Systematic analyses of natural variants and artificial mutants establish functional landscapes of BRCA1 for homology-directed repair (HDR) and therapy resistance and identify the BRCA1-PALB2 interaction as a key control point for HDR pathway choice.

53BP1 and BRCA1 antagonistically control a temporal choice of two distinct pathways to restart stalled replication forks in a DNA double stand repair-independent manner.

Small molecule inhibitors identified in a biophysical high-throughout screening assay confirm the importance of the interaction between single-stranded DNA and the protein RAD52 for the survival of BRCA2-depleted cells.

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

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.

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 specification of tegumental progenitor cells in Schistosoma mansoni relies on a pair of flatworm-specific transcription factors that are related to genes regulating epidermal specification in free-living flatworms.