Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A novel YY1-miR-1 regulatory circuit in skeletal myogenesis revealed by genome-wide prediction of YY1-miRNA network

ABSTRACT: microRNAs (miRNAs) are non-coding RNAs that regulate gene expression post-transcriptionally, and mounting evidences support the prevalence and functional significance of their interplay with transcription factors (TFs). Here we describe the identification of a regulatory circuit between muscle miRNAs (miR-1, miR-133 and miR-206) and Yin Yang 1 (YY1), an epigenetic repressor of skeletal myogenesis. Genome-wide identification of potential YY1 down-stream targets by combining computational prediction with expression profiling data reveals a large number of putative miRNA targets of YY1 during skeletal myoblasts differentiation into myotubes with muscle miRs rank on top of the list.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE32238 | GEO | 2011/12/31

SECONDARY ACCESSION(S): PRJNA147193

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

A novel YY1-miR-1 regulatory circuit in skeletal myogenesis revealed by genome-wide prediction of YY1-miRNA network

Project description:microRNAs (miRNAs) are non-coding RNAs that regulate gene expression post-transcriptionally, and mounting evidences support the prevalence and functional significance of their interplay with transcription factors (TFs). Here we describe the identification of a regulatory circuit between muscle miRNAs (miR-1, miR-133 and miR-206) and Yin Yang 1 (YY1), an epigenetic repressor of skeletal myogenesis. Genome-wide identification of potential YY1 down-stream targets by combining computational prediction with expression profiling data reveals a large number of putative miRNA targets of YY1 during skeletal myoblasts differentiation into myotubes with muscle miRs rank on top of the list. Murine skeletal muscle cells (C2C12 cells) were differentiated for 0, 1 or 3 days. Total RNAs were isolated from the cells and used for array profiling of miRNA expression.

2011-12-31 | E-GEOD-32238 | biostudies-arrayexpress

Transcriptome Analysis Identifies Linc-Yy1, A Novel Functional LincRNA During Myogenesis

Project description:Little is known how lincRNAs are involved in skeletal myogenesis. Here we describe the discovery of a novel lincRNA, Linc-YY1 from the promoter of transcription factor (TF) Yin Yang 1 (YY1) gene. We demonstrate that Linc-YY1 is dynamically regulated during myogenesis in vitro and in vivo. Gain or loss of function of Linc-YY1 in C2C12 myoblast cells or satellite cells alters myogenic differentiation and in injured muscles impacts the course of regeneration. Further studies suggest LincYY1 may interact with YY1 through its middle domain to evict YY1

2015-10-16 | GSE74049 | GEO

Expression data from mouse skeletal muscle

Project description:We generated skeletal muscle-specific knockout mice lacking the transcription factor Yin Yang 1 (YY1) and analyzed expression patterns in the skeletal muscle these mice. We used microarrays to detail the global programme of gene expression regulated by YY1. Wild type or knockout mice at 6 months were sacrificed and the soleus was isolated for RNA extraction.

2012-06-29 | E-GEOD-39009 | biostudies-arrayexpress

YY1 regulates skeletal muscle regeneration through controlling metabolic reprogramming during adult muscle stem cell activation

Project description:Skeletal muscle satellite cells (SCs) are adult muscle stem cells responsible for muscle regeneration after acute or chronic injuries. The lineage progression of quiescent satellite cells toward activation, proliferation and differentiation during the regeneration is orchestrated by cascades of transcription factors (TFs). Here we elucidate the functional role of a ubiquitously expressed TF, Yin Yang1 (YY1) in muscle regeneration. Muscle-specific deletion of YY1 in embryonic muscle progenitors leads to severe deformity of diaphragm muscle formation thus postnatal death. Inducible deletion of YY1 in satellite cells almost completely blocks the acute damage induced muscle repair and exacerbates the chronic injury induced dystrophic phenotype. Examination of SCs revealed that YY1 loss results in cell autonomous defect in cell activation and proliferation. Mechanistic search through genome-wide profiling of YY1 regulated transcriptome and YY1 binding revealed that YY1 binds and suppresses mitochondrial gene expression. Simultaneously, it also activates Hif1α mediated glycolytic genes to facilitate a metabolic reprogramming toward glycolysis which is needed for SC activation. Altogether our findings have identified YY1 as a key regulator of SC metabolic reprogramming during cell activation through its dual roles in modulating both mitochondrial and glycolytic pathways.

2019-04-09 | GSE108249 | GEO

Expression data from mouse skeletal muscle

2012-06-30 | GSE39009 | GEO

miR-206 modulates the pathogenesis of muscular dystrophy of mdx mice

Project description:In response to skeletal muscle injury, adult myogenic stem cells, known as satellite cells, are activated and undergo proliferation and differentiation to regenerate new muscle fibers. The skeletal muscle-specific microRNA, miR-206, is up-regulated in satellite cells following muscle injury, but its role in muscle regeneration has not been defined. Here we show that skeletal muscle regeneration in response to cardiotoxin injury is impaired in mice lacking miR-206. Loss of miR-206 also accelerates and exacerbates the dystrophic phenotype of mdx mice, a model for Duchenne muscular dystrophy. MiR-206 promotes satellite cell differentiation and fusion to form multinucleated myofibers by suppressing a collection of negative regulators of myogenesis. Our findings reveal an essential role for miR-206 in satellite cell differentiation during skeletal muscle regeneration and as a modulator of Duchenne muscular dystrophy. total RNA obtained from TA muscle of mdx and 3 miR-206 KO; mdx mice at 3 months of age.

2012-04-30 | E-GEOD-36077 | biostudies-arrayexpress

miR-206 modulates the pathogenesis of muscular dystrophy of mdx mice

2012-05-01 | GSE36077 | GEO

Genome-wide survey of YY1 targets in C2C12 cells by High-throughput sequencing

Project description:By applying ChIP-seq, we generated genome-wide maps of YY1 in skeletal myoblasts and myotubes. We found that YY1 binds to 1820 confident target with a large portion residing in the intergenic regions. In addition, YY1 was found to activate many loci, and there is no significant overlap between YY1 and Ezh2 targets, suggensting a Ezh2-independent manner. Further detailed study revealed that YY1 can regulate some lincRNAs which are fucntional in skeletal myogenesis. In this study, we identified a YY1-Yam-1-miR-715 (TF-lincRNA-miRNA) regulatory curcuit in myogensis. Examination of YY1 targets in myoblast versus myotubes

2013-08-15 | E-GEOD-45875 | biostudies-arrayexpress

miR‐206 family is important for mitochondrial and muscle function, but not essential for myogenesis in vitro [miRNA-Seq]

Project description:miR-206, miR-1a-1 and miR-1a-2, foundational members of the myomir family, promote skeletal muscle differentiation and have complete identity in the seed sequence, suggesting functional redundancy. To test if the essential role of these three microRNAs in skeletal myogenesis was masked by redundant function of at least one of the three miRNA left in the cells in previous reports, we generated triple KO (tKO) C2C12 cells by CRISPR/Cas9 (in vitro) and triple KO mice (in vivo model). tKO myoblasts differentiate, producing similar levels of promyogenic mRNAs and normal fusion index. RNAseq analysis confirms tKO clones differentiate but also reveals decrease in mRNA levels of genes related to mitochondrial oxidative phosphorylation. Dimished mitochondria function in tKO cells was confirmed using Seahorse assay. The targets of miR-206/-1a are specifically upregulated during differentiation of tKO myoblasts, when the microRNAs are normally induced, confirming the complete loss of the three microRNA genes. Although we observe partial embryonic lethality of tKO mice, the live mice grow normally to adulthood, have the same size of skeletal muscles as control animals, but perform worse on physical activity tests, which may be partially explained by smaller skeletal muscle fiber diameters. Thus these three myomiRs are not essential for skeletal muscle differentiation but are required for optimal differentiation and provide a clear example of the microRNAs not being a switch but a modulator of differentiation.

2020-04-15 | GSE133255 | GEO

miR‐206 family is important for mitochondrial and muscle function, but not essential for myogenesis in vitro [RNA-Seq]

2020-04-15 | GSE133260 | GEO