Transposition reactions that occur during DNA replication and involve the termini of adjacent transposons can induce genome expansion by re-replication of transposon-flanking sequences.

Recombinant mitochondrial genomes can be selected, traits can be genetically mapped and new genetic combinations can be made.

Polymerase θ is among the most proficient terminal transferases known and switches between three different mechanisms of terminal transferase activity.

The model organism Tetrahymena thermopile carries two nuclei with distinct genomes: an unrearranged germline genome with five chromosomes, and a somatic genome reduced in size by a third and with 181 chromosomes.

Phenotypic diversity and cell state transition (i.e., acquisition of a CD44+/CD24- cell state or exposure to TGF-beta) can spur intra-tumor genetic heterogeneity and contribute to acquired resistance.

The discovery of a mechanism that causes DNA deletions during non-canonical DNA replication termination is described.

In concert phosphorylation site modification of both XRCC4 and XLF C-terminal disordered tails promotes disassembly of XRCC4/XLF DNA tethers during c-NHEJ.

p53 suppresses genome instability by direct role at stalled replication forks for pathway regulation that explains transcription-independent p53 tumor-suppressor functions.

Using barcoded mutagenesis and a high-throughput genetic screen results in the identification of 150 genes that affect lipid accumulation in a non-model yeast system.

If released in the wild, current CRISPR-based gene drive systems designed to alter populations could spread much farther than intended, despite the evolution of drive resistance.