# DESMIN AND VIMENTIN DURING MYOGENESIS

> **NIH NIH R01** · BAYLOR COLLEGE OF MEDICINE · 1992 · $176,131

## Abstract

One of the first recognizable steps during embryonic muscle development is
the initiation of desmin expression in replicating presumptive myoblasts
proceeding the expression of the myogenic regulator myoD and possibly
myogenin.  Terminal differentiation of skeletal muscle is associated with
down regulation of vimentin and up regulation of desmin.  We do not know
the biological function of these two immediate filament proteins during
these processes.  The goal of the proposal is to use different approaches
to study the function of desmin and vimentin during early and terminal
muscle differentiation.  Our data so far has linked overexpression of
vimentin and inhibited differentiation.  C2 myoblasts transfected with
oncogenic ras genes fail to appropriately down regulate vimentin and up
regulate desmin.  We wish to address the association of this phenomenon
with the inability of these cells to differentiate.  The following lines of
investigation are employed:  The recently isolated and fully or partially
characterized mouse desmin an vimentin cDNAs and gene will be used to
manipulate the expression of vimentin and desmin during in vitro  and in
vivo myogenesis.  Specifically, constructs designed to express a)  high
levels of vimentin or desmin at the wrong stages during myogenesis, b)
high levels of antisense RNA that would inhibit mRMA accumulation and
translation, or c)  high levels of truncated polypeptides that will disrupt
normal filament assembly are introduced into both myogenic cells and
transgenic mice.  This will allow us to study:  a)  any possible dependence
of the expression of vimentin and desmin upon each other;  b)  any effect
of these proteins on the expression or function of other muscle specific
genes;  and c)  the functional consequences of such forced or inhibited
expression on muscle differentiation.  Alternatively, gene targeting
constructs will be made to be used in homologous recombination experiments
designed to disrupt the desmin gene and consequently study directly its
functional role during early and late muscle development.  For this
purpose, further characterization of this mouse desmin gene will be
performed and its precise expression during embryogenesis will be assessed
by in situ hybridization.  We also want to address the significance of the
similarities that vimentin and desmin have recently shown to share with
some growth (fos, jun) and myogenic (myoD, myogenin) transcription
regulators, respectively, by investigating:  a)  possible association with
these molecules, b)  involvement in their transport, and c)  modulation of
their function.

## Key facts

- **NIH application ID:** 3159797
- **Project number:** 5R01AR039617-05
- **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:** 1992
- **Award amount:** $176,131
- **Award type:** 5
- **Project period:** 1988-07-15 → 1996-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3159797

## Citation

> US National Institutes of Health, RePORTER application 3159797, DESMIN AND VIMENTIN DURING MYOGENESIS (5R01AR039617-05). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3159797. Licensed CC0.

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