Journal
NATURE COMMUNICATIONS
Volume 7, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms10458
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Funding
- Wellcome Trust [WT098503, 084071]
- Medical Research Council
- TSB/EPSRC [TS/H000933/1]
- Cambridge Hospitals National Institute for Health Research Biomedical Research Center
- ERC
- Fundacao para a Ciencia e a Tecnologia [SFRH/BD/69033/2010]
- MRC
- EU [257082, 282510]
- Royal Society Wolfson Research Merit Award [WM100023]
- Engineering and Physical Sciences Research Council [TS/H001220/1, TS/H000933/1] Funding Source: researchfish
- Medical Research Council [G0800784, MC_PC_12009, MR/J001597/1, G1000847] Funding Source: researchfish
- Wellcome Trust [095606/Z/11/Z] Funding Source: researchfish
- EPSRC [TS/H001220/1, TS/H000933/1] Funding Source: UKRI
- MRC [MR/J001597/1, G0800784, G1000847] Funding Source: UKRI
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Non-CG methylation is an unexplored epigenetic hallmark of pluripotent stem cells. Here we report that a reduction in non-CG methylation is associated with impaired differentiation capacity into endodermal lineages. Genome-wide analysis of 2,670 non-CG sites in a discovery cohort of 25 phenotyped human induced pluripotent stem cell (hiPSC) lines revealed unidirectional loss (Delta beta = 13%, P<7.4 x 10(-4)) of non-CG methylation that correctly identifies endodermal differentiation capacity in 23 out of 25 (92%) hiPSC lines. Translation into a simplified assay of only nine non-CG sites maintains predictive power in the discovery cohort (Delta beta = 23%, P<9.1 x 10(-6)) and correctly identifies endodermal differentiation capacity in nine out of ten pluripotent stem cell lines in an independent replication cohort consisting of hiPSCs reprogrammed from different cell types and different delivery systems, as well as human embryonic stem cell (hESC) lines. This finding infers non-CG methylation at these sites as a biomarker when assessing endodermal differentiation capacity as a readout.
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