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Unrestrained 53BP1 activity causes fusions of dysfunctional telomeres and embryonic lethality associated with misrepair of DNA double-strand breaks in BRCA1-deficient mice. However, the physiological role of 53BP1 remains unclear, because it presumably did not evolve to carry out these pathological functions. A new report proposes that 53BP1 activity prevents hyper-resection and thereby promotes error-free DNA repair while suppressing alternative mutagenic pathways.
Mutations in the BRCA1 and BRCA2 genes strongly predispose carriers to breast and ovarian cancers. Two new studies reveal that FANCD2, a key component of the Fanconi anemia pathway, is essential for the survival of cells with BRCA1 or BRCA2 mutations. These findings pave the way for new 'synthetic lethal' strategies to kill BRCA-mutated cancers.
Ribosome profiling provides a snapshot of the mRNA positions of all elongating ribosomes in the cell. A new powerful enhancement of the technique, translation complex profile sequencing (TCP–seq), extends this mapping to scanning ribosomal complexes. In addition to its usefulness as a tool for studying the regulation of translation initiation, TCP–seq provides specific and powerful signatures of bona fide translation.
The crystal structure of the putative exonuclease Exuperantia, required for Drosophila anterior patterning, reveals an EXO-SAM-like domain architecture that is catalytically inactive but mediates dimerization and RNA binding, which are essential for bicoid localization.
A new study reveals that 53BP1 influences high-fidelity homology-directed repair by showing that its depletion in the presence of increasing DNA-damage levels triggers a shift from RAD51-dependent gene conversion, an error-free process, to RAD52-mediated single-strand annealing, which is mutagenic.
Structural and functional analysis of the Swi2/Snf2 remodeler demonstrates that the catalytic core of the protein is a competent remodeling machine, which rests in an inactive conformation poised for activation.
Biochemical, structural and cell-based analyses reveal a chaperone-like function of glycyl-tRNA synthetase, which supports neddylation via direct interactions with NEDD8, E1 and E2.
Solid-state NMR analyses reveal that the free backbone carbonyl groups associated with proline residues in the transmembrane helices play a key role in mediating rhodopsin activation.
EPR spectroscopy analyses elucidate how lipids affect the conformational dynamics of a multidrug secondary transporter, LmrP, and indicate a key role of the lipid headgroups in shaping the conformational-energy landscape of the transporter.
A crystal structure of the Zika virus NS3 RNA helicase reveals similarities to the RNA helicase from Dengue virus, with variability in loops typically involved in binding ATP and RNA, and aids in identification of potentially druggable hotspots.
Probing the synthetic lethal effect of FANCD2 deletion in BRCA2-deficient cells reveals independent roles of FANCD2 and BRCA2 in stabilizing stalled replication forks to maintain genome stability and promote cell survival.
The complete architecture of the yeast COG tethering complex is revealed by negative-stain electron microscopy, showing an intricate shape with up to five flexible legs.
Electron microscopy analyses of tethering complexes from different families, GARP and HOPS, show that they share a similar architecture featuring long flexible legs. The findings suggest that multisubunit tethering complexes use related structural frameworks to accomplish their functions.