Transcriptional up‐regulation of the mouse gene for the muscle‐specific subunit of enolase during terminal differentiation of myogenic cells

Abstract

The glycolytic enzyme enolase (EC 4.2.1.11) exists as dimers formed from three structurally related subunits alpha, beta, and gamma, encoded by separate genes. The gene encoding the beta-subunit is expressed only in striated muscles. We have previously shown that the beta-enolase gene belongs to a small subset of muscle-specific genes showing transcriptional activity in cultured myoblasts, prior to withdrawal from the cell cycle. An increase in the level of beta-enolase mRNA occurs during terminal differentiation of myoblasts. To investigate the mechanisms underlying this increase, we have simultaneously estimated, under steady state conditions, the rate of synthesis and the stability of beta-enolase mRNA in proliferating C2.7 myoblasts as well as in differentiating myotubes. The method used is based on the isolation of newly synthesized RNA from the total RNA pool, following pulse-labeling of intact cells in the presence of 4-thiouridine. The results described here demonstrate a coordinate increase in newly synthesized and total beta-enolase mRNA, while the mRNA half-life, about 4 hr, remains unchanged in the course of terminal differentiation. The expression of the gene for insulin-like growth factor-II (IGF-II), a major positive regulator of myogenesis, was analyzed using the same approach. It is concluded that the up-regulation of beta-enolase as well as IGF-II gene expression in differentiating muscle cells reflects an increased rate of entry of newly synthesized mRNAs into the general pool of transcripts without changes in their respective half-lives.

Glycogen Debranching Enzyme 6 (AGL), Enolase 1 (ENOSF1), Ectonucleotide Pyrophosphatase 2 (ENPP2_1), Glutathione S-Transferase 3 (GSTM3_3) and Mannosidase (MAN2B2) Metabolism Computational Network Analysis Between Chimpanzee and Human Left Cerebrum

“…We inferred stronger lipid metabolism but weaker cell proliferation as a result of inducing cell differentiation in high-expression ENOSF1 metabolism network of human left cerebrum. We also found evidences from literatures to support this inference [33][34][35][36][37][38].…”

Assessing the translational landscape of myogenic differentiation by ribosome profiling

“…This led to the identification of 27 genes containing uORFs regulated during differentiation. Many of these genes, including Cryab (63,64), Vim (65), Spp1 (66), Eno3 (67,68), Pgam (69), Agl (70), Tmbim6 (71), Asb8 (72) and Cs (73), are known to be involved in the development, regeneration and/or homeostasis of skeletal muscles in humans (Table 1). Moreover Eno3 (74,75) and Spp1 (76) have been recently reported as biomarkers for Duchenne muscular dystrophy, where their protein expression levels changes in Duchenne patients through molecular mechanisms not yet fully understood.…”

Thyroid hormones differentially modulate enolase isozymes during rat skeletal and cardiac muscle development

“…48). The expression of IGF-II has been correlated with myogenic differentiation in vivo and in vitro (15,27,39). IGF-II mRNA is present in large amounts in fetal skeletal muscles, and its level decreases dramatically after birth (3) at the time of elimination of superfluous synapses (19).…”