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. Author manuscript; available in PMC: 2018 Sep 1.
Published in final edited form as: J Mol Cell Cardiol. 2017 Jul 20;110:80–95. doi: 10.1016/j.yjmcc.2017.07.005

Figure 4.

Figure 4

Figure 4

Cardiomyocyte-specific Bmal1 deletion alters autophagy markers in the heart. CBK and littermate control (CON) mouse hearts were collected at distinct times of day, followed by Western blot and RT-PCR analysis for mTOR (A; 3–7 independent observations), ULK1 (B; 3–7 independent observations), LC3 (C; 3–7 independent observations), and p62 (D; 3–7 independent observations). In a separate set of studies (E; 3–7 independent observations), CBK and CON mice were either fed ad libitum or fasted for 16 hours (ZT4 to ZT20), followed by collection of hearts (at ZT20), and subsequent assessment of LC3 lipidation, p62, and accumulation of autophagosomes. Data are represented as fold change from the trough of CON hearts (A, B, C, D), or as fold change from CON hearts from ad libitum fed mice (E). Data for ZT0 is duplicated as ZT24 for visualization purposes only (A, B, C, D). All data are shown as mean ± SEM. *, p<0.05 for CBK versus CON hearts within a ZT (A, B, C, D), or CBK versus CON hearts within a fed/fasted experimental group (E).