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DNA double-stranded breaks can be repaired through error-prone pathways. Here, van Schendel et al. demonstrate that C. elegansacquires inheritable mutations through the use of polymerase theta-mediated end joining.

How repair of DNA interstrand crosslinks contributes to mutagenesis is not understood. Here, the authors identify two mutagenic repair pathways in C. elegans: FAN1-mediated translesion synthesis causing SNVs, and POLQ-mediated end joining leading to deletions. They also uncover a role for TRAIP.

Manganese-based hydrogenation catalysts are sensitive to high temperatures and may degrade under industrially relevant conditions. Here, the authors report a highly efficient manganese pincer pre-catalyst displaying high TOF values (up to 41 000 h⁻¹) and stability (TON up to 200 000) at loadings as low as 5-200 ppm.

Here the authors show that DNA double-strand breaks move outside facultative heterochromatin for repair, which coincides with demethylation of H3K27me3. This movement, demethylation and subsequent correct repair depend on the histone demethylase dUtx.

The mechanism for T-DNA integration, a critical step of Agrobacterium-mediated transgenesis, remains elusive. Now, a study shows that polymerase θ controls T-DNA integration and generates the error-prone sequences at the sites of integration.

Human antibodies cross-reactive for several viruses within the Ebolavirus genus have been identified. Here the authors present the crystal structure of such a neutralizing monoclonal antibody (mAb) targeting the stalk of Bundibugyo virus glycoprotein and show that mAb binding may interfere with trimeric bundle assembly and/or the viral membrane.

Genomes contain tracts of tandem guanines, which can adopt stable G-quadruplex structures that obstruct replication fork movement. Here, Koole et al. describe a non-canonical polymerase Theta-dependent repair pathway that prevents genomic instability caused by these replication barriers.

CRISPR-Cas9 can introduce unintended off-target effects. Here authors show that unintended mutations produced by in vivo of zebrafish can be inherited by their off-spring.

Soil-borne Agrobacterium tumefaciens can transform plants by transferring part of its DNA, which subsequently integrates into the host genome. This study reveals how the 5′ end of this bacterial DNA becomes stably attached to plant genomic DNA.

To overcome challenges posted by vast number of GPCR genes and redundancy, the authors disrupted nearly all GPCR-encoding genes in C. elegans, enabling effective examination of GPCR signaling and offering a valuable resource for the research community.

Error-prone repair of DNA double-strand breaks have been implied to cause cancer-associated genome alterations, but the mechanism of their formation remains unclear. Here the authors find that DNA polymerase α primase plays part in tandem duplication formation at CRISPR/Cas9-induced complementary 3′ ssDNA protrusions.

Barriers to DNA replication are potent sources of genome instability. Here, the authors provide a mechanistic model for how a single persistent G-quadruplex structure generates multiple substrates for polymerase theta-mediated end-joining, thus causing multiple deletions during animal development.

Susan Gasser and colleagues find that methylation at histone H3 lysine 9 (H3K9me) is required for repression of simple repeats and transposons in Caenorhabditis elegans. Loss of H3K9me in worms leads to extensive accumulation of insertions and deletions at repeat elements, which correlate with R-loop formation and increased sensitivity to replication stress.