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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.

Farrerol promotes the efficiency of CRISPR/Cas9-mediated genome editing in both cells and embryos.

Genetic analysis of senataxin and RNase H2-deficient mice reveals that genome stability during class switch recombination and antibody generation can be uncoupled, suggesting a role for R loop metabolism dysfunction in lymphomagenesis in patients without immune deficiency.

Crispant analysis in zebrafish serves as a powerful tool for the rapid functional screening of genes implicated in bone fragility disorders, like osteogenesis imperfecta and osteoporosis.

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.

LeishBASEedit enables gene editing in Leishmania without requiring DNA double-strand breaks, homologous recombination, or donor DNA, thereby facilitating loss-of-function screens via delivery of plasmid libraries and regardless of limitations due to gene copy number variations and/or lack of RNAi components.

Generation of a home-and-rescue gene drive targeting an essential gene reveals confinable population modification.

The initiation of human genome replication requires the six-subunit origin recognition complex (ORC) and CDC6, with ORC playing additional roles during mitosis and in organization of the cell nucleus.

Template switching during DNA replication is a frequent source of adaptive gene amplification.