m6A pathway suppression reprograms gene expression during the integrated stress response

hY3 RNA binds and inhibits ribosomes and modulates the starvation-induced integrated stress response

Together, the findings establish hY3 as a ribosome-bound regulator of translation and stress responses, positioning it as a determinant of cell fate under metabolic stress.

Stress induces DCP2 translation via a stalling-dependent mechanism

DCP2, encoding a major mRNA decapping enzyme, is identified as a previously unrecognized ISR-induced transcript and it is shown that translational induction of DCP2 depends on an overlapping ORF whose conserved 3′ region, corresponding to a ribosome pausing site, acts as a potent inhibitory element.

Cellular stress triggers degradation and global redistribution of RNAPII

Transcription is essential for cellular stress response. However, how RNAPII respond to and are regulated during stress are poorly understood. We show that RNAPII is degraded during many types of cellular stresses. In osmotic stressed cells, the TNFα-p38 pathway was activated and promoted the neddylation of the CUL1 E3 ligase complex, which interacted with RPB1 through FBXO11 to ubiquitylate and degrade RNAPII. This caused genome wide RNAPII binding reduction, but prevented RNAPII binding loss from genes with low promoter GC content. This redistribution protected the RNAPII loss from stress response genes in the cell adhesion, MAPK and GPCR pathways. RNAPII redistribution is vital for cell survival, as degradation blockage resulted in the loss of RNAPII from low GC promoters and compromised stress response from disrupted cell adhesion to increased apoptosis. Thus, rapid RNAPII degradation and RNAPII redistribution are components of the cellular stress response to benefit cell survival.

Epitranscriptomic Regulation of mRNA Stability in Plants: Roles of m6A, m5C, and Pseudouridine

A model in which mRNA modifications act combinatorially to regulate mRNA homeostasis in plants is supported, including advances in profiling technologies, single-base resolution methods, and nanopore direct RNA sequencing.

The GCN2-ATF4 signaling axis orchestrates the hepatic transcriptional stress response to short-term sulfur amino acid deprivation.

GCN2 is established as a major sensor mediating the early hepatic response to SAA deprivation, and a transcriptional program essential for maintaining amino acid homeostasis is defined, highlighting a coordinated adaptive response to acute SAA deprivation.

SUMOylation of HSF1 orchestrates transcriptional and splicing programs during the proteotoxic stress response