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Genome-wide analyses of the effects of U1 snRNP inhibition in human cells shows that telescripting suppresses premature cleavage and polyadenylation in long introns to sustain expression of large genes important for cell cycle and development.
Crystal structures of a chimeric GABAA receptor define new allosteric binding sites for inhibitory and potentiating neurosteroids within the α subunit transmembrane domain.
Genome-wide analyses of somatic mutations across six cancer types show that mutation frequencies differ between chromosomal regions located at the nuclear core versus the periphery, and thus mutational patterns are influenced by nuclear architecture.
The near-atomic structure of the Chaetomium thermophilum 90S preribosome explains how assembly factors and pre-rRNA guide folding of pre-40S domains and suggests a proofreading model for the 90S–pre-40S transition.
The structure of zebrafish DUB USP30 in complex with a Lys6-linked diUb, along with biochemistry analyses, reveals the basis for Lys6-linkage specificity.
Structural and biochemical analyses of human USP30 explain the basis of Lys6-linkage preference and regulation by PINK1 and Parkin, shedding light onto how USP30 can act as a brake on mitophagy.
NMR spectroscopy analyses of the Abl regulatory module (RM), which tunes Abl kinase activity, explain the mechanism of certain RM-located drug-resistance mutations.
The 3.8-Å cryo-EM structure of the Saccharomyces cerevisiae small-subunit processome in a state that precedes pre-rRNA cleavage at site A1 provides an essentially complete near-atomic model of this assembly.
Cryo-EM and X-ray crystallography to determine the mammalian RNA Pol II–DSIF complex structure maps DSIF's polymerase, DNA-template and transcript contacts that facilitate transcription elongation.
Cryo-EM structures of two late-stage assembly intermediates of the human mitoribosomal large subunit reveal the timing of rRNA folding and protein incorporation during the final steps of ribosomal maturation and identify two new assembly factors.
Crystal structures of unprocessed and mature crRNA-bound LbaCas13a shed light upon catalytic residues involved in crRNA maturation and mechanisms blocking Cas13a nuclease activity before target-RNA binding.
The robustness of the circadian clock deteriorates with aging. Two new studies show that aging reprograms the circadian transcriptome in a cell-type-dependent manner and that such rewiring can be reversed by caloric restriction.
Group II chaperonins facilitate protein folding by undergoing ATP-driven conformational changes. A recent study reveals a tunable allosteric network in group II chaperonins that includes a residue at the intersubunit interface, which is important for assembly and allosteric coordination. The authors also propose that lower cooperativity allows group II chaperonins to achieve optimal substrate folding over a broad range of ATP concentrations.
The monoallelic expression of many imprinted genes in mammals depends on DNA methylation marks that originate from the germ cells. Recent studies in mice and fruit flies evoke a novel, transient mode of genomic imprinting in which oocyte-acquired histone H3 Lys27 trimethylation (H3K27me3) marks are transmitted to the zygote and modulate the allele specificity and timing of gene expression in the early embryo.
In this Review, Peña, Hurt and Panse discuss our current knowledge on the eukaryotic ribosome assembly, a complex process that takes place across different cellular compartments and involves over 200 assembly factors.
In vitro and in vivo data show that ER protein CNPY2 initiates the PERK–CHOP signaling pathway to trigger the unfolded protein response (UPR) and contributes to hepatic steatosis.
A comprehensive proteomics screen for ‘reader’ proteins that recognize m6A-modified RNA reveals that the modification both promotes and prevents the binding of factors that control mRNA homeostasis in mammalian cells.
The lncRNA NEAT1, a key component of paraspeckles, interacts with RNA-binding proteins, including NONO and PSF, and affects global pri-miRNA processing by recruiting the Drosha–DGCR8 Microprocessor.
A Shaker Kv-channel V478W mutant shows enhanced C-type inactivation with disruption of the outermost K+ site in the selectivity filter (IS1). The crystal structure of Kv1.2-2.1 bearing the equivalent mutation reveals an empty IS1.