MEG3

MEG3 (maternally expressed 3) is a maternally expressed, imprinted is_associated_with::long non-coding RNA is_associated_with::gene. At least 12 different isoforms of MEG3 are generated by is_associated_with::alternative splicing. Expression of MEG3 is lost in cancer cells. It acts as a growth suppressor in is_associated_with::tumour cells, and activates is_associated_with::p53. A is_associated_with::pituitary transcript variant has been associated with inhibited is_associated_with::cell proliferation. Studies in is_associated_with::mouse and is_associated_with::sheep suggest that an upstream is_associated_with::intergenic differentially is_associated_with::methylated region (is_associated_with::IG-DMR) regulates imprinting of the region. The expression profile in mouse of the co-regulated Meg3 and Dlk1 genes suggests a causative role in the pathologies found in is_associated_with::uniparental disomy animals, characterized by defects in is_associated_with::skeletal muscle maturation, is_associated_with::bone formation, is_associated_with::placenta size and organization and is_associated_with::prenatal lethality. The sheep homolog is associated with the callipyge mutation which in is_associated_with::heterozygous individuals affects a muscle-specific long-range control element located in the DLK1-GTL2 intergenic region and results in the callipyge muscular is_associated_with::hypertrophy. The non-is_associated_with::Mendelian inheritance pattern, known as is_associated_with::polar overdominance, likely results from the combination of the cis-effect on the expression levels of genes in the DLK1-GTL2 imprinted domain, and trans interaction between the products of reciprocally imprinted genes.