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DNA methylation is essential for mammalian development and physiology. Here we report that the developmentally regulated  H19  lncRNA binds to and inhibits S-adenosylhomocysteine hydrolase (SAHH), the only mammalian enzyme capable of hydrolysing S-adenosylhomocysteine (SAH). SAH is a potent feedback inhibitor of S-adenosylmethionine (SAM)-dependent methyltransferases that methylate diverse cellular components, including DNA, RNA, proteins, lipids and neurotransmitters. We show that  H19  knockdown activates SAHH, leading to increased DNMT3B-mediated methylation of an lncRNA-encoding gene  Nctc1  within the  Igf2-H19-Nctc1  locus. Genome-wide methylation profiling reveals methylation changes at numerous gene loci consistent with SAHH modulation by  H19 . Our results uncover an unanticipated regulatory circuit involving broad epigenetic alterations by a single abundantly expressed lncRNA that may underlie gene methylation dynamics of development and diseases and suggest that this mode of regulation may extend to other cellular components.

H19 lncRNA alters DNA methylation genome wide by regulating S-adenosylhomocysteine hydrolase