Identification and characterization of a virus-inducible non-coding RNA in mouse brain

Abstract

Japanese encephalitis virus or Rabies virus results in the activation of a gene encoding a novel, non-coding RNA (ncRNA) in the mouse central nervous system. This transcript, named virus-inducible ncRNA (VINC), is identical to a 3?18 kb transcript expressed in mouse neonate skin (GenBank accession no. AK028745) that, together with a number of unannotated cDNAs and expressed sequence tags, is grouped in the mouse unigene cluster Mm281895. VINC is expressed constitutively in early mouse embryo and several adult non-neuronal mouse tissues, as well as a murine renal adenocarcinoma (RAG) cell line. Northern blotting of nuclear and cytoplasmic RNAs revealed that VINC is localized primarily in the nucleus of RAG cells and is thus a novel member of the nuclear ncRNA family. Non-protein-coding eukaryotic genome sequences, often referred to as 'junk DNA', are estimated to encode several non-coding RNAs (ncRNAs), which may account for nearly 98 % of all genomic output in humans (http://research. imb.uq.edu.au/rnadb). In addition to the classical ncRNAs, such as rRNA, tRNA and small nucleolar RNAs, the eukaryotic genome encodes two distinct categories of ncRNAs, referred to as small ncRNAs and long mRNA-like ncRNAs. The long ncRNAs, which are transcribed by RNA polymerase II, spliced and polyadenylated, are implicated in a number of regulatory processes, such as imprinting, X-chromosome inactivation, DNA demethylation, transcription, RNA interference, chromatin-structure dynamics and antisense regulation. In addition, long mRNA-like ncRNAs such as MALAT-1, BC-1 and BC-200 serve as prognostic markers for cancer, whilst the prion-associated RNAs LIT-1, SCA-8 etc. are implicated in a number of neurological disorders (Costa, 2005). Thus, identification and characterization of novel ncRNAs and constant updating of the mammalian RNome are essential for the complete deciphering of genome biology and understanding mammalian gene regulation.

A novel non-protein-coding infection-specific gene family is clustered throughout the genome of Phytophthora infestans

“…that are directly or indirectly required for mRNA processing and translation. In contrast, regulatory ncRNAs are usually themselves tightly developmentally regulated (reviewed by Goodrich & Kugel, 2006;Hirsch et al, 2006;Saha et al, 2006), and they have been shown to be involved in diverse biological mechanisms, such as the control of chromosome architecture, transcriptional regulation, developmental timing of protein synthesis, and mRNA turnover, and they may also regulate alternative splicing (Ling et al, 2005; reviewed by Goodrich & Kugel, 2006;Mattick, 2003;Morey & Avner, 2004). At least one non-coding RNA gene, HAR1F in humans, shows significant evolutionary acceleration, and is associated with the unique biology of that species in terms of brain development (Pollard et al, 2006).…”

MEN ε/β nuclear-retained non-coding RNAs are up-regulated upon muscle differentiation and are essential components of paraspeckles

“…1), suggesting that Men e/ b transcripts are, in fact, present at a higher level in myotubes. In addition to muscle differentiation-related regulation, Men e transcripts have been reported to be up-regulated in mouse brain infected with Japanese encephalitis virus or Rabies virus (Saha et al 2006), although the biological significance of this induced expression remains to be explored.…”

Functional dissection of NEAT1 using genome editing reveals substantial localization of the NEAT1_1 isoform outside paraspeckles

“…NEAT1 transcription can be significantly influenced by p53 and is often up-regulated by stresses, such as hypoxia, viral infection/products, and genotoxic agents (Saha et al 2006;Choudhry et al 2014;Imamura et al 2014;Adriaens et al 2016). Unsurprisingly, there is also a strong link between high NEAT1 expression and more aggressive forms of cancer (Chakravarty et al 2014;Chai et al 2016;Chen et al 2016;Fu et al 2016;Ma et al 2016;Sun et al 2016;Wang et al 2016).…”