Transgenic mice that express Cre recombinase under control of a skeletal muscle-specific promoter frommef2c

Heidt, Analeah B.; Black, Brian L.

doi:10.1002/gene.20123

Cited by 21 publications

(18 citation statements)

References 21 publications

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“…mef2c -73k-Cre and nfatc1 flox/flox mice have been described (Aliprantis et al, 2008; Heidt and Black, 2005). To generate nfatc1 +/Δ mice, male nfatc1 flox/flox mice were crossed to female Mef2c -AHF-Cre mice (Rojas et al, 2008).…”

Section: Methodsmentioning

confidence: 99%

NFATc1 Controls Skeletal Muscle Fiber Type and Is a Negative Regulator of MyoD Activity

2014

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SUMMARY Skeletal muscle comprises a heterogeneous population of fibers with important physiological differences. Fast fibers are glycolytic and fatigue rapidly. Slow fibers utilize oxidative metabolism and are fatigue-resistant. Muscle diseases such as sarcopenia and atrophy selectively affect fast fibers, but the molecular mechanisms regulating fiber type-specific gene expression remain incompletely understood. Here, we show that the transcription factor NFATc1 controls fiber type composition and is required for fast-to-slow fiber type switching in response to exercise in vivo. Moreover, MyoD is a crucial transcriptional effector of the fast fiber phenotype, and we show that NFATc1 inhibits MyoD-dependent fast fiber gene promoters by physically interacting with the N-terminal activation domain of MyoD and blocking recruitment of the essential transcriptional coactivator p300. These studies establish a molecular mechanism for fiber type switching through direct inhibition of MyoD to control the opposing roles of MyoD and NFATc1 in fast versus slow fiber phenotypes.

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Section: Methodsmentioning

confidence: 99%

NFATc1 Controls Skeletal Muscle Fiber Type and Is a Negative Regulator of MyoD Activity

2014

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“…Mice were genotyped using previously described Cre-specific PCR primers (5′-TGC CAC GAC CAA GTG ACA GC-3′, 5′-CCA GGT TAC GGA TAT AGT TCA TG-3′) (Heidt and Black, 2005), and primers designed to distinguish between the control and floxed Hdac3 allele (5′-GCA GTG GTG GTG AAT GGC TT-3′, 5′-CCT GTG TAA CGG GAG CAG AAC TC-3′). Genotyping for the Z/EG transgene was performed by X-Gal staining tail samples.…”

Section: Methodsmentioning

confidence: 99%

Murine craniofacial development requires Hdac3-mediated repression of Msx gene expression

Singh

Gupta

Trivedi

et al. 2013

Developmental Biology

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Craniofacial development is characterized by reciprocal interactions between neural crest cells and neighboring cell populations of ectodermal, endodermal and mesodermal origin. Various genetic pathways play critical roles in coordinating the development of cranial structures by modulating the growth, survival and differentiation of neural crest cells. However, the regulation of these pathways, particularly at the epigenomic level, remains poorly understood. Using murine genetics, we show that neural crest cells exhibit a requirement for the class I histone deacetylase Hdac3 during craniofacial development. Mice in which Hdac3 has been conditionally deleted in neural crest demonstrate fully penetrant craniofacial abnormalities, including microcephaly, cleft secondary palate and dental hypoplasia. Consistent with these abnormalities, we observe dysregulation of cell cycle genes and increased apoptosis in neural crest structures in mutant embryos. Known regulators of cell cycle progression and apoptosis in neural crest, including Msx1, Msx2 and Bmp4, are upregulated in Hdac3-deficient cranial mesenchyme. These results suggest that Hdac3 serves as a critical regulator of craniofacial morphogenesis, in part by repressing core apoptotic pathways in cranial neural crest cells.

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“…loxP/loxP mice were crossed with a mouse strain expressing Cre recombinase under the control of the MEF2C promoter (mef2C-73K-Cre) (26). The expression of Mfn2 was analyzed in control (mef2C-Cre…”

Section: Mfn2mentioning

confidence: 99%

Mitofusin 2 (Mfn2) links mitochondrial and endoplasmic reticulum function with insulin signaling and is essential for normal glucose homeostasis

Sebastián

Hernández‐Álvarez

Segalés

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

560

496

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Mitochondria are dynamic organelles that play a key role in energy conversion. Optimal mitochondrial function is ensured by a quality-control system tightly coupled to fusion and fission. In this connection, mitofusin 2 (Mfn2) participates in mitochondrial fusion and undergoes repression in muscle from obese or type 2 diabetic patients. Here, we provide in vivo evidence that Mfn2 plays an essential role in metabolic homeostasis. Liver-specific ablation of Mfn2 in mice led to numerous metabolic abnormalities, characterized by glucose intolerance and enhanced hepatic gluconeogenesis. Mfn2 deficiency impaired insulin signaling in liver and muscle. Furthermore, Mfn2 deficiency was associated with endoplasmic reticulum stress, enhanced hydrogen peroxide concentration, altered reactive oxygen species handling, and active JNK. Chemical chaperones or the antioxidant N-acetylcysteine ameliorated glucose tolerance and insulin signaling in liver-specific Mfn2 KO mice. This study provides an important description of a unique unexpected role of Mfn2 coordinating mitochondria and endoplasmic reticulum function, leading to modulation of insulin signaling and glucose homeostasis in vivo.mitochondrial dynamics | insulin resistance | metabolism | oxidative stress

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Transgenic mice that express Cre recombinase under control of a skeletal muscle-specific promoter frommef2c

Cited by 21 publications

References 21 publications

NFATc1 Controls Skeletal Muscle Fiber Type and Is a Negative Regulator of MyoD Activity

NFATc1 Controls Skeletal Muscle Fiber Type and Is a Negative Regulator of MyoD Activity

Murine craniofacial development requires Hdac3-mediated repression of Msx gene expression

Mitofusin 2 (Mfn2) links mitochondrial and endoplasmic reticulum function with insulin signaling and is essential for normal glucose homeostasis

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