Transcriptome sequencing and metabolome analysis of food habits domestication from live prey fish to artificial diets in mandarin fish (Siniperca chuatsi).

BACKGROUND: As economical traits, food habits domestication can reduce production cost in aquaculture. However, the molecular mechanism underlying food habits domestication has remained elusive. Mandarin fish (Siniperca chuatsi) only feed on live prey fish and refuse artificial diets. In the present study, we domesticated mandarin fish to feed on artificial diets. The two groups were obtained, the fish did not eat artificial diets or ate artificial diets during all of the three domestication processes, named Group W or X, respectively. RESULTS: Using transcriptome and metabolome analysis, we investigated the differentially expressed genes and metabolites between the two groups, and found three common pathways related to food habit domestication, including retinol metabolism, glycerolipid metabolism, and biosynthesis of unsaturated fatty acids pathways. Furthermore, the western blotting and bisulfite sequencing PCR analysis were performed. The gene expression of TFIIF and histone methyltransferase ezh1 were significantly increased and decreased in the fish of Group X, respectively. The total DNA methylation levels of TFIIF gene and tri-methylation of histone H3 at lysine 27 (H3K27me3) were significantly higher and lower in the fish of Group X, respectively. CONCLUSION: It was speculated that mandarin fish which could feed on artificial diets, might be attributed to the lower expression of ezh1, resulting in the decreased level of H3K27me3 and increased level of DNA methylation of TFIIF gene. The high expression of TFIIF gene might up-regulate the expression of genes in retinol metabolism, glycerolipid metabolism and glycerophosphoric metabolism pathways. Our study indicated the relationship between the methylation of DNA and histone and food habits domestication, which might be a novel molecular mechanism of food habits domestication in animals.

Genes associated with sodium fluoride-induced human osteoblast apoptosis.

This study aims to explore the potential pathways and molecular characteristics of fluorine-induced osteoblast apoptosis. In vitro fluorine-induced model was established with an osteogenesis sarcoma cell line Saos-2. Then flow cytometry was used to determine the mitochondrial membrane potential at 24 h after the intervention. 84 apoptosis-related genes in the cells were determined using the functional polymerase chain reaction (PCR) chip and part of the differentially expressed genes was verified with immune blotting. When the stimulated concentration of sodium fluoride were 20 mg/L, 40 mg/L and 80 mg/L, the mitochondrial membrane potential of the osteoblast cells were 27.0%, 28.8% and 38.6%, respectively, significantly higher than that in the blank control group (P<0.05). The PCR chip detection found 13 up-regulating genes and 15 down-regulating genes, among which the expression of Bim, Caspase 9, Caspase 14, B-cell lymphoma-2 (BCL2) and BAX increased with the doses of sodium fluoride, while the expression of Caspase 3 down-regulated in 5 mg/L sodium fluoride but up-regulated at the concentration of sodium fluoride more than 10 mg/L. Caspase 7 expression showed no obvious difference between the different concentration groups. However, Caspase 10 decreased with the increasing doses of sodium fluoride. Fluoride-induced osteoblast apoptosis may be through the mitochondrial pathway (including endoplasmic reticulum stress pathway) and death receptor pathway.