{"doi":"10.1007/s00412-023-00813-7","title":"DNA replication and replication stress response in the context of nuclear architecture","abstract":"<jats:title>Abstract</jats:title><jats:p>The DNA replication process needs to be coordinated with other DNA metabolism transactions and must eventually extend to the full genome, regardless of chromatin status, gene expression, secondary structures and DNA lesions. Completeness and accuracy of DNA replication are crucial to maintain genome integrity, limiting transformation in normal cells and offering targeting opportunities for proliferating cancer cells. DNA replication is thus tightly coordinated with chromatin dynamics and 3D genome architecture, and we are only beginning to understand the underlying molecular mechanisms. While much has recently been discovered on how DNA replication initiation is organised and modulated in different genomic regions and nuclear territories—the so-called “DNA replication program”—we know much less on how the elongation of ongoing replication forks and particularly the response to replication obstacles is affected by the local nuclear organisation. Also, it is still elusive how specific components of nuclear architecture participate in the replication stress response. Here, we review known mechanisms and factors orchestrating replication initiation, and replication fork progression upon stress, focusing on recent evidence linking genome organisation and nuclear architecture with the cellular responses to replication interference, and highlighting open questions and future challenges to explore this exciting new avenue of research.</jats:p>","journal":"Chromosoma","year":2024,"id":647870,"datarank":0.43718191157595576,"base_score":2.5649493574615367,"endowment":2.5649493574615367,"self_citation_contribution":0.38474240361923057,"citation_network_contribution":0.052439507956725216,"self_endowment_contribution":0.38474240361923057,"citer_contribution":0.052439507956725216,"corpus_percentile":null,"corpus_rank":null,"citation_count":12,"citer_count":10,"citers_with_citation_signal":6,"citers_with_endowment":6,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":246978,"name":"Massimo Lopes","orcid":"0000-0003-3847-8133","position":1,"is_corresponding":false},{"id":1688102,"name":"Daniel González-Acosta","orcid":null,"position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"DNA replication and replication stress response in the context of nuclear architecture","abstract":"<jats:title>Abstract</jats:title><jats:p>The DNA replication process needs to be coordinated with other DNA metabolism transactions and must eventually extend to the full genome, regardless of chromatin status, gene expression, secondary structures and DNA lesions. Completeness and accuracy of DNA replication are crucial to maintain genome integrity, limiting transformation in normal cells and offering targeting opportunities for proliferating cancer cells. DNA replication is thus tightly coordinated with chromatin dynamics and 3D genome architecture, and we are only beginning to understand the underlying molecular mechanisms. While much has recently been discovered on how DNA replication initiation is organised and modulated in different genomic regions and nuclear territories—the so-called “DNA replication program”—we know much less on how the elongation of ongoing replication forks and particularly the response to replication obstacles is affected by the local nuclear organisation. Also, it is still elusive how specific components of nuclear architecture participate in the replication stress response. Here, we review known mechanisms and factors orchestrating replication initiation, and replication fork progression upon stress, focusing on recent evidence linking genome organisation and nuclear architecture with the cellular responses to replication interference, and highlighting open questions and future challenges to explore this exciting new avenue of research.</jats:p>","is_dataset_classified":null,"base_score":0.0,"endowment":0.0,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"38055079","pmcid":"PMC10904558","openalex_id":null,"authors":[],"funders":[{"funder_name":"European Molecular Biology Organization","grant_id":"ALTF 1135-2021","title":null},{"funder_name":"Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung","grant_id":"310030_189206","title":null},{"funder_name":"Swiss National Science Foundation","grant_id":"189206","title":"Replication fork remodelling and its multifaceted impact on genome stability and cancer"},{"funder_name":"University of Zurich","grant_id":"","title":null}],"total_grants":4,"fwci":null,"citation_percentile":null,"influential_citations":0,"citation_trend":[],"oa_status":"hybrid","license":"cc-by","oa_locations":[{"url":"https://link.springer.com/content/pdf/10.1007/s00412-023-00813-7.pdf","host_type":"publisher"},{"url":"https://link.springer.com/article/10.1007/s00412-023-00813-7/fulltext.html","host_type":"publisher"},{"url":"https://www.zora.uzh.ch/id/eprint/253601/1/s00412_023_00813_7.pdf","host_type":"repository"},{"url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC10904558/pdf/412_2023_Article_813.pdf","host_type":"repository"},{"url":"https://doi.org/10.5167/uzh-253601","host_type":""},{"url":"https://europepmc.org/articles/PMC10904558","host_type":"Europe_PMC"},{"url":"https://europepmc.org/articles/PMC10904558?pdf=render","host_type":"Europe_PMC"},{"url":"https://doi.org/10.1007/s00412-023-00813-7","host_type":""},{"url":"https://dx.doi.org/10.5167/uzh-253601","host_type":""},{"url":"https://pubmed.ncbi.nlm.nih.gov/38055079","host_type":""},{"url":"http://dx.doi.org/10.1007/s00412-023-00813-7","host_type":""},{"url":"https://www.zora.uzh.ch/id/eprint/253601/","host_type":""}],"fields_of_study":["0301 basic medicine","03 medical and health sciences"],"mesh_terms":["Chromatin","Humans","DNA Damage","Genomic Instability","DNA Replication"],"keywords":["DNA replication","Nuclear Dynamics","Nuclear Architecture","Replication Stress","Genome Organisation","2716 Genetics (clinical)","10061 Institute of Molecular Cancer Research","610 Medicine & health","Review","Chromatin","Genomic Instability","1311 Genetics","Humans","570 Life sciences; biology","610 Medicine &amp; health","DNA Damage"],"sdg_mappings":[],"linked_datasets":[],"clinical_trials":[],"software_tools":[],"database_accessions":[],"source":"live","citation_network_status":"fetched"},"created_at":"2026-08-10T01:58:32.200523Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}