences from Parp1+/+ at individual time point (Student’s t-test; ** p < 0.01, and *** p < 0.01).

(B) Mural Chaser Parp1+/+ or Parp1loxp/loxp mice were treated as described in (A). Fat mass (left panel) and lean mass (right panel) ratio (normalized to body weight) were measured after 8 weeks of high-fat/high sucrose diet feeding. Each bar represents the mean + SEM (n = 7 in Parp1+/+ group, and n = 10 in Parp1loxp/loxp group). Asterisks indicate significant differences from Parp1+/+ (Student’s t-test; ** p < 0.01).

(C) Model for NMNAT-1-dependent histone Glu/Asp ADPRylation by PARP-1 during the physiological process of adipogenesis. See details in the Discussion.