Abstract
Post-transcriptional control of gene expression is mediated by RNA-binding proteins (RBPs) and small non-coding RNAs (e.g., microRNAs) that bind to distinct elements in their mRNA targets. Here, we review recent examples describing the synergistic and/or antagonistic effects mediated by RBPs and miRNAs to determine the localisation, stability and translation of mRNAs in mammalian cells. From these studies, it is becoming increasingly apparent that dynamic rearrangements of RNA-protein complexes could have profound implications in human cancer, in synaptic plasticity, and in cellular differentiation.
Highlights
The post-transcriptional control of gene expression is fundamental for proper cell homeostasis [1].In particular, the fate of messenger RNAs must be tightly regulated to prevent aberrant synthesis of proteins that could lead to anomalous development and eventual disease [1,2,3]
Regulation of messenger RNAs (mRNAs) is thereby achieved by different RNA-binding proteins (RBPs) and non-coding RNAs, such as microRNAs, which interact with distinct elements in the mRNA, forming so-called ribonucleoprotein (RNP) complexes [4]
Cytoplasmic RBPs preferentially interact with sequences or structural elements located in the 3'-untranslated region (3'-UTR) of mRNAs, allowing targeting of a subset of mRNAs to implement specific control
Summary
The post-transcriptional control of gene expression is fundamental for proper cell homeostasis [1]. Regulation of mRNAs is thereby achieved by different RNA-binding proteins (RBPs) and non-coding RNAs, such as microRNAs (miRNAs), which interact with distinct elements in the mRNA, forming so-called ribonucleoprotein (RNP) complexes [4]. Cytoplasmic RBPs preferentially interact with sequences or structural elements located in the 3'-untranslated region (3'-UTR) of mRNAs, allowing targeting of a subset of mRNAs to implement specific control. We discuss recent examples that support the notion of extensive combinatorial post-transcriptional control of mRNA stability and of translation through interactions with RBPs and/or miRNAs. We focus on recent mechanistic studies exemplifying antagonistic or synergistic arrangements of: (i) RBPs and miRNAs; (ii) RBPs and RBPs and (iii) miRNAs on cytoplasmic mRNAs and their impact in cell biology
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