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Targeted inactivation of myogenic factor genes reveals their role during mouse myogenesis: a review.
Int J Dev Biol. 1996 Feb; 40(1):345-53.IJ

Abstract

The role of the four myogenic regulating genes Myf-5, myogenin, MyoD, and MRF4 (herculin, Myf-6) during mouse embryogenesis has been investigated by targeted gene inactivation. Null mutations for the MyoD gene generate no skeletal muscle phenotype due to a compensatory activation of the Myf-5 gene. Mice carrying a homozygous Myf-5 mutation exert considerably delayed myotome formation with unexpected consequences. While skeletal myogenesis in these mutant mice resumes normally at the onset of MyoD expression, a skeletal defect of the ribs persists. Apparently, Myf-5 and MyoD individually are not absolutely essential for skeletal muscle development, most likely because they have overlapping or redundant functions. In fact, double mutants lacking both, MyoD and Myf-5, fail to develop skeletal musculature and the muscle forming regions seem to be devoid of myoblasts. Homozygous inactivation of the myogenin gene leads to drastically reduced myofiber formation. These mice accumulate apparently normal numbers of myoblasts which are arrested in their terminal differentiation program. Myf-6 null mutant mice exhibit drastically reduced expression of Myf-5 for reasons presently unknown. The phenotype is very similar to Myf-5 mutants with an additional reduction of deep back muscles and minor alterations in sarcomeric protein isoforms. Based on the phenotypes obtained from these various gene "knock-out" mice, we now begin to understand the regulatory network and the homostatic relationship of genes which are critically involved in myogenesis of vertebrates.

Links

Publisher Full Text
intjdevbiol.com
intjdevbiol.com

Authors+Show Affiliations

Arnold HH
Department of Cell and Molecular Biology, Technical University of Braunschweig, Germany.
Braun T
No affiliation info available

MeSH

AnimalsDNA-Binding ProteinsGene Expression Regulation, DevelopmentalGene TargetingHomozygoteMiceMice, KnockoutMuscle ProteinsMuscle, SkeletalMyoD ProteinMyogenic Regulatory Factor 5Myogenic Regulatory FactorsMyogeninPhenotypeTrans-Activators

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

8735947

Citation

Arnold, H H., and T Braun. "Targeted Inactivation of Myogenic Factor Genes Reveals Their Role During Mouse Myogenesis: a Review." The International Journal of Developmental Biology, vol. 40, no. 1, 1996, pp. 345-53.
Arnold HH, Braun T. Targeted inactivation of myogenic factor genes reveals their role during mouse myogenesis: a review. Int J Dev Biol. 1996;40(1):345-53.
Arnold, H. H., & Braun, T. (1996). Targeted inactivation of myogenic factor genes reveals their role during mouse myogenesis: a review. The International Journal of Developmental Biology, 40(1), 345-53.
Arnold HH, Braun T. Targeted Inactivation of Myogenic Factor Genes Reveals Their Role During Mouse Myogenesis: a Review. Int J Dev Biol. 1996;40(1):345-53. PubMed PMID: 8735947.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Targeted inactivation of myogenic factor genes reveals their role during mouse myogenesis: a review. AU - Arnold,H H, AU - Braun,T, PY - 1996/2/1/pubmed PY - 1996/2/1/medline PY - 1996/2/1/entrez SP - 345 EP - 53 JF - The International journal of developmental biology JO - Int J Dev Biol VL - 40 IS - 1 N2 - The role of the four myogenic regulating genes Myf-5, myogenin, MyoD, and MRF4 (herculin, Myf-6) during mouse embryogenesis has been investigated by targeted gene inactivation. Null mutations for the MyoD gene generate no skeletal muscle phenotype due to a compensatory activation of the Myf-5 gene. Mice carrying a homozygous Myf-5 mutation exert considerably delayed myotome formation with unexpected consequences. While skeletal myogenesis in these mutant mice resumes normally at the onset of MyoD expression, a skeletal defect of the ribs persists. Apparently, Myf-5 and MyoD individually are not absolutely essential for skeletal muscle development, most likely because they have overlapping or redundant functions. In fact, double mutants lacking both, MyoD and Myf-5, fail to develop skeletal musculature and the muscle forming regions seem to be devoid of myoblasts. Homozygous inactivation of the myogenin gene leads to drastically reduced myofiber formation. These mice accumulate apparently normal numbers of myoblasts which are arrested in their terminal differentiation program. Myf-6 null mutant mice exhibit drastically reduced expression of Myf-5 for reasons presently unknown. The phenotype is very similar to Myf-5 mutants with an additional reduction of deep back muscles and minor alterations in sarcomeric protein isoforms. Based on the phenotypes obtained from these various gene "knock-out" mice, we now begin to understand the regulatory network and the homostatic relationship of genes which are critically involved in myogenesis of vertebrates. SN - 0214-6282 UR - https://www.unboundmedicine.com/medline/citation/8735947/Targeted_inactivation_of_myogenic_factor_genes_reveals_their_role_during_mouse_myogenesis:_a_review_ L2 - http://www.intjdevbiol.com/paper.php?doi=8735947 DB - PRIME DP - Unbound Medicine ER -