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It was recently shown that a long non-coding RNA (lncRNA), that we named the  91H  RNA (i.e. antisense  H19  transcript), is overexpressed in human breast tumours and contributes in  trans  to the expression of the  Insulin-like Growth Factor 2  ( IGF2 ) gene on the paternal chromosome. Our preliminary experiments suggested that an  H19  antisense transcript having a similar function may also be conserved in the mouse. In the present work, we further characterise the mouse  91H  RNA and, using a genetic complementation approach in  H19  KO myoblast cells, we show that ectopic expression of the mouse  91H  RNA can up-regulate  Igf2  expression in  trans  despite almost complete unmethylation of the Imprinting-Control Region (ICR). We then demonstrate that this activation occurs at the transcriptional level by activation of a previously unknown  Igf2  promoter which displays, in mouse tissues, a preferential mesodermic expression (Pm promoter). Finally, our experiments indicate that a large excess of the  H19  transcript can counteract  91H -mediated  Igf2  activation. Our work contributes, in conjunction with other recent findings, to open new horizons to our understanding of  Igf2  gene regulation and functions of the  91H / H19  RNAs in normal and pathological conditions.

H19 Antisense RNA Can Up-Regulate Igf2 Transcription by Activation of a Novel Promoter in Mouse Myoblasts