Ribosomal protein mutations, mutations that affect ribosomal RNA synthesis, or function of the mature ribosome, trigger a transcriptional response mediated by Xrp1 expression which reduces cellular translation via eIF2-alpha phosphorylation and renders cells liable to competition with wild-type neighbors.

Molecular signals from chloroplasts can synergistically interact with the plant hormone, abscisic acid (ABA), to regulate non-canonical signaling pathways mediating fundamental cellular processes including stomatal closure, seed dormancy and germination.

The Dengue virus contains discretely folded RNA structures that confer the ability to resist a powerful host cell enzyme and produce a disease-inducing noncoding RNA.

The transcription factor Xrp1 mediates a previously unrecognized branch of stress-response signaling, specifically as a downstream effector of eIF2alpha kinases.

Xrp1 contributes to cell competition as a heterodimer with the Drosophila C/EBP homolog Irbp18 and although rapidly evolving is itself conserved beyond Drosophila.

A tissue-specific transcription factor is involved in the regulation of alternative polyadenylation in conjunction with a transcription termination factor.

RNA decay is used at multiple points in the budding yeast unfolded protein response to regulate its suppression and activation, and possibly its attenuation.

Interconnected RNA processing mechanisms ensure the fidelity of non-conventional mRNA splicing during the unfolded protein response.

Dcp2 C-terminal domain cis-regulatory elements collaborating with specific activators control decapping enzyme targeting and activation by orchestrating sequential assembly of distinct decapping complexes.