The genes for beta-myosin heavy chain and glycogen phosphorylase are discoordinately regulated during compensatory growth of plantaris muscle in the adult rat.
It has been shown previously that compensatory hypertrophy of the plantaris muscle in adult rats can be induced by surgical removal of the synergistic gastrocnemius muscle. During hypertrophy, muscle transformation also occurs and there is a shift in the fiber type population of the muscle from fast to slow. Towards obtaining a better understanding of the molecular mechanisms controlling this process, we have carried out a kinetic analysis of the change in expression of two muscle-specific genes encoding the slow beta-heavy chain isoform of myosin and the muscle isoform of glycogen phosphorylase. This analysis indicated that significant increases (2-3 fold) in the steady-state levels of slow myosin heavy chain mRNA and protein did not occur until several weeks following ablation of the gatrocnemius muscle. Increases in slow fiber type paralleled the change in beta-myosin heavy chain expression. In contrast, the activity of phosphorylase, as well as the level of its corresponding mRNA, decreased approx. 1.5-2 fold shortly after (2-4 days) ablation of the gastrocnemius and levels remained low for at least several weeks. Significant changes in expression of these genes did not occur in plantaris muscle from sham operated contralateral legs. These studies indicated that changes in the expression of both genes was governed primarily by accumulation of their mRNAs. However, these genes were not coordinately regulated, indicating either that multiple control mechanisms regulate gene expression in this system or that the same controlling factor(s) regulates expression of these genes in temporally different ways.
Crerar
M M
MM
Department of Biology, York University, Ont., Canada.
Hamilton
N C
NC
Blank
S
S
Urdea
M S
MS
Ianuzzo
C D
CD
D000818:Animals; D005786:Gene Expression Regulation; D005796:Genes; D006984:Hypertrophy / Q000378:metabolism; D008297:Male; D009132:Muscles / Q000378:metabolism* / Q000473:pathology; D009218:Myosins / Q000096:biosynthesis / Q000235:genetics*; D006005:Phosphorylases / Q000096:biosynthesis / Q000235:genetics*; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D011919:Rats, Inbred Strains
D012333:RNA, Messenger; D006005:Phosphorylases; D009218:Myosins