Project description:The Chinese sturgeon (Acipenser sinensis) is anadromous fish distributed in Yangtze River and East China Sea. In this study, we reported cleft-palate Chinese sturgeons in artificial population for the first time. In order to explore the genetic basis of palate malformation in A. sinensis, Illumina RNA-seq technology was used to analyze the transcriptome data of normal and cleft-palate individuals in farmed Chinese sturgeons. Raw reads were obtained and assembled into 808,612 unigenes, with an average length of 509.33 bp and an N50 of 574 bp. Sequence similarity analyses against four public databases (Nr, Uniprot, KEGG and COGs) found 158,642 unigenes that can be annotated. GABAergic synapse and TGF-β signal pathway were the most two enriched pathways with high Richfactor in the analyses of different expressed genes. In these two signal pathways, six genes (GABRA4, GS, GNS, S6K, PITX2, and BMP8) were found as cleft-palate genes in Chinese sturgeon. These findings contribute to our understanding of the genetic basis of cleft palate in sturgeon, while simultaneously adding to our knowledge about craniofacial development.
Project description:Background: Liver cancer is the third deadliest type of cancer, posing a serious threat to human health. Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer. C. sinensis, classified as a definite group I carcinogen by the IARC (International Agency for Research on Cancer), is an important risk factor for HCC. Although many studies have shown that C. sinensis infection affects the prognosis of HCC patients, the specific mechanisms are still unclear, especially the dynamics and regulatory roles of chromatin accessibility. Results: In this study, we integrated ATAC-seq, RNA-seq, and ChIP-seq data to elucidate changes in the epigenetics of HCC after the C. sinensis infection. Many different accessibility regions (DARs) were identified both in tumors and adjacent tissue after the C. sinensis infection. Meanwhile, top TFs whose motifs were enriched in DAR were found, such as HNF4a, FOXI1, etc. Although there were slight deviations, epigenetic changes were found to be consistent with gene expression levels. We also revealed that H3K9ac, H3K4me2, H3K4me3, H3K27ac, and H3K4me1 were associated with chromatin accessibility. Importantly, we also found potential evidence that C. sinensis infection would alter the spatial structure of the HCC genome. Finally, both molecular experimental results and clinical data certified that C. sinensis infection would promote the metastasis of HCC. Conclusions: C. sinensis infection will remodel the chromatin accessibility of HCC, leading to changes in gene expression levels. This study provides conclusive evidence that C. sinensis infection alters the epigenetics of HCC.