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New work on DNA polymerase λ highlights its remarkable flexibility. This fits with the generally adaptable nature of the DNA-repair process in which this enzyme is involved—nonhomologous end-joining—which allows this mechanism to handle diverse types of broken DNA ends in order to restore the duplex structure, albeit with a loss of information at the join.
Nuclear actin polymerization helps facilitate chromosome compartment switches that can shift damaged DNA toward a nuclear environment that is favorable for DNA repair. Yet shifting multiple broken DNA strands together can also increase the likelihood of misjoining of the DNA ends and subsequent formation of translocations.
Here the authors report a genomic view of 3D chromatin reorganization following DNA damage. Movement of damaged DNA into nuclear domains, which is brought about by nuclear actin, favors error-free damage repair at the expense of rare chromosome rearrangements with oncogenic potential.
The authors find that silent chromatin is more diverse than just facultative and constitutive heterochromatin. These inactive types have distinct three-dimensional interaction characteristics that are transposable if the underlying chromatin state is altered.
Yelland et al. use yeast genetics and cryo-EM to show how 2′-O-methylation on a single rRNA base gates the assembly of the ribosome via regulating interaction with the essential GTPase Nog2.
Chandramouly et al. discover that human Polλ exhibits robust microhomology-mediated end-joining (MMEJ) activity like PolΦ. Polλ promotes MMEJ in mammalian cells independently of essential nonhomologous end-joining factors LIG4/XRCC4 and Polq, which indicates a distinct Polλ-dependent MMEJ mechanism.
Different patterns of nucleosome exposure by developmentally indispensable pioneer transcription factors and enabling of a nucleosome remodeler complex reveal mechanisms of gene regulatory initiation within compacted chromatin.
GPAT1 is a mitochondrial outer membrane protein that catalyzes the first step of glycerolipid biosynthesis. Cryo-EM structures and functional studies of human GPAT1 uncover the molecular architecture and mechanism of this important acyltransferase.
The structure of a heteromeric volume-regulated LRRC8A/C channel shows a hexameric assembly of four clustered A subunits interspersed by two C subunits, which increase the mobility of the protein, thus facilitating channel activation.
The mechanism controlling SWI/SNF chromatin remodeler targeting is incompletely understood. This study demonstrates that AP-1 transcription factors guide SWI/SNF to genomic regions, resulting in 3D genomic architecture alterations.
ABC-type heterotrimeric proteins can be designed de novo using coiled coils and helical bundles as starting scaffolds, extended using helical repeat proteins and then used as building blocks for higher-order oligomeric assemblies.
LRRK2 is one of the most commonly mutated genes in familial Parkinson’s disease. Here, the authors report a cryo-EM structure of the catalytic half of LRRK2 bound to microtubules, revealing determinants of binding that are independent of LRRK2 kinase activity.
Here the authors show that DNMT3A and DNMT3B are differentially regulated during endoderm and mesoderm differentiation in mouse development and characterize the dynamic DNMT3A and DNMT3B sequence specificity during gastrulation.
In this Perspective the authors discuss the major challenges when studying the role of enhancers in disease etiology, highlighting a path forward for future studies aiming to understand the molecular basis of enhanceropathies.
The authors perform parallel transcriptome sequencing, tRNA qPCR array, ribosome profiling and mass spectrometry across five stages of mouse neocortex development to model the dynamic transcriptome-to-proteome transition, discovering a critical prenatal window during which translational control is predominant.
The authors describe how three types of cis-element (CTCF sites, active TSSs and TTSs) regulate cohesin trafficking along chromosomes. They uncover that this cohesin traffic pattern is genetically linked to gene regulation and RNA processing.