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Title: OVEREXPRESSION OF THE REPRESSOR PROTEIN ID-I IN SKELETAL MUSCLE IMPAIRS MYOFIBRILLAR GENE EXPRESSION BUT NOT MYOFIBRILLAR PROTEIN SYNTHESIS

Author
item Fiorotto, Marta
item ROSENBERGER, JUDY - BAYLOR COLL OF MEDICINE
item DONOVAN, MICHAEL - BAYLOR COLL OF MEDICINE

Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract Only
Publication Acceptance Date: 3/23/2004
Publication Date: 4/17/2004
Citation: Fiorotto, M.L., Rosenberger, J., Donovan, M. 2004. Overexpression of the repressor protein Id-I in skeletal muscle impairs myofibrillar gene expression but not myofibrillar protein synthesis [abstract]. Federation of American Societies for Experimental Biology Conference. 18(4):A356.

Interpretive Summary: Not needed for an Abstract

Technical Abstract: Fast-twitch skeletal muscle growth is impaired when Id overexpression is high. We hypothesized that Id proteins, by inhibiting muscle-specific transcription factor activity, reduce the abundance of myofibrillar mRNAs and, consequently, the capacity to synthesize myofibrillar proteins. The objective of the study was to delineate the contribution of mRNA abundance to the synthesis rate of individual myofibrillar proteins in transgenic mice with muscle-specific overexpression of Id-1. Studies were performed in 5, 10, 20, and 35-d-old transgenic and wild-type littermates (n=5-6 per group). In vivo fractional synthesis rates of myosin heavy chain (MHC), actin, and myosin light chains (MLC) 1 and 2 (fast isoforms) were measured using a flooding dose of [3H]-phenylalanine. The corresponding mRNAs were quantified and expressed relative to total muscle poly(A) and 18S rRNA abundances. We determined that the abundances of all myofibrillar mRNAs were 50-70% lower in transgenic compared to wild-type mice at 5, 10, and 20 d of age, yet the synthesis rates of only the MLCs were reduced (by 10%), with no effect on MHC and actin synthesis rates. We conclude that suppression of muscle growth by Id proteins is not mediated by an impairment in the relative synthesis rate of myofibrillar proteins consequent to the inhibition of muscle-specific gene expression.