STUDIES ON THE EVOLUTION AND FUNCTION OF DIFFERENT FORMS OF THE MOUSE MYOGENIC GENE MYO-D1 AND UPSTREAM FLANKING REGION

PH KAY, SA MARLOW, Christopher Mitchell, JM PAPADIMITRIOU

Research output: Contribution to journalArticle

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Abstract

The product of the murine Myo-D1 gene is able to initiate the complete sequence of genetic events required for formation of skeletal muscle. Because efficiency of regeneration of skeletal muscle is more pronounced in SJL/J mice, as compared to other strains, differences in the structure of Myo-D1 and the upstream regulatory region were sought to determine whether efficiency of tissue repair was influenced by the structure of the gene itself. Analysis of the restriction-fragment length polymorphism (RFLP) of genomic DNA from SJL/J and different sub-strains of mouse indicated that there are at least three different structural forms of Myo-D1, one of which is unique to SJL/J mice and may have been derived from a double recombinational event involving founder forms of Myo-D1. The unique form of Myo-D1 in SJL/J mice also exhibits a PvuII RFLP upstream from the gene, which may reflect some form of rearrangement or variation in methylation of a potential Myo-D1-binding region. Reference to the size of fragments hybridising with the Myo-D1 probe, following digestion of genomic DNA with TaqI, suggests that in most tissues, adenine residues within Myo-D1 may be extensively methylated. Segregation of Myo-D1 allotypes with response to mechanical injury to skeletal muscle in F2 offspring derived from SJL/J and BALB/c parental strains reveals that increased efficiency of tissue repair is associated with the SJL/J type of Myo-D1 gene. These observations provide new approaches to investigation of genetic control of tissue regeneration and cellular differentiation and proliferation in general.
LanguageEnglish
Pages215-222
JournalGene
Volume124
Issue number2
Publication statusPublished - Feb 1993

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Skeletal Muscle
Restriction Fragment Length Polymorphisms
Genes
Regeneration
Nucleic Acid Regulatory Sequences
DNA
Adenine
Methylation
Digestion
Cell Proliferation
Wounds and Injuries

Cite this

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title = "STUDIES ON THE EVOLUTION AND FUNCTION OF DIFFERENT FORMS OF THE MOUSE MYOGENIC GENE MYO-D1 AND UPSTREAM FLANKING REGION",
abstract = "The product of the murine Myo-D1 gene is able to initiate the complete sequence of genetic events required for formation of skeletal muscle. Because efficiency of regeneration of skeletal muscle is more pronounced in SJL/J mice, as compared to other strains, differences in the structure of Myo-D1 and the upstream regulatory region were sought to determine whether efficiency of tissue repair was influenced by the structure of the gene itself. Analysis of the restriction-fragment length polymorphism (RFLP) of genomic DNA from SJL/J and different sub-strains of mouse indicated that there are at least three different structural forms of Myo-D1, one of which is unique to SJL/J mice and may have been derived from a double recombinational event involving founder forms of Myo-D1. The unique form of Myo-D1 in SJL/J mice also exhibits a PvuII RFLP upstream from the gene, which may reflect some form of rearrangement or variation in methylation of a potential Myo-D1-binding region. Reference to the size of fragments hybridising with the Myo-D1 probe, following digestion of genomic DNA with TaqI, suggests that in most tissues, adenine residues within Myo-D1 may be extensively methylated. Segregation of Myo-D1 allotypes with response to mechanical injury to skeletal muscle in F2 offspring derived from SJL/J and BALB/c parental strains reveals that increased efficiency of tissue repair is associated with the SJL/J type of Myo-D1 gene. These observations provide new approaches to investigation of genetic control of tissue regeneration and cellular differentiation and proliferation in general.",
author = "PH KAY and SA MARLOW and Christopher Mitchell and JM PAPADIMITRIOU",
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STUDIES ON THE EVOLUTION AND FUNCTION OF DIFFERENT FORMS OF THE MOUSE MYOGENIC GENE MYO-D1 AND UPSTREAM FLANKING REGION. / KAY, PH; MARLOW, SA; Mitchell, Christopher; PAPADIMITRIOU, JM.

In: Gene, Vol. 124, No. 2, 02.1993, p. 215-222.

Research output: Contribution to journalArticle

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