Related Experiment Video

Updated: Aug 8, 2026

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
07:49

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods

Published on: July 17, 2019

Developmental regulation of intermediate filament and actin mRNAs during myogenesis is disrupted by oncogenic ras

E N Olson1, Y G Capetanaki

  • 1Department of Biochemistry and Molecular Biology, University of Texas, M.D. Anderson Cancer Center, Houston 77030.

Oncogene
|July 1, 1989
PubMed

Insights

Oncogenic ras genes disrupt normal muscle cell differentiation by preventing the down-regulation of specific actin and vimentin mRNAs, even when cells stop dividing. This interference impacts muscle development and gene regulation.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Developmental Biology

Background:

  • Skeletal myoblast differentiation involves coordinated changes in actin and intermediate filament gene expression.
  • Vimentin and beta-, gamma-actins are typically down-regulated, while desmin and alpha-sarcomeric actin are up-regulated during terminal differentiation.
  • The role of cell cycle withdrawal versus differentiation in regulating these gene expression changes is not fully understood.

Purpose of the Study:

  • To investigate whether the down-regulation of vimentin and beta-, gamma-actin mRNAs is linked to cell cycle exit or terminal differentiation.
  • To examine the effect of oncogenic ras genes on the expression of actin and intermediate filament mRNAs during myogenesis.

Main Methods:

  • Analysis of mRNA expression in C2 myoblasts transfected with oncogenic Harvey (H)-ras genes.
  • Culturing cells in mitogen-deficient medium to induce cell cycle withdrawal.
  • Quantification of specific actin and vimentin mRNA levels using molecular techniques.

Main Results:

  • Myoblasts expressing oncogenic ras ceased dividing but failed to down-regulate vimentin and beta-, gamma-actin mRNAs.
  • Vimentin mRNA levels increased approximately 2.5-fold in ras-transfected cells.
  • Alpha-sarcomeric actin and desmin mRNAs remained at basal levels in these cells.
  • The interference with gene regulation was dependent on the mutational activation of ras, not observed with proto-oncogenic alleles.

Conclusions:

  • Oncogenic ras interferes with the down-regulation of specific actin and vimentin genes during myoblast differentiation.
  • Ras oncogenes prevent the normal decline in expression of certain cytoskeletal genes, impacting muscle development.
  • The effect of ras is specific to its activated form and disrupts developmental gene regulation mechanisms.

More Related Videos

Identification of EGFR and RAS Inhibitors using Caenorhabditis elegans08:12

Identification of EGFR and RAS Inhibitors using Caenorhabditis elegans

Published on: October 5, 2020

Optogenetic Inhibition of Rho1-Mediated Actomyosin Contractility Coupled with Measurement of Epithelial Tension in Drosophila Embryos12:35

Optogenetic Inhibition of Rho1-Mediated Actomyosin Contractility Coupled with Measurement of Epithelial Tension in Drosophila Embryos

Published on: April 14, 2023

Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
Formation of Muscle Fibers from Myoblasts01:13

Formation of Muscle Fibers from Myoblasts

De novo myogenesis, or the formation of muscle fibers, begins during the early embryonic stages. The skeletal muscle is formed from somites– blocks of embryonic cell layers. The somites are further divided into dermatomes, myotomes, sclerotomes, and syndetomes. Among these, the myotomes give rise to muscle fibers.
Muscle progenitor cells (MPCs) are formed from the myotomes. MPCs express genes that encode the transcription factors Pax3 and Pax7. Along with Pax 3/7, other transcription factors...
Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...