Project description:We show that treatment with HPUra (for S. pneumoniae) and trimethoprim (for E. coli) leads to a skewed gene dosage profile (increase around the origin of replication), which is also propagated to the transcriptome level. Kanamycin, however, does not have this effect. In case of S. pneumoniae this shift in gene dosage distribution leads to the population-wide activation of competence. Pairwise comparison of untreated to antibiotic-treated cells (either DNA-seq or RNA-seq). It was performed with deep sequencing, using an Illumina HiSeq 2000 machine with 100 bp read length. S. pneumoniae samples treated with kanamycin was analysed from a single sample, while all other conditions were from duplicate samples.

2014-04-10 | E-GEOD-54199 | biostudies-arrayexpress

DYNAMICS OF REPLICATION ORIGIN OVER-ACTIVATION

Project description:DYNAMICS OF REPLICATION ORIGIN OVER-ACTIVATION

| PRJNA723279 | ENA

Single-nucleotide variant and marker frequency analysis of Sinorhizobium meliloti strains with rearranged genomic DNA.

Project description:S. meliloti strains with a bi- and monopartite genome configuration were constructed by consecutive Cre/lox-mediated site-specific fusions of the secondary replicons. Beside the correct genomic arrangements, these strains and precursors were tested for variations in the nucleotide sequence. Further, a marker frequency analysis was performed to test if replication is initiated at all origins and to determine the replication termination regions of the triple replicon fusion molecule. To gain the sequence data for these analyses, respective strains were applied to whole genome sequencing using an Illumina MiSeq-System.

2022-10-10 | E-MTAB-11878 | biostudies-arrayexpress

oriZ replication profiles

Project description:Replication dynamics in double origin E. coli strains

| PRJEB9476 | ENA

DNA replication timing directly regulates the frequency of oncogenic chromosomal translocations [HiC]

Project description:Many cancers originate from misregulation of gene expression caused by chromosomal translocations which result from ligation of DNA double-strand breaks (DSBs). Indeed, translocations may be causal in ~20% of human cancer morbidity 1. Although the sources of DSBs are numerous2-5, we have virtually no knowledge of the steps linking DSB formation to DSB ligation. Here, we show that early replication timing of translocation partner loci, mediated by the activity of replication origins, is a critical regulator of lymphomagenic Myc translocations generated by activation-induced deaminase (AID) during antibody maturation in B-cells. Reduced levels of the replicative helicase, the minichromosome maintenance (MCM) complex6, impairs translocation genesis, decreases firing of replication origins at AID target genes and globally abrogates the replication timing program without altering cell proliferation, gene expression or genome architecture. Strikingly, deleting a single origin of replication at Myc induces a switch from early-to-late replication at Myc with concomitantly impaired translocation frequency. This phenotype is reversed by restoring early replication at Myc thereby demonstrating a direct, causal role of replication origin activity and replication timing in translocation genesis. Finally, this replication timing-mediated step acts downstream of DSBs and is independent of DSB frequency, constituting a novel regulatory step in translocation biogenesis.

2022-09-15 | GSE161817 | GEO

Marker Frequency analysis on Escherichia coli RecB mutants

Project description:Nucleic Acid Sequencing for the study of division induced double strand breaks in the terminus region of Escherichia coli cells lacking RecBCD DNA repair enzymes.

2017-09-18 | E-MTAB-6030 | biostudies-arrayexpress

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