Selective degradation of mature miRNAs shapes temporal miRNA expression patterns and is important for proper regulation of target genes to support normal development of Drosophila embryos.

Mutation of Glycine 34 to Arginine within the N-terminal tail of histone H3 alters post-translational modifications on Lysine 36 and is associated with a delay in replication restart, defective homologous recombination and an increase in genomic instability.

The Hippo pathway downstream effector YAP regulates S-phase progression to protect neural stem cells of the retina from experiencing genomic instability.

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

In addition to causing DNA damage, R-loops cause genomic instability by interfering with DNA repair.

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

SPOP mutations underlie a novel, genomically unstable subclass of prostate cancer by altering DNA repair.

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.

MicroRNAs tightly control the cellular level of homologous recombination (HR) factors in the G1 phase, and failure of this control system results in an ectopic increase in HR proteins in G1 cells leading to impaired DNA repair.

The ribosomal protein, Rps27l, plays an oncogenic role by promoting p53 degradation via stabilizing the Mdm2-Mdm4 complex, but a tumor suppressor role by preventing the aneuploidy and loss of p53 heterozygosity.