Abstract:
AIM:Disclosing the mechanisms that regulate reprogramming memory. MATERIALS & METHODS:We established computational procedure to find DNA methylation somatic memory sites (SMSs) at single CpGs and integrated them with genomics, epigenomics, transcriptomics and imprinting information. RESULTS & CONCLUSION:Reprogramming memory persists at late passages in low methylated regions. Contrarily to hypomethylated, hypermethylated SMSs occur at evolutionary conserved sites overlapping active transcription loci in dynamic chromatin regions. The epigenetic-memory molecular origin is the expression of source-cell transcription factors protecting hypomethylated SMSs in euchromatin from de novo methylation, keeping source-cell lineage-specific loci in induced pluripotent stem (iPS) cells incompletely silenced. Sites in lineage-specific genes of different-from-those-of-the-source-cell lineages remain hypermethylated in heterochromatin regions becoming permanently silenced. SMSs cause differential expression between iPS cells and embryonic stem cells through two mechanisms: 'epigenetic/expression memory rule', the DNA unreprogramming methylation status coupled with chromatin states induces differentially expressed genes. 'Imprinting control', the change of DNA methylation status in imprinting control regions induces differential expression of imprinted genes.
journal_name
Epigenomicsjournal_title
Epigenomicsauthors
Luu PL,Gerovska D,Schöler HR,Araúzo-Bravo MJdoi
10.2217/epi-2017-0098subject
Has Abstractpub_date
2018-02-01 00:00:00pages
149-174issue
2eissn
1750-1911issn
1750-192Xjournal_volume
10pub_type
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