Project description:DNA duplication is intimately connected to setting up post-replicative chromosome structures and events, but molecular details of this coordination are not well understood. A striking example occurs during yeast meiosis, where replication locally influences timing of the DNA double-strand breaks (DSBs) that initiate recombination. We show here that replication-DSB coordination is eliminated by overexpressing Dbf4-dependent Cdc7 kinase (DDK) or removing Tof1 or Csm3, components of the replication fork protection complex (FPC). DDK physically associates with Tof1, and Tof1 is dispensable for replication-DSB coordination if DDK is artificially tethered to replisomes. Furthermore, DDK phosphorylation of the DSB-promoting factor Mer2 is locally coordinated with replication, dependent on Tof1. These findings indicate that DDK recruited by FPC to replisomes phosphorylates chromatin-bound Mer2 in the wake of the replication fork, thus synchronizing replication with an early prerequisite for DSB formation. This may be a general mechanism to ensure spatial and temporal coordination of replication with other chromosomal processes. Ninety-six samples total: 12 time points (each time points contains ChIP and input samples) from Rec114-myc ARS+, Rec114-myc arsM-bM-^HM-^F strains, Rec114-myc tof1M-bM-^HM-^FARS+ and Rec114-myc tof1M-bM-^HM-^F arsM-bM-^HM-^F strains
Project description:DNA duplication is intimately connected to setting up post-replicative chromosome structures and events, but molecular details of this coordination are not well understood. A striking example occurs during yeast meiosis, where replication locally influences timing of the DNA double-strand breaks (DSBs) that initiate recombination. We show here that replication-DSB coordination is eliminated by overexpressing Dbf4-dependent Cdc7 kinase (DDK) or removing Tof1 or Csm3, components of the replication fork protection complex (FPC). DDK physically associates with Tof1, and Tof1 is dispensable for replication-DSB coordination if DDK is artificially tethered to replisomes. Furthermore, DDK phosphorylation of the DSB-promoting factor Mer2 is locally coordinated with replication, dependent on Tof1. These findings indicate that DDK recruited by FPC to replisomes phosphorylates chromatin-bound Mer2 in the wake of the replication fork, thus synchronizing replication with an early prerequisite for DSB formation. This may be a general mechanism to ensure spatial and temporal coordination of replication with other chromosomal processes. Forty-eight samples total: 8 time points from WT ARS+, WT arsM-bM-^HM-^F, DDK OP ARS+, DDK OP arsM-bM-^HM-^F,tof1M-bM-^HM-^F ARS+,tof1M-bM-^HM-^F arsM-bM-^HM-^F strains
Project description:Microbiome sequencing model is a Named Entity Recognition (NER) model that identifies and annotates microbiome nucleic acid sequencing method or platform in texts. This is the final model version used to annotate metagenomics publications in Europe PMC and enrich metagenomics studies in MGnify with sequencing metadata from literature. For more information, please refer to the following blogs: http://blog.europepmc.org/2020/11/europe-pmc-publications-metagenomics-annotations.html https://www.ebi.ac.uk/about/news/service-news/enriched-metadata-fields-mgnify-based-text-mining-associated-publications
Project description:An updated representation of S. meliloti metabolism that was manually-curated and encompasses information from 240 literature sources, which includes transposon-sequencing (Tn-seq) data and Phenotype MicroArray data for wild-type and mutant strains.
Project description:Lipomyces genome scale model based on the Lipomyces starkeyi NRRL-11557 genome.
Published in:
Genome-Scale Model Development and Genomic Sequencing of the Oleaginous Clade Lipomyces
Frontiers in Bioengineering and Biotechnology
Industrial Biotechnology
Volume 12 - 2024 | doi: 10.3389/fbioe.2024.1356551
Project description:Primary objectives: The primary objective is to investigate circulating tumor DNA (ctDNA) via deep sequencing for mutation detection and by whole genome sequencing for copy number analyses before start (baseline) with regorafenib and at defined time points during administration of regorafenib for treatment efficacy in colorectal cancer patients in terms of overall survival (OS).
Primary endpoints: circulating tumor DNA (ctDNA) via deep sequencing for mutation detection and by whole genome sequencing for copy number analyses before start (baseline) with regorafenib and at defined time points during administration of regorafenib for treatment efficacy in colorectal cancer patients in terms of overall survival (OS).