Epigenomic signatures underpin the axonal regenerative ability of dorsal root ganglia sensory neurons.
Ilaria PalmisanoVance P LemmonThomas H HutsonLuming ZhouEilidh McLachlanElisabeth SergerKirill ShkuraPrashant K SrivastavaArnau HerveraNick O' NeillTong LiuHassen DhrifZheng WangMiroslav KubatStefan WuchtyMatthias MerkenschlagerLiron LeviEvan ElliottJohn L BixbyVance P LemmonSimone Di GiovanniPublished in: Nature neuroscience (2019)
Axonal injury results in regenerative success or failure, depending on whether the axon lies in the peripheral or the CNS, respectively. The present study addresses whether epigenetic signatures in dorsal root ganglia discriminate between regenerative and non-regenerative axonal injury. Chromatin immunoprecipitation for the histone 3 (H3) post-translational modifications H3K9ac, H3K27ac and H3K27me3; an assay for transposase-accessible chromatin; and RNA sequencing were performed in dorsal root ganglia after sciatic nerve or dorsal column axotomy. Distinct histone acetylation and chromatin accessibility signatures correlated with gene expression after peripheral, but not central, axonal injury. DNA-footprinting analyses revealed new transcriptional regulators associated with regenerative ability. Machine-learning algorithms inferred the direction of most of the gene expression changes. Neuronal conditional deletion of the chromatin remodeler CCCTC-binding factor impaired nerve regeneration, implicating chromatin organization in the regenerative competence. Altogether, the present study offers the first epigenomic map providing insight into the transcriptional response to injury and the differential regenerative ability of sensory neurons.
Keyphrases
- gene expression
- stem cells
- mesenchymal stem cells
- cell therapy
- spinal cord
- dna methylation
- genome wide
- transcription factor
- tissue engineering
- spinal cord injury
- machine learning
- neuropathic pain
- dna damage
- single cell
- optic nerve
- bone marrow
- dna binding
- circulating tumor
- nucleic acid
- simultaneous determination
- heat shock protein