期刊
PLOS ONE
卷 7, 期 5, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0037923
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资金
- Association pour la Recherche contre le Cancer [ARC] [SFI20101201555]
- Agence Nationale de la Recherche [ANR-07-BLAN-0052-02, NT09_669034]
- CEFIC-Long-range Research Initiative [LRI-EMSG49-CNRS-08]
- Ligue Nationale contre le Cancer (comite de l'Herault)
- Centre National de la Recherche Scientifique (CNRS)
- fellowship from the Ligue Nationale contre le cancer (comite de l'Ardeche)
- governmental fellowship from the socialist republic of Vietnam
- Agence Nationale de la Recherche (ANR) [ANR-07-BLAN-0052] Funding Source: Agence Nationale de la Recherche (ANR)
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.
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