Mutational inactivation of the JNK signaling pathway causes genomic instability and breast cancer development.

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.

Interaction with PUMILIO is essential for maintenance of genomic stability by the cytoplasmic long noncoding RNA NORAD, whereas binding to RBMX is dispensable for this function.

Genetic predisposition to uterine leiomyomas arises from variation at loci for genetic stability and genitourinary development, and in part explains the frequent occurrence of the condition in women with African origin.

Fifteen continuous high-grade serous ovarian carcinoma patient-derived organoids are characterized by transcriptomic, genomic, and drug sensitivity assays to reveal that they comprise communities of clonal populations and represent models of different causes of chromosomal instability and degrees of genome complexity.

c-di-GMP and HipH function as a toxin-antitoxin-like module to regulate persister cell formation in bacterial biofilms.

The genomic regions that cause male hybrids between house mouse subspecies to have low fertility have been identified.

A new role for Endonuclease G with respect to the generation of mtDNA deletions is identified, which is dependent on the formation of G4 DNA within human mitochondria.

RNA Polymerase II transcriptional termination of a nuclear long non-coding RNA is required to maintain the mitochondrial genome and hence promotes budding yeast growth.

Transposable elements are not reactivated in natural hybrids of the yeast Saccharomyces paradoxus, but their accumulation is genotype-specific and is not predicted by the evolutionary divergence between a hybrid's parents.