Genome-Wide Analysis of RNA Secondary Structure

Abstract

Single-stranded RNA molecules fold into extraordinarily complicated secondary and tertiary structures as a result of intramolecular base pairing. In vivo, these RNA structures are not static. Instead, they are remodeled in response to changes in the prevailing physicochemical environment of the cell and as a result of intermolecular base pairing and interactions with RNAbinding proteins. Remarkable technical advances now allow us to probe RNA secondary structure at single-nucleotide resolution and genome-wide, both in vitro and in vivo. These data sets provide new glimpses into the RNA universe. Analyses of RNA structuromes in HIV, yeast, Arabidopsis, and mammalian cells and tissues have revealed regulatory effects of RNA structure on messenger RNA (mRNA) polyadenylation, splicing, translation, and turnover. Application of new methods for genome-wide identification of mRNA modifications, particularly methylation and pseudouridylation, has shown that the RNA "epitranscriptome" both influences and is influenced by RNA structure. In this review, we describe newly developed genome-wide RNA structure-probing methods and synthesize the information emerging from their application.

Nuclease escape elements protect messenger RNA against cleavage by multiple viral endonucleases

“…Thus, RNA structure appears to be a central component of an SRE and is likely to influence recruitment or arrangement of proteins involved in escape. This is in line with the fact that RNP assembly can be more heavily impacted by structural fidelity than primary sequence recognition [59]. We hypothesize that there is a core set of proteins required for SRE function, such as HuR, but that individual SREs recruit distinct accessory factors that dictate the conditions or mechanism by which that SRE protects against nuclease targeting.…”

From chemical metabolism to life: the origin of the genetic coding process

“…They are flexible molecules that explore the formation of double-stranded regions based on a relaxed complementarity code (A–U and G–C or G–U), forming stems and loops. This situation has long been investigated [53]. It is the basis of a considerable number of works about RNAs involved in a large number of functions, including catalytic activities (ribozymes).…”

DNA aptamers against the DUX4 protein reveal novel therapeutic implications for FSHD

“…It has been shown, for instance, that the bulge loops in DNA aptamers against streptavidin are critical for the affinity . Bulge loops can also occur naturally in structural elements of RNA which are known to be recognized by RNA‐binding proteins . In genomic DNA, bulge loops are considered as erroneous structures and trigger repair mechanisms .…”