Homologous recombination is the default response to replication impedance by the RTS1 barrier, leading to restarted replication forks that suffer frequent collapse, triggering further rounds of recombination downstream of the barrier.

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

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.

Unloading the polymerase sliding clamp PCNA from DNA by Elg1 promotes recombination at the RTS1 replication fork barrier by limiting Fbh1 and Srs2 activity.

Genomic deletions and gene conversions, caused by template switching associated with restarted DNA replication, are detected downstream of a collapsed replication fork and are suppressed by several conserved DNA helicases.

Translesion polymerase kappa promotes replication fork restart to maintain genome stability during conditions of nucleotide deprivation.

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

Reconstitution of orientation-specific R-loop-replisome collisions with purified proteins reveals the differential impact of R-loop-associated RNA:DNA hybrids and G-quadruplexes on replication fork progression.

Rtf2 is shown to associate with multiple splicing factors and influence splicing of a subset of introns explaining why previous work erroneously assigned it as a replication restart factor in fission yeast.

Sirtuin, Hst4 is a novel DDK kinase target, which is modified and degraded in response to replication stress, increasing H3K56 acetylation, to stabilize DNA replication forks via fork protection complex which maintains genome stability and has potential in cancer therapeutics.