Sarah Lambert

ORCID: 0000-0002-1403-3204
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About
Contact & Profiles
Research Areas
  • DNA Repair Mechanisms
  • Genomics and Chromatin Dynamics
  • CRISPR and Genetic Engineering
  • Fungal and yeast genetics research
  • Microtubule and mitosis dynamics
  • RNA and protein synthesis mechanisms
  • PARP inhibition in cancer therapy
  • RNA Research and Splicing
  • Insect Resistance and Genetics
  • Insect and Arachnid Ecology and Behavior
  • Ubiquitin and proteasome pathways
  • Carcinogens and Genotoxicity Assessment
  • Genetic Neurodegenerative Diseases
  • Cancer therapeutics and mechanisms
  • DNA and Nucleic Acid Chemistry
  • Bacterial Genetics and Biotechnology
  • Gene Regulatory Network Analysis
  • RNA modifications and cancer
  • Chromosomal and Genetic Variations
  • Cancer-related Molecular Pathways
  • Epigenetics and DNA Methylation
  • Nuclear Structure and Function
  • Mitochondrial Function and Pathology
  • Plant Genetic and Mutation Studies
  • Plant Gene Expression Analysis

Université Paris-Saclay
2016-2024

Centre National de la Recherche Scientifique
2014-2024

Institut Curie
2015-2024

Université Paris Sciences et Lettres
2016-2024

La Ligue Contre le Cancer
2021-2024

Inserm
2021-2024

Université Paris-Sud
2007-2024

Commissariat à l'Énergie Atomique et aux Énergies Alternatives
1999-2024

Synchrotron soleil
2024

Direction de la Recherche Fondamentale
2024

Gene amplification plays important roles in the progression of cancer and contributes to acquired drug resistance during treatment. Amplification can initiate via dicentric palindromic chromosome production subsequent breakage–fusion–bridge cycles. Here we show that, fission yeast, acentric chromosomes form by homologous recombination protein-dependent fusion nearby inverted repeats, that these fusions occur frequently when replication forks arrest within repeats. Genetic molecular analyses...

10.1101/gad.1863009 article EN Genes & Development 2009-12-15

Abstract Replication requires homologous recombination (HR) to stabilize and restart terminally arrested forks. HR-mediated fork processing single stranded DNA (ssDNA) gaps not necessarily double strand breaks. We used genetic molecular assays investigate fork-resection at dysfunctional, unbroken forks in Schizosaccharomyces pombe . Here, we report that is a two-step process regulated by the non-homologous end joining factor Ku. An initial resection mediated MRN-Ctp1 removes Ku from forks,...

10.1038/s41467-017-02144-5 article EN cc-by Nature Communications 2017-12-01

Homologous recombination is a universal mechanism that allows repair of DNA and provides support for replication. therefore major pathway suppresses non-homology-mediated genome instability. Here, we report recovery impeded replication forks by homologous error-prone. Using fork-arrest-based assay in fission yeast, demonstrate single collapsed fork can cause mutations large-scale genomic changes, including deletions translocations. Fork-arrest-induced gross chromosomal rearrangements are...

10.1371/journal.pgen.1002976 article EN cc-by PLoS Genetics 2012-10-18

Nuclear Pore complexes (NPCs) act as docking sites to anchor particular DNA lesions facilitating repair by elusive mechanisms. Using replication fork barriers in fission yeast, we report that relocation of arrested forks NPCs occurred after Rad51 loading and its enzymatic activity. The E3 SUMO ligase Pli1 acts at safeguard integrity nascent strands generates poly-SUMOylation which promote but impede the resumption synthesis homologous recombination (HR). Anchorage allows removal SENP...

10.1038/s41467-020-19516-z article EN cc-by Nature Communications 2020-11-06

Nuclear pore complexes (NPCs) have emerged as genome organizers, defining a particular nuclear compartment enriched for SUMO protease and proteasome activities, act docking sites the repair of DNA damage. In fission yeast, anchorage perturbed replication forks to NPCs is an integral part recombination-dependent restart mechanism (RDR) that resumes synthesis at terminally dysfunctional forks. By mapping polymerase usage, we report Ulp1-associated ensure efficient initiation restarted...

10.1093/nar/gkae526 article EN cc-by Nucleic Acids Research 2024-06-25

During replication arrest, the DNA checkpoint plays a crucial role in stabilization of replisome at stalled forks, thus preventing collapse active forks and formation aberrant structures. How this acts to preserve integrity structures fork is poorly understood. In Schizosaccharomyces pombe, kinase Cds1 negatively regulates structure-specific endonuclease Mus81/Eme1 genomic when perturbed. Here, we report that, response hydroxyurea (HU) treatment, prevents S-phase-specific breakage resulting...

10.1091/mbc.e07-07-0728 article EN Molecular Biology of the Cell 2007-11-22

Homologous recombination is a universal mechanism that allows DNA repair and ensures the efficiency of replication. The substrate initiating process homologous single-stranded promotes strand exchange reaction resulting in genetic diversity repair. molecular mechanisms by which repairs double-strand break have been extensively studied are now well characterized. However, contribute to replication eukaryotes remains poorly understood. Studies bacteria identified multiple roles for machinery...

10.3390/biom3010039 article EN cc-by Biomolecules 2012-12-27
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