# DESMIN AND VIMENTIN DURING MYOGENESIS

> **NIH NIH R01** · BAYLOR COLLEGE OF MEDICINE · 1989 · $98,850

## Abstract

Patterns of intermediate filament (IF) protein expression have
provided several model systems in which to study the regulation of
both gene expression and morphogenesis during cell differentiation.
During myogenesis in vitro, the expression of the vimentin gene
decreases, whereas expression of desmin is induced upon myoblast
fusion and partially replaces vimentin expression during terminal
differentiation.  We have previously shown that the developmental
regulation of these IF subunits is controlled at the mRNA level.
C2 myoblasts transferred with the oncogenic ras genes lose their
ability to differentiate.  We have recently found that these
transformed cells, when induced, fail to appropriately down
regulate vimentin and up regulate desmin mRNAs.  How are these two
phenomena related?  At what level is the normal and disrupted
developmental expression of vimentin regulated?  Is it at the
transcriptional or post-transcriptional level?  What is the role
of these two proteins in this differentiating system and how does
it correlate with their expression pattern?  This proposal will
examine some of the above issues.  We will determine the level of
regulation of vimentin and desmin expression during normal and
disrupted mouse myogenesis by measuring initial transcription rates
and mRNA stabilization.  Using recently developed gene transfer
techniques, we will investigate possible modes of function of these
two proteins during muscle differentiation.  The following lines
of investigation will be employed.  cDNA or genomic constructs
designed to either express high levels of vimentin or desmin at the
wrong stage during myogenesis or produce high levels of antisense
RNAs (which will arrest the expression of the endogenous gene),
will be introduced into myogenic cells.  This will allow us to
study: A) any possible dependence of the expression of these to
genes upon each other; and b) the functional consequences of such
forced or inhibited expression on muscle differentiation.  For
these antisense experiments, we need the corresponding mouse DNAs
which will be isolated by using the available chicken probe.
Alternatively, we will use antisense oligonucleotides to inhibit
the translation of these proteins.  Eventually, antisense
constructs as well as constructs that will overproduce vimentin or
desmin will be used in mouse transformations and the consequences
of the absence or over accumulation of these proteins in normal and
abnormal muscle function will be investigated in vivo.

## Key facts

- **NIH application ID:** 3159795
- **Project number:** 5R01AR039617-02
- **Recipient organization:** BAYLOR COLLEGE OF MEDICINE
- **SAM.gov UEI:** FXKMA43NTV21
- **Principal Investigator:** YASSEMI CAPETANAKI
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1989
- **Award amount:** $98,850
- **Award type:** 5
- **Project period:** 1988-07-15 → 1991-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3159795

## Citation

> US National Institutes of Health, RePORTER application 3159795, DESMIN AND VIMENTIN DURING MYOGENESIS (5R01AR039617-02). Retrieved via MORVS 2026-10-24 from https://api.morvs.ai/grant/nih/3159795. Licensed CC0.

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