LAUSR

Numerous human genome sequencing projects have clearly indicated that only ≈2% of the human genome is constituted by protein-coding genes and that >90% of the genome is actively transcribed. This apparent lack of efficiency of mammalian cells has been explained with the existence of classes of RNAs biochemically similar to mRNA, but functionally different because they do not act as a template for protein synthesis. LncRNAs (long noncoding RNAs) belong to one of these classes and their crucial role in both cardiac physiology and disease has been clearly demonstrated for some of them, such as CHAST (cardiac hypertrophy–associated transcript), MIAT (myocardial infarction-associated transcript), CHRF (cardiac hypertrophy–related factor), and BACE1-AS (beta-secretase 1-antisense).1–4 The function of the vast majority of them remains, however, unknown. Article, see p 1347 LncRNAs have been identified both in the nucleus and in the cytoplasm and can function through their sequence and structure. Indeed, by associating with DNA, RNA, and proteins, they can modify gene expression and activity, either transcriptionally or posttranscriptionally. One of the functions of lncRNAs is to regulate genomic imprinting, that is, the monoallelic silencing of specific genes, based on the parent-of-origin of the allele. In mammals, during early gametogenesis, almost 1% of protein-coding genes are epigenetically marked so that their expression occurs in a parent of origin-specific manner.5 Genomic imprinting relies on cis -acting long-distance gene regulatory mechanisms that make use of chromatin insulators and lncRNAs.5 There are several imprinted RNAs maternally or paternally expressed, and …