Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

In vivo transcriptome of Listeria monocytogenes EGDe

ABSTRACT: Time course study of the mouse infection by comparing the genomic transcriptional patterns of Listeria monocytogenes EGDe grown under laboratory conditions (exponential growth phase) with that of in vivo-grown bacteria (in mouse spleens) over three days of infection. Time course study of the mouse infection by comparing the genomic transcriptional patterns of Listeria monocytogenes EGDe grown under laboratory conditions (exponential growth phase) with that of in vivo-grown bacteria (in mouse spleens) over three days of infection.

ORGANISM(S): Listeria monocytogenes EGD-e

SUBMITTER: Didier Cabanes

PROVIDER: E-GEOD-13057 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

In vivo transcriptional profiling of Listeria monocytogenes and mutagenesis identify new virulence factors involved in infection.

Camejo Ana A Buchrieser Carmen C Couvé Elisabeth E Carvalho Filipe F Reis Olga O Ferreira Pierre P Sousa Sandra S Cossart Pascale P Cabanes Didier D

PLoS pathogens 20090529 5

Listeria monocytogenes is a human intracellular pathogen able to colonize host tissues after ingestion of contaminated food, causing severe invasive infections. In order to gain a better understanding of the nature of host-pathogen interactions, we studied the L. monocytogenes genome expression during mouse infection. In the spleen of infected mice, approximately 20% of the Listeria genome is differentially expressed, essentially through gene activation, as compared to exponential growth in rich ...[more]

PMID: 19478867

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Project description:Copy number expansions such as amplifications and duplications contribute to human phenotypic variation, promote molecular diversification during evolution, and drive the initiation and/or progression of various cancers. The mechanisms underlying these copy number changes are still incompletely understood, however. We recently demonstrated that transient, limited re-replication from a single origin in Saccharomyces cerevisiae efficiently induces segmental amplification of the re-replicated region. Structural analyses of such re-replication induced gene amplifications (RRIGA) suggested that RRIGA could provide a new mechanism for generating copy number variation by non-allelic homologous recombination (NAHR). Here we elucidate this new mechanism and provide insight into why it is so efficient. We establish that sequence homology is both necessary and sufficient for repetitive elements to participate in RRIGA and show that their recombination occurs by a single-strand annealing (SSA) mechanism. We also find that re-replication forks are prone to breakage, accounting for the widespread DNA damage associated with deregulation of replication proteins. These breaks appear to stimulate NAHR between re-replicated repeat sequences flanking a re-initiating replication origin. Our results support a RRIGA model where the expansion of a re-replication bubble beyond flanking homologous sequences followed by breakage at both forks in trans provides an ideal structural context for SSA–mediated NAHR to form a head-to-tail duplication. Given the remarkable efficiency of RRIGA, we suggest it may be an unappreciated contributor to copy number expansions in both disease and evolution. The arrays in this series are primary comparative genomic hybridizations to determine genomic changes after re-replication. Genomic DNA was purified from reference Saccharomyces cerevisiae cells or survivors of re-replication, differentially labeled with Cy3 and Cy5, and competitively hybridized to a spotted microarray containing ORF and intergenic PCR products. Cy5/Cy3 ratios (or the inverse in the case of dye swapped samples) are normalized so that the average ratio of all elements was 1 (except for arrays measuring re-replication induction where this ratio was set to 2). A small number of the arrays were used to determine the extent and location of re-replication under different conditions. For those, genomic DNA was purified from non-replicating and re-replicating cells and treated as above. Series contains a total of 333 hybridizations. Note that the VALUE field reported for all of the sample tables in this series are the log2 of the normalized Cy5/Cy3 (or Cy3/Cy5) ratio. To convert these into usable copy number profiles raise 2 to the indicated VALUE.

Dataset Information

In vivo transcriptome of Listeria monocytogenes EGDe

Publications

In vivo transcriptional profiling of Listeria monocytogenes and mutagenesis identify new virulence factors involved in infection.

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