Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR507301_1.fastq.gz | Fastqsanger.gz | |||
| ERR507301_2.fastq.gz | Fastqsanger.gz | |||
| ERR507302_1.fastq.gz | Fastqsanger.gz | |||
| ERR507302_2.fastq.gz | Fastqsanger.gz | |||
| ERR507303_1.fastq.gz | Fastqsanger.gz |
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Project description:Due to difficulties inherent in designating conservation units for effective species management and conservation, the use of multiple complementary sources of information is required to identify and assess the designation of conservation units based on the degree of variation among populations within a species. In this study, we combined estimates of microsatellite and transcriptomic variation to assess the population structure and potential for adaptive variation of threatened Atlantic salmon, Salmo salar, among rivers in the Bay of Fundy. In general, population structure identified by genetic differentiation was consistent with the patterns of variation in gene expression. Both data sets provided clear indication of strong regional differentiation between rivers located within the inner Bay of Fundy relative to rivers located within the outer Bay of Fundy or the Southern Uplands region. There was also support for more refined population structure; there was some differentiation in both microsatellite and gene expression patterns between salmon from rivers in the two regions of the inner Bay of Fundy: Chignecto Bay and Minas Basin. Consistent patterns apparent in the genetic and transcriptomic dataset indicate that Atlantic salmon populations from the inner and outer Bay of Fundy reflect unique genetic lineages, with some evidence of unique genetic legacies between regions of the inner Bay of Fundy, and even between individual rivers within a region. Consistency of the microarray data across two years helps to validate the use of this technique as a useful tool in assessment of variation among wild populations for species conservation.
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Project description:Although therapy responsiveness to therapy in Burkitt lymphoma (BL) is high, relapsed disease and and chemoresistance remain a clinical challenge, and complete mechanisms underlying BL chemoresistance and how it can be circumvented is yet to be fully elucidated. In this study we present data showing that chymotrypsin-like serine proteases inhibitor Nα-tosyl-L-phenylalanine chloromethylketone (TPCK) and specific NF-κB inhibitor Bay-11 7082 can induce caspase-independent apoptosis in chemoresistant BL cells. We also demonstrate that both TPCK and Bay-11 7082-treatment leads to decreased NF-κB nuclear activity and that this is associated with sensitization of chemoresistant Burkitt lymphoma cells. Furthermore we investigated global transcriptional changes induced by Bay-11 7082 and TPCK in the DG-75 and Raji cell lines, respectively, by microarray analysis using Illumina BeadChips. TPCK-treatment of Raji and DG-75 cells resulted in 59 and 21 differently expressed genes, respectively, while Bay-11-treated Raji and DG-75 cells displayed 1403 and 8 differently expressed genes, respectively. Gene Ontology (GO) categorization confirmed enrichment of multiple GOs in Bay 11-treated Raji and DG-75 cells. Fifty percent of the 61 categories in Raji cells were categories sorting under Biological Processes and represented mostly increased gene expression. In DG-75 cells Bay-11 7082 induced significant gene ontology enrichment in only two categories, where the increased/decreased ratio was 1:1. Further unsupervised and supervised bioinformatics processing by Ingenuity Pathway Analysis indicated significant networks in response to TPCK and Bay 11 respectively, including association to NF-κB. Bay-11 7082 demonstrated deregulated NF-κB related members of receptor mediated cell death signaling, i.e TRAF2 and TRADD, as well as deregulated members of the NF-κB signaling pathway from the cytoplasmic compartment, i.e RELB, in Raji cells. Comparably NF-κB network analysis of Raji- and DG-75 cells treated with Bay-11 7082 and Raji cells treated with TPCK demonstrated deregulation of NF-κB target genes CD69 and IL8. These data indicates that NF-kB may play a role in overcoming chemoresistance in BL cells with defective classical apoptosis signaling. NF-κB network analysis of Raji- and DG-75 cells treated with Bay-11 7082 and Raji cells treated with TPCK
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