Petr Ćejka

Prime editing enables high-throughput identification and characterization of selective MutSβ inhibitors

This study uses prime editing to identify and characterize MutSβ inhibitors that reduce (CAG)n repeat expansion.

Non-canonical ATR signalling via NBS1 phosphorylation propagates fork slowing from stressed to unperturbed nuclear regions

Meiotic pairing through barcode-like satellite DNA repeats

The paper demonstrates that satellite DNA barcodes facilitate meiotic pairing in Drosophila by showing that repeat mismatches disrupt pairing and that pairing defects correlate with oocyte death.

Critical roles of MCM8 in meiotic recombination during mouse spermatogenesis

This study investigates the role of MCM8 in meiotic recombination in mouse spermatocytes, showing it regulates DSB number and post-resection intermediate formation.

SMARCAL1 is a candidate therapeutic target for ALT-positive tumors

The paper identifies SMARCAL1 as a key regulator of ALT metabolism and a potential therapeutic target for ALT-positive tumors.

Rad51 determines pathway usage in post-replication repair

This study identifies Rad51 mutations that shift post-replication repair pathway usage from homologous recombination to alternate pathways by affecting fork protection.

IFI16 senses and protects stalled replication forks

This paper shows that IFI16 detects stalled replication forks and triggers an innate immune response, while also protecting nascent DNA from degradation and aiding in fork protection in BRCA-deficient cells.

Nuclear mechanostability emerges from satellite DNA condensation into chromocenters

This study shows that nuclear mechanostability arises from satellite DNA condensation into chromocenters, which help dissipate mechanical stress and protect genome integrity.

The PIN1-p38-CtIP signaling axis protects stalled replication forks from deleterious degradation

This study identifies the PIN1-p38-CtIP signaling pathway as essential for protecting stalled replication forks from degradation, independent of its role in homologous recombination.

FIGNL1 inhibits homologous recombination in BRCA2 deficient cells by dissociating RAD51 filaments

This study shows that FIGNL1 inhibits homologous recombination in BRCA2-deficient cells by preventing RAD51 filament removal, maintaining genome stability and viability.

HLTF Prevents G4 Accumulation and Promotes G4-induced Fork Slowing to Maintain Genome Stability

This paper shows that HLTF has two roles in managing G4s: preventing their accumulation and slowing replication forks to maintain genome stability.

Inhibition of MRN activity by a telomere protein motif

The paper shows that the MIN motif in Rif2 inhibits MRN complex activity at telomeres, preventing DDR activation and NHEJ in yeast.

The Pif1 helicase is actively inhibited during meiotic recombination which restrains gene conversion tract length

The paper shows that the Pif1 helicase is inhibited by the Mer3-MutLβ complex during meiotic recombination, limiting gene conversion tract length.

Mechanism of in vivo activation of the MutLγ-Exo1 complex for meiotic crossover formation

The paper identifies the role of the MutLγ-Exo1 complex in meiotic crossover formation by showing Exo1 recruits Cdc5 to activate MutLγ and highlights its spatial regulation near DSB hotspots.

Identification of MCM8IP, an interactor of MCM8-9 and RPA1 that promotes homologous recombination and DNA synthesis in response to DNA damage

This study identifies MCM8IP as a DNA repair factor that promotes homologous recombination and DNA synthesis in response to DNA damage by interacting with MCM8-9 and RPA1.

Removal of Spo11 from meiotic DNA breaks in vitro but not in vivo by Tyrosyl DNA Phosphodiesterase 2

This study shows TDP2 can remove Spo11 from Spo11-DSBs in vitro but not in vivo, suggesting structural barriers prevent TDP2 access to Spo11-DNA in living cells.

The crossover function of MutSγ is activated via Cdc7-dependent stabilization of Msh4

This study shows that MutSγ activation during meiosis depends on Cdc7-mediated phosphorylation of Msh4, stabilizing the complex and enabling crossover formation.