Limits...
Growth and muscle defects in mice lacking adult myosin heavy chain genes.

Acakpo-Satchivi LJ, Edelmann W, Sartorius C, Lu BD, Wahr PA, Watkins SC, Metzger JM, Leinwand L, Kucherlapati R - J. Cell Biol. (1997)

Bottom Line: The three adult fast myosin heavy chains (MyHCs) constitute the vast majority of the myosin in adult skeletal musculature, and are >92% identical.Both strains exhibit growth and muscle defects, but the defects are different between the two strains and do not correlate with the abundance or distribution of each gene product.Most striking is that while both strains exhibit physiological defects in isolated muscles, the defects are distinct.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Genetics, Albert Einstein College of Medicine, New York 10461, USA.

ABSTRACT
The three adult fast myosin heavy chains (MyHCs) constitute the vast majority of the myosin in adult skeletal musculature, and are >92% identical. We describe mice carrying mutations in each of two predominant adult fast MyHC genes, IIb and IId/x. Both strains exhibit growth and muscle defects, but the defects are different between the two strains and do not correlate with the abundance or distribution of each gene product. For example, despite the fact that MyHC-IIb accounts for >70% of the myosin in skeletal muscle and shows the broadest distribution of expression, the phenotypes of IIb mutants are generally milder than in the MyHC-IId/x strain. In addition, in a muscle which expresses both IIb and IId/x MyHC in wild-type mice, the histological defects are completely different for expression of the two genes. Most striking is that while both strains exhibit physiological defects in isolated muscles, the defects are distinct. Muscle from IIb mice has significantly reduced ability to generate force while IId mouse muscle generates normal amounts of force, but has altered kinetic properties. Many of the phenotypes demonstrated by these mice are typical in human muscle disease and should provide insight into their etiology.

Show MeSH

Related in: MedlinePlus

Representative examples of single twitches from whole  EDL muscles (A) and small diaphragm strips (B) at 22°C. Muscle  length and stimulation voltage (0.5-ms duration) was set to produce maximum twitch force. Muscle was stimulated at time zero.  Mouse genotype is as indicated.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC2140209&req=5

Figure 8: Representative examples of single twitches from whole EDL muscles (A) and small diaphragm strips (B) at 22°C. Muscle length and stimulation voltage (0.5-ms duration) was set to produce maximum twitch force. Muscle was stimulated at time zero. Mouse genotype is as indicated.

Mentions: The reduced grip strength found in mice could be explained by an alteration of contractile function in the striated muscles from these animals. To directly test whether maximum force generating capacity is affected in −/− animals, we examined peak isometric tetanic tension in EDL and diaphragm muscle strips isolated from 5–7-mo-old IIb and IId/x−/− animals, respectively. These muscles were selected for study because of their significant content of IIb and IId/x myosin, respectively in wild-type mice (Jansen et al., 1996). Results of this analysis are summarized in Table II and graphed in Fig. 8.


Growth and muscle defects in mice lacking adult myosin heavy chain genes.

Acakpo-Satchivi LJ, Edelmann W, Sartorius C, Lu BD, Wahr PA, Watkins SC, Metzger JM, Leinwand L, Kucherlapati R - J. Cell Biol. (1997)

Representative examples of single twitches from whole  EDL muscles (A) and small diaphragm strips (B) at 22°C. Muscle  length and stimulation voltage (0.5-ms duration) was set to produce maximum twitch force. Muscle was stimulated at time zero.  Mouse genotype is as indicated.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2140209&req=5

Figure 8: Representative examples of single twitches from whole EDL muscles (A) and small diaphragm strips (B) at 22°C. Muscle length and stimulation voltage (0.5-ms duration) was set to produce maximum twitch force. Muscle was stimulated at time zero. Mouse genotype is as indicated.
Mentions: The reduced grip strength found in mice could be explained by an alteration of contractile function in the striated muscles from these animals. To directly test whether maximum force generating capacity is affected in −/− animals, we examined peak isometric tetanic tension in EDL and diaphragm muscle strips isolated from 5–7-mo-old IIb and IId/x−/− animals, respectively. These muscles were selected for study because of their significant content of IIb and IId/x myosin, respectively in wild-type mice (Jansen et al., 1996). Results of this analysis are summarized in Table II and graphed in Fig. 8.

Bottom Line: The three adult fast myosin heavy chains (MyHCs) constitute the vast majority of the myosin in adult skeletal musculature, and are >92% identical.Both strains exhibit growth and muscle defects, but the defects are different between the two strains and do not correlate with the abundance or distribution of each gene product.Most striking is that while both strains exhibit physiological defects in isolated muscles, the defects are distinct.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Genetics, Albert Einstein College of Medicine, New York 10461, USA.

ABSTRACT
The three adult fast myosin heavy chains (MyHCs) constitute the vast majority of the myosin in adult skeletal musculature, and are >92% identical. We describe mice carrying mutations in each of two predominant adult fast MyHC genes, IIb and IId/x. Both strains exhibit growth and muscle defects, but the defects are different between the two strains and do not correlate with the abundance or distribution of each gene product. For example, despite the fact that MyHC-IIb accounts for >70% of the myosin in skeletal muscle and shows the broadest distribution of expression, the phenotypes of IIb mutants are generally milder than in the MyHC-IId/x strain. In addition, in a muscle which expresses both IIb and IId/x MyHC in wild-type mice, the histological defects are completely different for expression of the two genes. Most striking is that while both strains exhibit physiological defects in isolated muscles, the defects are distinct. Muscle from IIb mice has significantly reduced ability to generate force while IId mouse muscle generates normal amounts of force, but has altered kinetic properties. Many of the phenotypes demonstrated by these mice are typical in human muscle disease and should provide insight into their etiology.

Show MeSH
Related in: MedlinePlus