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Murine EDMD

ABSTRACT: Study muscle regeneration in Emerin and Lamin AC KO mice. Gastrocnemius muscles were injected with cardiotoxin. Muscles were isolated at different time points. Keywords: Time-Series

ORGANISM(S): Mus musculus

PROVIDER: GSE5304 | GEO | 2006/07/13

SECONDARY ACCESSION(S): PRJNA96307

REPOSITORIES: GEO

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Transcription profiling of gastrocneumius muscle from Emerin and Lamin A/C knockout mice after recovery from cardiotoxin injection to study muscle regeneration

Project description:Study muscle regeneration in Emerin and Lamin AC KO mice. Gastrocnemius muscles were injected with cardiotoxin. Muscles were isolated at different time points. Keywords: Time-Series The specific aim is to generate staged muscle degeneration/regeneration of Emerin deficient and Lamin A/C deficient mice. Muscles will then be express profiled using Affymetrix arrays.

2006-07-12 | E-GEOD-5304 | biostudies-arrayexpress

Effects of muscle regeneration after injury on overloading-induced hypertrophy

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Project description:Utilizing glycerol and cardiotoxin (CTX) injections in the tibialis anterior muscles of M. musculus provides models of skeletal muscle damages followed by skeletal muscle regeneration. In particular, glycerol-induced muscle regeneration is known to be associated with ectopic adipogenesis. We characterized genome-wide expression profiles of tibialis anterior muscles from wild-type mice injured by either glycerol or CTX injection. Our goal was to detect gene expression changes during the time course of glycerol-induced and CTX-induced muscle regeneration models, that can lead to ectopic adipocyte accumulation. Tibialis anterior muscle of 12 week old wildtype C57BL/6J male mice injected i.m with either glycerol or CTX were collected 3, 7, 14 or 21 days after injection. 6 biological replicates were used for each time points. Please note that a few replicate samples did not pass QC test, thus, were removed from the submission. Unchallenged tibialis anterior muscles from a group of 5 wildtype C57BL/6J mice were also as a control. Total RNA was extracted, QCed and hybridized to Affymetrix microarrays.

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Project description:RNA sequencing was performed on proliferating and differentiating emerin-null myogenic progenitors expressing emerin and EDMD-causing emerin mutants to identify molecular pathways implicated in Emery-Dreifuss Muscular Dystrophy.

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Project description:One gastrocnemius muscle was injected with the ERS-drug tunicamycin, the other with control saline solution and muscles were used to prepare RNA.

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RNA-seq: Loss of a heterochromatin anchor rescues altered genome organization and EDMD muscle defects triggered by a laminopathy mutation

Project description:Point mutations in nuclear structural protein lamin A produce rare, tissue-specific diseases called laminopathies. The introduction of a human Emery Dreifuss Muscular Dystrophy (EDMD)-inducing mutation (lamin A-Y45C) into C. elegans lamin (LMN-Y59C), recapitulates many EDMD phenotypes, and correlates with hyper-sequestration of heterochromatic arrays at the nuclear periphery. Using muscle-specific emerin Dam-ID, we also document the misorganization of endogenous chromatin in the LMN-Y59C mutant. We score increased perinuclear positioning along chromosome arms, and enhanced release within chromosomal cores. Coincidentally, Y59C worms have reduced locomotion and compromised sarcomere integrity. By coupling the Y59C mutation with deletion of the perinuclear chromodomain protein CEC-4, which tethers H3K9-methylated chromatin, we rescue the EDMD-like physiology and ultrastructural defects in sarcomeres. Deletion of cec-4 also rescued the Y59C-induced changes in chromatin organization. The promoters of genes that change position in the LMN-Y59C mutant, are enriched for E2F (EFL-1/-2) binding sites, consistent with previous studies implicating the Rb-E2F interaction with lamin A in muscle dysfunction. Gene expression changes provoked by LMN-Y59C are also largely reversed by cec-4 deletion. In summary, the ablation of a perinuclear H3K9me-anchor can counteract the dominant muscle-specific defects provoked by a laminopathic mutation, implicating peripheral chromatin organization in the control of muscle integrity.

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RNA-seq for miRNAs in fibrocyte-adipocyte progenitors (FAPs) or myogenic progenitors (MPs) during muscle regeneration

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