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The Role of Epigenetics in Skeletal Muscle Adaptations to Exercise and Exercise Training
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
It is generally well accepted that repeated bouts of acute exercise and corresponding dynamic alterations in the expression of exercise-responsive genes play an important role in skeletal muscle adaptations to exercise training. However, a key question is whether exercise training induces stable epigenetic alterations that could confer a persistent memory of muscle adaptation. A number of studies have observed hypomethylation of exercise-responsive genes in skeletal muscle following exercise training interventions (28, 35, 46), which were generally associated with gene expression patterns. Gene ontology analysis found that many of the gene regions that displayed reduced methylation following exercise training were associated with various metabolic processes and insulin signalling (46). Interestingly, many of these same pathways were also identified in ontology analysis of gene regions that displayed increased methylation after training (46). The functional significance of these findings remains unclear, but could be explained by other findings that have questioned the extent to which methylation contributes to the global control of gene expression levels in differentiated tissue (20, 69). Nitert and colleagues (46) directly addressed this question by analysing the effect of methylation on promoter reporters of a number of genes found to be hypomethylated in skeletal muscle following exercise training. These experiments showed that methylation of the promoters of the NDUFC2, RUNX1, MEF2A, and THADA genes significantly reduced reporter expression (46), providing strong evidence that hypomethylation of these gene regions enhances the transcription of these genes. The concept of an exercise training transcriptional memory has also been examined more directly in a well-controlled study where subjects completed two 3-month training periods, separated by a 9-month period of detraining (34). Following the 9-month detraining period, there was no retention of the training-induced transcriptional profile, although there were subtle differences in the transcriptional response to the second training period (34). At present no studies have rigorously assessed whether histone modifications are persistently altered following exercise training. However, given the short half-life and enzymatic reversibility of these modifications, it is difficult to envisage a scenario where persistent histone modifications contribute to maintenance of a training phenotype. On balance, these data collectively suggest that there is not a clearly defined epigenetic memory of exercise training that is retained beyond the termination of training.
Effects of psychoactive drugs on cellular bioenergetic pathways
Published in The World Journal of Biological Psychiatry, 2021
Chiara C. Bortolasci, Briana Spolding, Srisaiyini Kidnapillai, Mark F. Richardson, Nina Vasilijevic, Sheree D. Martin, Laura J. Gray, Sean L. McGee, Michael Berk, Ken Walder
After genome-wide correction for multiple testing using FDR, valproate significantly increased the expression of NDUFA4 (q = 0.019) and NDUFAF4 (q = 0.004) from Complex 1, COX5A (q = 0.010) from Complex 4 and ATP5B (q = 0.00045) from Complex 5. Quetiapine increased the expression of NDUFA6-AS1 (q = 0.039, Complex 1), UQCRC2 (q = 0.0019, Complex 3) and COX7A2L (q = 0.00027, Complex 4). Quetiapine also decreased the expression of NDUFA1 (q = 0.025), NDUFA12 (q = 0.041), NDUFAF4 (q = 0.0037), NDUFB3 (q = 0.0053), NDUFC2 (q = 0.0086), NDUFS1 (q = 0.00014), NDUFS2 (q = 0.0029), NDUFS3 (q = 2.3E-06) and NDUFS5 (q = 0.0015) from Complex 1, as well as SDHA (q = 0.023, Complex 2), UQCR10 (q = 0.0060), UQCR11 (q = 0.0045) and UQCRC2 (q = 0.0019) from Complex 3, COX6B1 (q = 0.022) and COX7A2L (q = 0.00027, Complex 4), and ATP5A1 (q = 0.025), ATP5B (q = 5.1E-09), ATP5F1 (q = 0.00017), ATP5G1 (q = 0.00056), ATP5H (q = 0.0085), ATP5J (q = 0.048) and ATP5J2 (q = 0.015) from Complex 5. Lithium increased the expression of ATP5J2 (q = 0.028, Complex 5), while lamotrigine did not significantly affect expression of any of the OXPHOS genes measured.