Environmental cues signal through circadian control of sarcomeric gene expression during cardiomyocyte hypertrophy

Figures

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  Figure 1.. Postnatal and circadian regulation of Tcap and Myl2 expression.

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  Figure 2.. TCAP and Myl2 partially localize to the chromatin compartment of the nucleus.

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  Figure 3.. An isoproterenol phase response curve on NRVM treated with phenylephrine reveals effects of β-adrenergic stimulation on myocyte hypertrophy/atrophy and transcription of clock-controlled genes.

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  Figure 4.. An isoproterenol phase response curve on NRVM treated with phenylephrine reveals effects of β-adrenergic stimulation on TCAP and MYL2 expression. Following the experimental workflow described in Figure 2(A), TCAP, MYL2, and GAPDH immunoblots were performed (A, C) and quantified in (B, D). Indicated p-values generated by ordinary one-way ANOVA with Tukey’s post hoc analysis for pairwise comparisons.

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  Figure 5.. NRVM treated with phenylephrine reveals time-of-day dependent effects of α-adrenergic stimulation on expression of the secreted protein ANP and the ER-resident protein‑folding chaperones GRP94, GRP78, and PDIA6.

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  Figure 6.. Myocyte biomass influences the kinetics of myocyte growth and Per2 and TCAP transcription.

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  Figure 7.. Decreased oxygen causes myocyte atrophy in parallel with changes in clock-controlled gene expression and histone stoichiometry.

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  Figure 8.. The circadian clock transcriptionally remodels Tcap expression during hypoxia-driven changes in chromatin organization.

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  Figure 9.. TCAP depletion impairs expression of clock-controlled and hypertrophic genes. NRVM were transfected with control or TCAP-targeted siRNA followed by subjection to 0 % O2 for 24 h. Cultures were imaged for cell‑size measurements, followed by collection of whole‑cell protein lysate and total RNA.