Subtractive cDNA cloning as a tool to analyse secondary effects of a muscle disease. Characterization of affected genes in the myotonic ADR mouse

Schleef, Martin; Zühlke, Christine; Schöffl, Fritz; Jockusch, Harald

doi:10.1016/0960-8966(94)90021-3

Cited by 15 publications

(8 citation statements)

References 63 publications

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“…The chronic electrical activity of this myotonia is similar to a chronic stimulation at low frequency (as normally observed in slow twitch fibers). Indeed, the expression pattern of several genes is modified in the ADR mice in a similar fashion to those in chronically stimulated muscles (22)(23)(24). In particular, the expression pattern of MyHC isoforms is changed in ADR mice, with a disappearance of MyHC-2B replaced by the 2X, 2A, and 1 isoforms and a shift to an oxidative phenotype (22,24,39).…”

Section: Denervation Of Adult Transgenic Mice Induces An Early Shut-dmentioning

confidence: 86%

“…To further investigate the influence of muscle activity on aldolase A expression, we crossed our transgenic mice with ADR mice that were affected by a recessive myotonia (21). ADR mice constitute a model of muscle hyperactivity (22,23) showing biochemical changes reminiscent of those observed in chronically stimulated muscle (24). Expression of the pM310CAT transgene is severely reduced in ADR both in formerly fast and slow muscles, suggesting that some elements of the pM promoter respond to muscle activity regardless of the fiber type.…”

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confidence: 99%

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Proximal Sequences of the Aldolase A Fast Muscle-specific Promoter Direct Nerve- and Activity-dependent Expression in Transgenic Mice

Spitz¹,

Vasconcelos²,

Châtelet³

et al. 1998

Journal of Biological Chemistry

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Muscle activity is known to modulate the muscle fiber phenotype. Changes in muscle activity (normal or experimentally induced) lead to modifications of the expression status of several muscle-specific genes. However, the transcription regulatory elements involved in the adaptative response are mainly unknown. The aldolase A muscle-specific promoter, pM, is expressed in adult fast twitch muscle with a preferential expression in fast glycolytic-2B fibers. Its activity is induced during postnatal muscle maturation, suggesting a role of nerve and/or muscle activity. Indeed, denervation of gastrocnemius in newborn mice prevented the activation of the promoter in this muscle, despite the nerve-independent formation of 2B fibers. Although the nerve was necessary for pM onset during development, denervating the gastrocnemius in adults had only mild effects on pM activity. By contrast, a transgene including the pM proximal regulatory sequences that are sufficient to reproduce the 2B fiber-specific expression of the endogenous promoter was shown to be highly sensitive to both neonatal and adult denervation. Transgenes containing muscle-specific pM proximal promoter elements were used to delineate the regulatory elements involved in this response to innervation and changes in the contractile activity pattern. Nerve-and activity-dependent elements could be localized in the 130-base pair-long proximal promoter region of the human aldolase A gene.

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Section: Denervation Of Adult Transgenic Mice Induces An Early Shut-dmentioning

confidence: 86%

mentioning

confidence: 99%

Proximal Sequences of the Aldolase A Fast Muscle-specific Promoter Direct Nerve- and Activity-dependent Expression in Transgenic Mice

Spitz¹,

Vasconcelos²,

Châtelet³

et al. 1998

Journal of Biological Chemistry

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show abstract

“…In association with the troponin complex, tropomyosin regulates the calcium-sensitive interaction of actin and myosin. The mouse and rat -tropomyosin genes have 13 exons (37,38). At least nine isoforms are derived from the rat -tropomyosin gene by use of alternative promoters, splicing, and polyadenylation sites (38,39).…”

Section: Characterization Of Clones Associated With Changes In Mrna Ementioning

confidence: 99%

Alterations in skeletal muscle gene expression of ob/ob mice by mRNA differential display.

Vicent

Piper²,

Gammeltoft³

et al. 1998

Diabetes

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To identify molecules that contribute to insulin resistance, we compared the patterns of gene expression in skeletal muscle of the obese ob/ob mouse, a genetic model of obesity and severe insulin resistance, with that of its thin littermate (ob/+) using the mRNA differential display method. From about 9,000 cDNAs displayed, we found 12 differentially expressed in ob/ob mice skeletal muscle that could be recovered from the differential display gels and confirmed by Northern blot analysis and sequenced. Eight mRNAs were overexpressed in ob/ob muscle: Id2 (a negative regulator of the basic helix-loop-helix family of transcription factors), fast skeletal muscle troponin T, ribosomal protein L3, the integral protein of the peroxisomal membrane 22PMP, the mammalian homolog of geranylgeranyl pyrophosphate synthase, an mRNA related to phosphatidylinositol-glycan-specific phospholipase D, and two unknown mRNAs. The level of overexpression of these mRNAs in skeletal muscle varied from a 500% increase to as little as a 25% increase. Two mRNAs were underexpressed 20-35%, including the f-subunit of mitochondrial ATP synthase and a retrovirus-related DNA. Two proteins with multiple transcripts, skeletal muscle alpha-tropomyosin and one for a repetitive sequence, showed a change in mRNA pattern of expression in the muscle of the ob/ob mouse. Because the primary genetic defect in the ob/ob mouse is known to be in the leptin gene, these data indicate how acquired alterations in gene expression of multiple classes of proteins may play a role in the complex pathogenesis of insulin resistance in obesity and diabetes.

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“…ant., tibialis anterior. albumin (PV), a 700-bp mouse cDNA from the coding region of mouse parvalbumin 44,52 ; and ␣-actin, a 500-bp cDNA from the coding region of human skeletal ␣-actin.…”

Section: Figurementioning

confidence: 99%

“…The adr mutation, which causes hyperexcitability of muscle fibers by reducing sarcolemmal chloride conductance, 39 has played a decisive role in the molecular identification of myotonia genes in mouse 23,47 and man. 32 In addition, physiological and developmental aspects of the disease were studied in the ADR mouse model, and primary 12,25,49 as well as secondary 24,31,44 effects on muscle physiology and gene expression have been unraveled, in part by experimental procedures that are only feasible with animal models, such as genetic complementation tests 26 and surgical transplantation.…”

mentioning

confidence: 99%

Expression of nerve-regulated genes in muscles of mouse mutants affected by spinal muscular atrophies and muscular dystrophies

1997

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Subtractive cDNA cloning as a tool to analyse secondary effects of a muscle disease. Characterization of affected genes in the myotonic ADR mouse

Cited by 15 publications

References 63 publications

Proximal Sequences of the Aldolase A Fast Muscle-specific Promoter Direct Nerve- and Activity-dependent Expression in Transgenic Mice

Proximal Sequences of the Aldolase A Fast Muscle-specific Promoter Direct Nerve- and Activity-dependent Expression in Transgenic Mice

Alterations in skeletal muscle gene expression of ob/ob mice by mRNA differential display.

Expression of nerve-regulated genes in muscles of mouse mutants affected by spinal muscular atrophies and muscular dystrophies

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