ArticleThe Journal of biological chemistry2020
PDS5 proteins are required for proper cohesin dynamics and participate in replication fork protection.
Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 75 citations in OpenAlex.
- Folding a broken genome: the versatile roles of cohesin in genome maintenance.Nature reviews. Genetics · 2026Review
- Article
- Multifaceted roles of PDS5B in RAD51-dependent homology-directed DNA repair and replication fork protection.Nature communications · 2026Article
- Cohesin cofactor dosage sets the rate of loop extrusion, rendering genome folding tunable yet vulnerable to genetic disruption.Molecular cell · 2026Article
- Clinical,medRxiv : the preprint server for health sciences · 2026Article
- CTCF/cohesin-binding sites are susceptible to replication-associated DNA damage and genomic instability in cancer cells.iScience · 2026Article
- Linking Genotype to Clinical Features inGenes · 2025Review
- Development of a New Personalized Molecular Test Based on Endometrial Receptivity and Maternal-Fetal Dialogue: Adhesio.Biochemical genetics · 2025Article
- Dosage sensitivity of the loop extrusion rate confers tunability to genome folding while creating vulnerability to genetic disruption.bioRxiv : the preprint server for biology · 2025Article
- NIPBL and STAG1 enable loop extrusion by providing differential DNA-cohesin affinity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Dynamic barriers modulate cohesin positioning and genome folding at fixed occupancy.Genome research · 2025Article
- Co-essentiality analysis identifies PRR12 as a cohesin interacting protein and contributor to genomic integrity.Developmental cell · 2025Article
- The cohesin-associated protein Pds5A governs the meiotic spindle assembly via deubiquitination of Kif5B in oocytes.Science advances · 2025Article
- Roles for the 3D genome in the cell cycle, DNA replication, and double strand break repair.Frontiers in cell and developmental biology · 2025Review
- Chromoanasynthesis.Methods in molecular biology (Clifton, N.J.) · 2025Article
- STAG2 loss in Ewing sarcoma alters enhancer-promoter contacts dependent and independent of EWS::FLI1.EMBO reports · 2024Article
- Dynamic barriers modulate cohesin positioning and genome folding at fixed occupancy.bioRxiv : the preprint server for biology · 2024Article
- FIGNL1-FIRRM is essential for meiotic recombination and prevents DNA damage-independent RAD51 and DMC1 loading.Nature communications · 2024Article
- H3K4me1 recruits DNA repair proteins in plants.The Plant cell · 2024Article
- Oncogenic c-Myc induces replication stress by increasing cohesins chromatin occupancy in a CTCF-dependent manner.Nature communications · 2024Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cohesin is a chromatin-bound complex that mediates sister chromatid cohesion and facilitates long-range interactions through DNA looping. How the transcription and replication machineries deal with the presence of cohesin on chromatin remains unclear. The dynamic association of cohesin with chromatin depends on WAPL cohesin release factor (WAPL) and on PDS5 cohesin-associated factor (PDS5), which exists in two versions in vertebrate cells, PDS5A and PDS5B. Using genetic deletion in mouse embryo fibroblasts and a combination of CRISPR-mediated gene editing and RNAi-mediated gene silencing in human cells, here we analyzed the consequences of PDS5 depletion for DNA replication. We found that either PDS5A or PDS5B is sufficient for proper cohesin dynamics and that their simultaneous removal increases cohesin's residence time on chromatin and slows down DNA replication. A similar phenotype was observed in WAPL-depleted cells. Cohesin down-regulation restored normal replication fork rates in PDS5-deficient cells, suggesting that chromatin-bound cohesin hinders the advance of the replisome. We further show that PDS5 proteins are required to recruit WRN helicase-interacting protein 1 (WRNIP1), RAD51 recombinase (RAD51), and BRCA2 DNA repair associated (BRCA2) to stalled forks and that in their absence, nascent DNA strands at unprotected forks are degraded by MRE11 homolog double-strand break repair nuclease (MRE11). These findings indicate that PDS5 proteins participate in replication fork protection and also provide insights into how cohesin and its regulators contribute to the response to replication stress, a common feature of cancer cells.
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