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A genetic screen in C. elegans identifies a suppressor of siRNA and a new subset of 22G-RNAs that act through the nuclear RNAi pathway to downregulate pre-rRNA under stress conditions.
STAT2, previously known as a positive effector of interferon signaling, is now shown to participate in negative feedback and suppression of this signaling pathway, by recruiting USP18 to the type I IFN receptor subunit IFNAR2.
Single-cell RNA sequencing of preimplantation mouse embryos demonstrates that lack of paternal Xist leads to genome-wide transcriptional misregulation in the early blastocyst and a failure to activate the extraembryonic pathway.
Guanine-rich sequences with a tendency to form G4 structures are a hallmark of hominoid-specific L1 retrotransposons, and their stabilization increases L1 mobility, thus potentially affecting genome evolution.
Structural, biochemical and in vivo analyses reveal that Rad50 zinc-hook and coiled-coil domains form a novel dimerization interface essential for Mre11-complex function in DNA damage response and repair.
The molecular chaperone HSP90 is found to affect the expression of mouse endogenous retrovirus elements and neighboring genes through the KAP1–SETDB1 epigenetic-repression machinery.
Using a family of spectrin domain variants and a combination of structural, biochemical and biophysical approaches, it is shown that cotranslational folding cannot be predicted on the basis of the folding behavior of isolated proteins.
Nascent-strand mapping of active DNA replication origins before and after gastrulation in C. elegans reveals that replication initiation is coordinated with transcriptional programs during embryonic development.
Crystal structures of the linker region of TRPML1 reveal that the luminal domain forms a tetrameric pore. Along with electrophysiology studies, this work provides insight into the mechanism of channel regulation by Ca2+ and H+.
The cryo-EM structure of pre-60S purified via Nmd3 provides molecular insights into the roles of assembly factors Nmd3, Lsg1, Tif6 and Reh1 in the last steps of ribosomal large-subunit maturation.
A comprehensive analysis of the human SUMO proteome, in HeLa and U2OS cell lines and under different conditions, identifies new SUMOylated sites and reveals cross-talk between SUMO and other post-translational modifications, such as phosphorylation.
Crystal structures of a localization element of ASH1 mRNA alone, in complex with its nuclear shuttling protein She2p, and in the cytoplasmic complex with She2p and She3p reveal a step-wise maturation pathway.
Cryo-EM structures of full-length human PC2 reveal two distinct channel states: an open conformation and a blocked conformation with Ca2+ bound at the entrance of the selectivity filter.
The cryo-EM structure of immature Zika virus shows partially ordered capsid proteins and reveals differences between pre-epidemic and epidemic strains at protein interfaces within the trimeric spikes.
A combination of SILAC-MS, genome-wide nucleosome mapping and live-cell imaging reveal rapid histone degradation and global chromatin decompaction after the induction of DNA double-strand breaks in S. cerevisiae.
The yeast ribosome-associated complex (RAC) is formed by Hsp40 protein Zuo1 and the atypical Hsp70 chaperone Ssz1. Structural analyses show Ssz1 in a hybrid conformation between the open and closed state and its substrate-binding domain completed by Zuo1.
Cryo-EM structures of secretin GspD in type II secretion systems from Escherichia coli and Vibrio cholera reveal a pentadecameric architecture, with three rings in the periplasm and β-strand-enriched gates on the outer membrane.
Cryo-EM and NMR analyses of the E. coli replisome show how DNA-end fraying after mismatch incorporation at the polymerase active site enables substrate ends to reach the ‘proofreading’ exonuclease site for mismatch removal.
Loss of function of the CFTR anion channel leads to cystic fibrosis, the most common inherited condition in humans of European origin. A recently reported structure for CFTR at 3.7-Å resolution reveals an unexpected 'lasso' domain and provides new insights into channel function in healthy individuals and in people with cystic fibrosis.
Determining the molecular mechanisms responsible for trinucleotide DNA repeat expansions is critical, as such expansions underlie many neuromuscular and neurodegenerative disorders. Mirkin and colleagues now propose that large-scale expansions of trinucleotide repeats can be generated by DNA-break-induced replication.