Project description:Differential transcriptomic responses of Biomphalaria glabrata (Gastropoda, Mollusca) to bacteria and metazoan parasites Schistosoma mansoni and Echinostoma paraensei (Digenea, Platyhelminthes). Transcriptional profiling of Biomphalaria glabrata comparing control uninfected M-line B. glabrata with five experimental groups. The experimental groups are: wounded but not infected M-line, Escherichia coli infected, Micrococcus luteus infected, Echinostoma paraensei infected and Schistosoma mansoni infected at 12 hours time point post infection.
Project description:Genotyping studies suggest that there is genetic variability among P. gingivalis strains, however the extent of variability remains unclear, and the regions of variability have only partially been identified. We previously used heteroduplex analysis of the ribosomal operon intergenic spacer region (ISR) to type P. gingivalis strains in several diverse populations, identifying 6 predominant heteroduplex types and many minor ones. In addition we used ISR sequence analysis to determine the relatedness of P. gingivalis strains to one another, and demonstrated a link between ISR sequence phylogeny and the disease-associated phenotype of P. gingivalis strains. The availability of whole genome microarrays based on the genomic sequence of strain W83 has allowed a more comprehensive analysis of P. gingivalis strain variability, using the entire genome. The objectives of this study were to define the phylogeny of P. gingivalis strains using the entire genome, to compare the phylogeny based on genome content to the phylogeny based on a single locus (ISR), and to identify genes that are associated with the strongly disease-associated strain W83 that could be important for virulence. Keywords: Comparative genomic hybridization
Project description:Malignant melanoma is an aggressive cancer known for its notorious resistance to most current therapies. The basic helix-loop-helix microphthalmia transcription factor (MITF) is the master regulator determining the identity and properties of the melanocyte lineage, and is regarded as a lineage-specific ‘oncogene’ that has a critical role in the pathogenesis of melanoma. MITF promotes melanoma cell proliferation, whereas sustained supression of MITF expression leads to senescence. By combining chromatin immunoprecipitation coupled to high throughput sequencing (ChIP-seq) and RNA sequen- cing analyses, we show that MITF directly regulates a set of genes required for DNA replication, repair and mitosis. Our results reveal how loss of MITF regulates mitotic fidelity, and through defective replication and repair induces DNA damage, ultimately ending in cellular senescence. These findings reveal a lineage-specific control of DNA replication and mitosis by MITF, providing new avenues for therapeutic intervention in melanoma. The identification of MITF-binding sites and gene- regulatory networks establish a framework for under- standing oncogenic basic helix-loop-helix factors such as N-myc or TFE3 in other cancers. 4 samples corresponding to genomic occupancy profiling of MITF (Cl8), PolII (501Mel), H3K4me3 501Mel). Anti-HA ChIP-seq on untagged cell line (501Mel) was used as a control.