| bioproject id |
PRJNA344676
to NCBI
|
| key word |
Challenge; GCRV; CIK; GRASS CARP REOVIRUS; MESSENGER-RNA EXPRESSION; ABERRANT DNA METHYLATION; CTENOPHARYNGODON-IDELLA; MICRORNA EXPRESSION; HUMAN-DISEASE; B2 RECEPTOR; GENOME; GENE; RESISTANCE |
| experiment type |
challenge |
| publication |
Shang X et al., "The destiny of the resistance/susceptibility against GCRV is controlled by epigenetic mechanisms in CIK cells.", Scientific Reports, 2017; 7(1): 4551 |
| description |
In this study, the resistant and susceptible monoclonal CIK cell lines were first established which would be the ponderable research models for the nosogenesis mechanism of the hemorrhagic disease. C1 (CIK cells), R2 (resistant cells) and S3 (susceptible cells) samples were carried out RNA-Seq, MeDIP-Seq and small RNA-Seq by the next-generation sequencing strategy, bioinformatics analysis as well as experimental verification. It was discovered that the aboriginality of CIK cells were gravitated to the susceptible trait. And the discrepancies between resistance and susceptibility against GCRV could primarily attribute to antioxidant activity, cell killing activity and cell proliferation regulation. Here we comprehensively present the profiling and characteristics of DNA methylation and microRNA in the resistant and susceptible CIK cells and proposed that high mCHH methylation distribution might be a characteristic modulator in C. idella. What’s more, a series of genes modulated by DNA methylation or microRNA were designated as potential biomarkers for the resistance breeding. This study laid the foundation and opened novel avenues for nosogenesis research on hemorragic disease of C. idella. Overall design: C1 (CIK cells), R2 (resistant cells) and S3 (susceptible cells) samples were carried out RNA-Seq, MeDIP-Seq and small RNA-Seq by the next-generation sequencing strategy. |
| abstract |
Hemorrhagic disease caused by grass carp reovirus (GCRV) has severely threatened the grass carp (Ctenopharyngodon idella) cultivation industry. It is noteworthy that the resistance against GCRV infection was reported to be inheritable, and identified at both individual and cellular levels. Therefore, this work was inspired and dedicated to unravel the molecular mechanisms of fate decision post GCRV infection in related immune cells. Foremost, the resistant and susceptible CIK (C. idella kidney) monoclonal cells were established by single cell sorting, subculturing and infection screening successively. RNA-Seq, MeDIP-Seq and small RNA-Seq were carried out with C1 (CIK cells), R2 (resistant cells) and S3 (susceptible cells) groups. It was demonstrated that genome-wide DNA methylation, mRNA and microRNA expression levels in S3 were the highest among three groups. Transcriptome analysis elucidated that pathways associated with antioxidant activity, cell proliferation regulation, apoptosis activity and energy consuming might contribute to the decision of cell fates post infection. And a series of immune-related genes were identified differentially expressed across resistant and susceptible groups, which were negatively modulated by DNA methylation or microRNAs. To conclude, this study systematically uncovered the regulatory mechanism on the resistance from epigenetic perspective and provided potential biomarkers for future studies on resistance breeding. |
Gene
RNA