Project description:Hepatic steatosis is the initial manifestation of abnormal liver functions and often leads to liver diseases such as non-alcoholic fatty liver disease in humans and fatty liver syndrome in animals. In this study, we conducted a comprehensive analysis of a large chicken population consisting of 705 adult hens by combining host genome resequencing, liver transcriptome, proteome, and metabolome analysis, as well as microbial 16S rRNA gene sequencing of each gut segment.
Project description:Dr. Eric Vivier's lab would like to tackle the enzymes involved in PEN5 carbohydrate metabolism. We have generated these cell lines by repeated cell sorting and cell cloning of the parental HSB-2 T cell line and the parental JY B cell line. H+ are PEN5+ HSB-2 cells, H- are PEN5- HSB-2 cells; JY+ are PEN5+ HSB-2 cells, JY- are PEN5- HSB-2 cells. We have originally described a cell surface molecule called PEN5, as a sulfated lactosamine, that is selectively expressed on a mature subset of human NK cells (Vivier, J. Exp. Med. 1993). Later, we have shown that the PEN5 carbohydrate decorates PSGL-1, confering L-selectin binding properties (André et al. PNAS, 2000). We have recently performed a Glycan Array Screening via Core H (Glycomics 917). These studies indeed reveal a very nice binding of the anti-PEN5 mAb to a subset of sulfated lactosamines. We would like to tackle the enzymes involved in PEN5 carbohydrate metabolism. We thus requesting a Gene microarray analysis performed using RNA extracted from PEN5+ and PEN5- NK cells, as well from the H+, H-, JY+ and JY- stable cell lines. We have generated these cell lines by repeated cell sorting and cell cloning of the parental HSB-2 T cell line and the parental JY B cell line. H+ are PEN5+ HSB-2 cells, H- are PEN5- HSB-2 cells; JY+ are PEN5+ HSB-2 cells, JY- are PEN5- HSB-2 cells. RNA preparations from variants of the HSB-2 (human T leukemia) and JY (human B lymphoma) cell lines, which were express or not PEN5 were sent to Microarray Core (E). These stable variants are referred to as H+ (HSB-2 cells expressing PEN5), H- (HSB-2 cells NOT expressing PEN5), JY+ (JY cells expressing PEN5), and JY- (JY cells NOT expressing PEN5). Samples were prepared at 3 different time points. The RNA was amplified, labeled, and hybridized to the GLYCOv3 microarrays. Data was sent to Dr. Eric Vivier for analysis.
Project description:Dr. Eric Vivier's lab would like to tackle the enzymes involved in PEN5 carbohydrate metabolism. We have generated these cell lines by repeated cell sorting and cell cloning of the parental HSB-2 T cell line and the parental JY B cell line. H+ are PEN5+ HSB-2 cells, H- are PEN5- HSB-2 cells; JY+ are PEN5+ HSB-2 cells, JY- are PEN5- HSB-2 cells.
Project description:<p>Hepatic steatosis is the initial manifestation of abnormal liver functions and often leads to liver diseases such as non-alcoholic fatty liver disease in humans and fatty liver syndrome in animals. In this study, we conducted a comprehensive analysis of a large chicken population consisting of 705 adult hens by combining host genome resequencing, liver transcriptome, proteome and metabolome analysis, as well as microbial 16S rRNA gene sequencing of each gut segment. The results showed the heritability (h2 = 0.25) and duodenal microbiability (m2 = 0.26) of hepatic steatosis were relatively high, indicating a large effect of host genetics and duodenal microbiota on chicken hepatic steatosis. Individuals with hepatic steatosis had low microbiota diversity and a decreased genetic potential to process triglyceride output from hepatocytes, fatty acid β-oxidation activity and resistance to fatty acid peroxidation. Furthermore, we revealed a molecular network linking host genomic variants (GGA6: 5.59-5.69 Mb), hepatic gene/protein expression (PEMT, phosphatidyl-ethanolamine N-methyltransferase), metabolite abundances (folate, S-adenosylmethionine, homocysteine, phosphatidyl-ethanolamine and phosphatidylcholine) and duodenal microbes (genus Lactobacillus) to hepatic steatosis, which could provide new insights into the regulatory mechanism of fatty liver development.</p>
Project description:To investigate the genome-wide DNA binding of chicken p53, we overexpressed chicken p53 with a flag in LMH cells. We then performed genome-wide DNA binding analysis using data obtained from ChIP-seq of LMH cells.
2022-10-05 | GSE200405 | GEO
Project description:Jinghong layer chicken genome resequencing data adapter
| PRJNA939426 | ENA
Project description:Resequencing data for Pu'an chicken
| PRJNA1022041 | ENA
Project description:Resequencing data for Luning Chicken
| PRJNA1025327 | ENA
Project description:Resequencing data for Yanying chicken
| PRJNA1018287 | ENA
Project description:Resequencing data for nami chicken