H19 antisense RNA can up-regulate Igf2 transcription by activation of a novel promoter in mouse myoblasts.
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 experi...
Guardado en:
| Autores principales: | , , , , , , , , , , , , , , |
|---|---|
| Formato: | article |
| Lenguaje: | EN |
| Publicado: |
Public Library of Science (PLoS)
2012
|
| Materias: | |
| Acceso en línea: | https://doaj.org/article/ee39985557a84364b441e1ede4cdd599 |
| Etiquetas: |
Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
|
| id |
oai:doaj.org-article:ee39985557a84364b441e1ede4cdd599 |
|---|---|
| record_format |
dspace |
| spelling |
oai:doaj.org-article:ee39985557a84364b441e1ede4cdd5992021-11-18T07:17:14ZH19 antisense RNA can up-regulate Igf2 transcription by activation of a novel promoter in mouse myoblasts.1932-620310.1371/journal.pone.0037923https://doaj.org/article/ee39985557a84364b441e1ede4cdd5992012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22662250/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203It 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.Van Giang TranFranck CourtAnne DuputiéEtienne AntoineNathalie AptelLaura MilliganFrançoise CarbonellMarie-Noëlle Lelay-TahaJacques PietteMichaël WeberDidier MontarrasChristian PinsetLuisa DandoloThierry FornéGuy CathalaPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 5, p e37923 (2012) |
| institution |
DOAJ |
| collection |
DOAJ |
| language |
EN |
| topic |
Medicine R Science Q |
| spellingShingle |
Medicine R Science Q Van Giang Tran Franck Court Anne Duputié Etienne Antoine Nathalie Aptel Laura Milligan Françoise Carbonell Marie-Noëlle Lelay-Taha Jacques Piette Michaël Weber Didier Montarras Christian Pinset Luisa Dandolo Thierry Forné Guy Cathala H19 antisense RNA can up-regulate Igf2 transcription by activation of a novel promoter in mouse myoblasts. |
| description |
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. |
| format |
article |
| author |
Van Giang Tran Franck Court Anne Duputié Etienne Antoine Nathalie Aptel Laura Milligan Françoise Carbonell Marie-Noëlle Lelay-Taha Jacques Piette Michaël Weber Didier Montarras Christian Pinset Luisa Dandolo Thierry Forné Guy Cathala |
| author_facet |
Van Giang Tran Franck Court Anne Duputié Etienne Antoine Nathalie Aptel Laura Milligan Françoise Carbonell Marie-Noëlle Lelay-Taha Jacques Piette Michaël Weber Didier Montarras Christian Pinset Luisa Dandolo Thierry Forné Guy Cathala |
| author_sort |
Van Giang Tran |
| title |
H19 antisense RNA can up-regulate Igf2 transcription by activation of a novel promoter in mouse myoblasts. |
| title_short |
H19 antisense RNA can up-regulate Igf2 transcription by activation of a novel promoter in mouse myoblasts. |
| title_full |
H19 antisense RNA can up-regulate Igf2 transcription by activation of a novel promoter in mouse myoblasts. |
| title_fullStr |
H19 antisense RNA can up-regulate Igf2 transcription by activation of a novel promoter in mouse myoblasts. |
| title_full_unstemmed |
H19 antisense RNA can up-regulate Igf2 transcription by activation of a novel promoter in mouse myoblasts. |
| title_sort |
h19 antisense rna can up-regulate igf2 transcription by activation of a novel promoter in mouse myoblasts. |
| publisher |
Public Library of Science (PLoS) |
| publishDate |
2012 |
| url |
https://doaj.org/article/ee39985557a84364b441e1ede4cdd599 |
| work_keys_str_mv |
AT vangiangtran h19antisensernacanupregulateigf2transcriptionbyactivationofanovelpromoterinmousemyoblasts AT franckcourt h19antisensernacanupregulateigf2transcriptionbyactivationofanovelpromoterinmousemyoblasts AT anneduputie h19antisensernacanupregulateigf2transcriptionbyactivationofanovelpromoterinmousemyoblasts AT etienneantoine h19antisensernacanupregulateigf2transcriptionbyactivationofanovelpromoterinmousemyoblasts AT nathalieaptel h19antisensernacanupregulateigf2transcriptionbyactivationofanovelpromoterinmousemyoblasts AT lauramilligan h19antisensernacanupregulateigf2transcriptionbyactivationofanovelpromoterinmousemyoblasts AT francoisecarbonell h19antisensernacanupregulateigf2transcriptionbyactivationofanovelpromoterinmousemyoblasts AT marienoellelelaytaha h19antisensernacanupregulateigf2transcriptionbyactivationofanovelpromoterinmousemyoblasts AT jacquespiette h19antisensernacanupregulateigf2transcriptionbyactivationofanovelpromoterinmousemyoblasts AT michaelweber h19antisensernacanupregulateigf2transcriptionbyactivationofanovelpromoterinmousemyoblasts AT didiermontarras h19antisensernacanupregulateigf2transcriptionbyactivationofanovelpromoterinmousemyoblasts AT christianpinset h19antisensernacanupregulateigf2transcriptionbyactivationofanovelpromoterinmousemyoblasts AT luisadandolo h19antisensernacanupregulateigf2transcriptionbyactivationofanovelpromoterinmousemyoblasts AT thierryforne h19antisensernacanupregulateigf2transcriptionbyactivationofanovelpromoterinmousemyoblasts AT guycathala h19antisensernacanupregulateigf2transcriptionbyactivationofanovelpromoterinmousemyoblasts |
| _version_ |
1718423700539179008 |