bioRxivGeneticsPreprint
miR-486 is an epigenetic modulator of Duchenne muscular dystrophy pathologies
Rylie M. HightoweriD, Adrienne SamaniiD, Andrea L. ReidiD, Katherine G. EnglishiD, Michael A. LopeziD, J. Scott Doyle, Michael J. ConkliniD, David Alan SchneideriD, Marcas M. BammaniD, Jeffrey J. WidrickiD, David K. CrossmaniD, Min XieiD, David I.H. Jee, Eric C. LaiiD, Matthew S. AlexanderiD
Abstract
Duchenne muscular dystrophy (DMD) is an X-linked progressive muscle disorder resulting in muscle weakness and cardiomyopathy. MicroRNAs have been shown to play essential roles in muscle development, metabolism, and disease pathologies. We demonstrated that miR-486 expression is reduced in DMD muscles and its expression levels correlate with dystrophic disease severity. MicroRNA-486 knockout mice developed disrupted myofiber architecture, decreased myofiber size, decreased locomotor activity, increased cardiac fibrosis, and metabolic defects that were exacerbated on the dystrophic mdx5cv background. We integrated RNA-sequencing and chimeric eCLIP-sequencing data to identify direct in vivo targets of miR-486 and associated dysregulated gene signatures in skeletal muscle. In comparison to our DMD mouse muscle transcriptomes, we identified several of these miR-486 muscle targets including known modulators of dystrophinopathy disease symptoms. Together, our studies identify miR-486 as a driver of muscle remodeling in DMD, a useful biomarker for dystrophic disease progression, and highlight chimeric eCLIP-sequencing as a useful tool to identify direct in vivo microRNA target transcripts. O_FIG O_LINKSMALLFIG WIDTH=122 HEIGHT=200 SRC="FIGDIR/small/448387v1_ufig1.gif" ALT="Figure 1"> View larger version (61K): org.highwire.dtl.DTLVardef@13eeaf5org.highwire.dtl.DTLVardef@1b3b2dborg.highwire.dtl.DTLVardef@a36782org.highwire.dtl.DTLVardef@1e0b95f_HPS_FORMAT_FIGEXP M_FIG C_FIG
- organism: mouse
- assay: bulk RNA-seq
- research focus: differential expression
- research focus: gene regulatory network inference
- approach: statistical model
- Citations
- 4
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