Regulation of MHC-I and MHC-II expression by CIITA in transmissible devil facial tumour cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB45867 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR6109006.fastq.gz | Fastqsanger.gz | |||
| ERR6109007.fastq.gz | Fastqsanger.gz | |||
| ERR6109008.fastq.gz | Fastqsanger.gz | |||
| ERR6109009.fastq.gz | Fastqsanger.gz |
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Project description:Ciita has been suggested to control the expression of a number of genes based on ChIP-Seq or reporter anaysis but in vivo regulation beyong MHC class II has largely not been confirmed. We crossed Ciita knock out mice to Zbtb46 GFP knock-in knock out mice to identify classical dendritic cells in vivo in a Ciita deficient background. Expression microarray analysis of CD24+ and CD172a+ DCs from homeostatic spleen or activated BM Flt3l cultures show a highly resitrcited transcriptional footprint of Ciita. These findings underscore the fact that canonical binding sites active in transient expression assays may not always be functional in vivo. In addition, ChIP-Seq alone is not sufficient to discriminate binding from control of expression of a nearby gene.
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Project description:Devil facial tumour disease (DFTD) is a fatal contagious cancer that has decimated Tasmanian devil populations. The tumour has spread without invoking immune responses, possibly due to low levels of Major Histocompatibility Complex (MHC) diversity in Tasmanian devils. Animals from a region in north-western Tasmania have lower infection rates than those in the east of the state. This area is a genetic transition zone between sub-populations, with individuals from north-western Tasmania displaying greater diversity than eastern devils at MHC genes, primarily through MHC class I gene copy number variation. Here we test the hypothesis that animals that remain healthy and tumour free show predictable differences at MHC loci compared to animals that develop the disease.We compared MHC class I sequences in 29 healthy and 22 diseased Tasmanian devils from West Pencil Pine, a population in north-western Tasmania exhibiting reduced disease impacts of DFTD. Amplified alleles were assigned to four loci, Saha-UA, Saha-UB, Saha-UC and Saha-UD based on recently obtained genomic sequence data. Copy number variation (caused by a deletion) at Saha-UA was confirmed using a PCR assay. No association between the frequency of this deletion and disease status was identified. All individuals had alleles at Saha-UD, disproving theories of disease susceptibility relating to copy number variation at this locus. Genetic variation between the two sub-groups (healthy and diseased) was also compared using eight MHC-linked microsatellite markers. No significant differences were identified in allele frequency, however differences were noted in the genotype frequencies of two microsatellites located near non-antigen presenting genes within the MHC.We did not find predictable differences in MHC class I copy number variation to account for differences in susceptibility to DFTD. Genotypic data was equivocal but indentified genomic areas for further study.
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