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Exercise causes repositioning of the ‐1 nucleosome within the PGC1α promoter in association with altered gene expression in skeletal muscle (705.7)
Author(s) -
Henagan Tara,
Covington Jeffrey,
Stewart Laura,
Galgani Jose,
Ravussin Eric,
Bajpeyi Sudip
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.705.7
Subject(s) - methylation , dna methylation , promoter , gene expression , biology , nucleosome , gene , endocrinology , medicine , genetics , histone
Skeletal muscle PGC1α expression is epigenetically regulated by promoter methylation. Methylation status at the ‐260 nucleotide (nt) within the promoter plays an important regulatory role in determining PGC1α expression and consequently mitochondrial number and function and insulin sensitivity. Here we identified ‐1 nucleosome (‐1N) position within the PGC1α promoter in muscle from sedentary, lean men (n=18, aged 24±1 yrs, BMI 23.8±0.4) before and immediately after an acute bout of exercise (50% VO2max, ~650 kcal). Nucleosome position was measured by scanning PCR. At baseline, the ‐1N position spanned the promoter region from nt ‐350 to ‐190, covering the regulatory ‐260 nt methylation site. Following the exercise bout, the ‐1N was repositioned upstream, spanning the region from nt ‐500 to ‐300. PGC1α expression was significantly increased (1.05±.08 to 1.29±0.11 fold change, P = 0.02) following the exercise bout. Increased PGC1α expression was correlated with the upstream ‐1N position following the exercise bout (R2 = 0.43, P = 0.03). We provide evidence that an acute bout of exercise repositions the ‐1N in the PGC1α promoter upstream of the regulatory ‐260 nt methylation site, which may prevent DNA methyltransferase recruitment and methylation thus causing increased gene expression. Grant Funding Source : Support by NIH NIDDK 5T32‐DK064584‐09 (TMH)