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ABSTRACT IS WITHDRAWN. (1164.8)
Author(s) -
Kirby Tyler,
Fry Christopher,
Jackson Janna,
Chaillou Thomas,
Peterson Charlotte,
McCarthy John
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.1164.8
Subject(s) - ribosome biogenesis , satellite , muscle hypertrophy , rna , biology , cell growth , cell , microbiology and biotechnology , ribosomal rna , medicine , ribosome , endocrinology , gene , biochemistry , engineering , aerospace engineering
We previously reported that hypertrophy of skeletal muscle can occur independent of satellite cell fusion; however, the compensatory mechanism allowing this growth to occur remains unknown. mTOR signaling and total protein content were unaffected by the loss of satellite cell fusion, arguing against a compensatory mechanism involving translation. Alternatively, total RNA content was maintained even though DNA accrual was blocked by the absence of satellite cell fusion. Based on this finding, we postulated that in the absence of satellite cell fusion, myonuclei would increase their transcriptional output in order to maintain RNA levels and thus muscle growth. Preliminary data revealed that RNA:DNA ratio and RNA content per myonucleus was greater in satellite cell‐depleted muscle, which was accompanied by an increase in myonuclear size. Though the significance of this observation remains to be determined, we hypothesize the change in myonuclear shape is indicative of an increase in transcriptional output, specifically ribosomal RNA. Consistent with this idea, we measured under hypertrophic conditions a difference in 28S and 18S content as well as pre‐47S transcript levels in satellite cell‐depleted muscle relative to muscle with a full complement of satellite cells. Thus, it appears myonuclei are able to compensate for the loss of satellite cell fusion during hypertrophy by increasing ribosomal biogenesis. Grant Funding Source : Supported by R01AR060701