Project description:Ambient salinity is one of the crucial abiotic factors that poses substantial impacts on fish growth, development and reproduction. Greater amberjack (Seriola dumerili) is of high economic value because, and its reproduction and survival are sensitive to water salinity. To better understand the molecular adaptive mechanism to salinity fluctuations in greater amberjack, we performed comparative transcriptome analysis for gill and kidney between the optimum salinity (30 ppt, CK) and undesired regimes (10 and 40 ppt). For the gill, the skeletal development was provoked upon either hypo- or hyper-salinity stimuli, and the development of pronephros, as well as vascular endothelial cells and cortisol-mediated mitochondria-rich cell, was activated in response to the salinity alterations in kidney. These enhancements may encourage the maintenance of the gill and kidney structures and alleviate the salinity-induced damage. Ion channels NKCC1 and CFTR and the transporters for ammonium and other substances were highly upregulated in the gills and kidney, respectively, which act important roles in the osmoregulation of greater amberjack. More important, undesirable alterations of ambient salinity were found to pose adverse impacts on the immune function of greater amberjack, which may increase the risk of pathogen infection and reduce the security and yield of aquaculture of greater amberjack. In addition, deviation from the optimum salinity condition may result in undesirable uptake and accumulation of environmental toxins in greater amberjack, which attracts further attention to the food safety. Collectively, these novel findings advance our knowledge on adaptative mechanisms to ambient salinity oscillations in greater amberjack and provide a theoretical guidance for the optimal breeding mode for the aquaculture of greater amberjack.
Project description:DNA regulatory elements are reported to be enriched for variants identified by genome-wide association studies to be significantly assocaited with risk of complext traits. Here, we have performed genome-wide mapping of histone modifications in two endometrial cancer cell lines and performed interestions of these sites with genetic risk variants identified by genome-wide association study of endometrial cancer. Histone modifications indicative of enhancers (H3K4Me1 and H3K27Ac) and promoters (H3K27Ac and H3K4Me3) were identified by ChIP-seq in Ishikawa and JHUEM-14 cells, pre- and post-stimulation by estrogen. Overall, 73% of endometrial cancer genetic risk variants overlapped at least histone modification site. This overlap was significantly greater than the overlap observed for these histone marks with genetic risk variants related to, for example, endometriosis (51%; Fisher’s Exact p = 8.7x10-8) or schizophrenia (40%; Fisher’s Exact p < 2.2x10-16). These findings indicate the relevance of the selected cell and tissue types for informing endometrial cancer biology. Overlaps between genetic risk variants and histone modification sites increased significantly after stimulation with estrogen (50% versus 38% for unstimulated features; Fisher’s Exact p = 5.6x10-3), emphasizing the importance of estrogen in endometrial cancer aetiology.