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Studies of the regulation of gene expression historically focused on transcription. However, during stress and apoptosis, profound gene expression changes occur more rapidly and globally than is possible by regulating transcription. Posttranscriptional changes in mRNA processing and translation in response to diverse stresses shut down most protein translation to conserve energy and lead to rapid remodeling of the proteome to promote repair. Pre-mRNA splicing and mRNA stability are fundamentally altered under some stress conditions. Stress pathways coordinate a cytoprotective repair response, while simultaneously initiating signaling that can ultimately trigger cell death. How the cell mediates the decision between repair and apoptosis is largely not understood. In some stresses, microRNAs may tip the balance. Here, we review what is known about posttranscriptional gene regulation during stress, focusing on what is still unknown and how new technologies might be used to understand what changes are most physiologically important in different forms of stress and death., (© 2013 John Wiley & Sons A/S. Published by Blackwell Publishing Ltd.)

The important role of microRNAs in directing immune responses has become increasingly clear. Here, we highlight discoveries uncovering the role of specific microRNAs in regulating the development and function of natural killer (NK) cells. Furthermore, we discuss the impact of NK cells on the entire immune system during global and specific microRNA ablation in the settings of inflammation, infection, and immune dysregulation., (© 2013 John Wiley & Sons A/S. Published by Blackwell Publishing Ltd.)

Post-transcriptional mechanisms that modulate global and/or transcript-specific mRNA stability and translation contribute to the rapid and flexible control of gene expression in immune effector cells. These mechanisms rely on RNA-binding proteins (RBPs) that direct regulatory complexes (e.g. exosomes, deadenylases, decapping complexes, RNA-induced silencing complexes) to the 3'-untranslated regions of specific immune transcripts. Here, we review the surprising variety of post-transcriptional control mechanisms that contribute to gene expression in the immune system and discuss how defects in these pathways can contribute to autoimmune disease., (© 2013 John Wiley & Sons A/S. Published by Blackwell Publishing Ltd.)

Suppression of viral infection by RNA in a nucleotide sequence homology-dependent manner was first reported in plants in early 1990 s. Studies in the past 15 years have established a completely new RNA-based immune system against viruses that is mechanistically related to RNA silencing or RNA interference (RNAi). This viral immunity begins with recognition of viral double-stranded or structured RNA by the Dicer nuclease family of host immune receptors. In fungi, plants and invertebrates, the viral RNA trigger is processed into small interfering RNAs (siRNAs) to direct specific silencing of the homologous viral genomic and/or messenger RNAs by an RNaseH-like Argonaute protein. Deep sequencing of virus-derived siRNAs indicates that the immunity against viruses with a positive-strand RNA genome is induced by Dicer recognition of dsRNA formed during the initiation of viral progeny (+)RNA synthesis. The RNA-based immune pathway in these organisms overlaps the canonical dsRNA-siRNA pathway of RNAi and may require amplification of viral siRNAs by host RNA-dependent RNA polymerase in plants and nematodes. Production of virus-derived small RNAs is undetectable in mammalian cells infected with RNA viruses. However, infection of mammals with several nucleus-replicating DNA viruses induces production of virus-derived microRNAs capable of silencing host and viral mRNAs as found for viral siRNAs. Remarkably, recent studies indicate that prokaryotes also produce virus-derived small RNAs known as CRISPR RNAs to guide antiviral defense in a manner that has yet to be defined. In this article, we review the recent progress on the identification and mechanism of the key components including viral sensors, viral triggers, effectors, and amplifiers, of the small RNA-directed viral immunity. We also highlight some of the many unresolved questions.