Quantification of expression and methylation of the Igf2r imprinted gene in segmental trisomic mouse model
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
12906851
DOI
10.1016/s0888-7543(03)00118-6
PII: S0888754303001186
Knihovny.cz E-resources
- MeSH
- RNA, Antisense metabolism MeSH
- Genomic Imprinting * MeSH
- DNA Methylation * MeSH
- Disease Models, Animal MeSH
- Mice MeSH
- Organ Specificity MeSH
- Receptor, IGF Type 2 genetics metabolism MeSH
- Trisomy genetics MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- RNA, Antisense MeSH
- Receptor, IGF Type 2 MeSH
Insulin-like growth factor 2 receptor (Igf2r), a maternally expressed imprinted gene, is triplicated in Ts43H trisomic mice. To verify its expression in a trisomic mode, we examined the allele-specific transcripts and relative levels of Igf2r mRNA in trisomic and control mice. Igf2r was expressed from the maternal allele(s) and silenced on the paternal allele(s) in most tissues of maternally or paternally derived Ts43H mice. The triallelic expression was observed in adult brain and testis and in embryonic head, but the antisense transcript, Air, was strictly paternal, and methylation of region 2 was strictly maternal in all tissues. The Igf2r expression in maternally derived trisomics, with two active copies of the gene, did not exceed the average mRNA levels of euploid controls with monoallelic expression. Thus, an indication is presented for a dosage compensation mechanism of Igf2r in the trisomic context.
References provided by Crossref.org
Segmental trisomy of chromosome 17: a mouse model of human aneuploidy syndromes
Segmental trisomy of mouse chromosome 17: introducing an alternative model of Down's syndrome