Background Feed efficiency is a crucial economic trait in poultry industry.Both host genetics and gut microbiota influence feed efficiency.How ever,the associations between gut microbiota and host genetics,as well as ...Background Feed efficiency is a crucial economic trait in poultry industry.Both host genetics and gut microbiota influence feed efficiency.How ever,the associations between gut microbiota and host genetics,as well as their combined contributions to feed efficiency in laying hens during the late laying period,remain largely unclear.Methods In total,686 laying hens were used for whole-genome resequencing and liver transcriptome sequencing.16S rRNA gene sequencing was conducted on gut chyme(duodenum,jejunum,ileum,and cecum)and fecal samples from 705 individuals.Bioinformatic analysis was performed by integrating the genome,transcriptome,and microbiome to screen for key genetic variations,genes,and gut microbiota associated with feed efficiency.Results The heritability of feed conversion ratio(FCR)and residual feed intake(RFI)was determined to be 0.28and 0.48,respectively.The ileal and fecal microbiota accounted for 15%and 10%of the FCR variance,while the jejunal,cecal,and fecal microbiota accounted for 20%,11%and 10%of the RFI variance.Through SMR analysis based on summary data from liver eQTL mapping and GWAS,we further identified four protein-coding genes,SUCLA2,TNFSF13B,SERTM1,and MARVELD3,that influence feed efficiency in laying hens.The SUCLA2 and TNFSFI 3B genes were significantly associated with SNP 1:25664581 and SNP rs312433097,respectively.SERTM1 showed significant associations with rs730958360 and 1:33542680 and is a potential causal gene associated with the abundance of Corynebacteriaceae in feces.MARVELD3 was significantly associated with the 1:135348198 and was significantly correlated with the abundance of Enterococcus in ileum.Specifically,a lower abundance of Enterococcus in ileum and a higher abundance of Corynebacteriaceae in feces were associated with better feed efficiency.Conclusions This study confirms that both host genetics and gut microbiota can drive variations in feed efficiency.A small portion of the gut microbiota often interacts with host genes,collectively enhancing feed efficiency.Therefore,targeting both the gut microbiota and host genetic variation by supporting more efficient taxa and selective breeding could improve feed efficiency in laying hens during the late laying period.展开更多
Background Hepatic steatosis is a prevalent manifestation of fatty liver, that has detrimental effect on the health and productivity of laying hens, resulting in economic losses to the poultry industry. Here, we aimed...Background Hepatic steatosis is a prevalent manifestation of fatty liver, that has detrimental effect on the health and productivity of laying hens, resulting in economic losses to the poultry industry. Here, we aimed to systematically investigate the genetic regulatory mechanisms of hepatic steatosis in laying hens.Methods Ninety individuals with the most prominent characteristics were selected from 686 laying hens according to the accumulation of lipid droplets in the liver, and were graded into three groups, including the control, mild hepatic steatosis and severe hepatic steatosis groups. A combination of transcriptome, proteome, acetylome and lipidome analyses, along with bioinformatics analysis were used to screen the key biological processes, modifications and lipids associated with hepatic steatosis.Results The rationality of the hepatic steatosis grouping was verified through liver biochemical assays and RNA-seq. Hepatic steatosis was characterized by increased lipid deposition and multiple metabolic abnormalities. Integration of proteome and acetylome revealed that differentially expressed proteins(DEPs) interacted with differentially acetylated proteins(DAPs) and were involved in maintaining the metabolic balance in the liver. Acetylation alterations mainly occurred in the progression from mild to severe hepatic steatosis, i.e., the enzymes in the fatty acid oxidation and bile acid synthesis pathways were significantly less acetylated in severe hepatic steatosis group than that in mild group(P < 0.05). Lipidomics detected a variety of sphingolipids(SPs) and glycerophospholipids(GPs) were negatively correlated with hepatic steatosis(r ≤-0.5, P < 0.05). Furthermore, the severity of hepatic steatosis was associated with a decrease in cholesterol and bile acid synthesis and an increase in exogenous cholesterol transport.Conclusions In addition to acquiring a global and thorough picture of hepatic steatosis in laying hens, we were able to reveal the role of acetylation in hepatic steatosis and depict the changes in hepatic cholesterol metabolism. The findings provides a wealth of information to facilitate a deeper understanding of the pathophysiology of fatty liver and contributes to the development of therapeutic strategies.展开更多
基金supported by National Key Research and Development Program of China(2021YFD1300600 and 2022YFF1000204)the National Natural Science Foundation of China(31930105)+1 种基金China Agriculture Research Systems[CARS-40]the 2115 Talent Development Program of China Agricultural University。
文摘Background Feed efficiency is a crucial economic trait in poultry industry.Both host genetics and gut microbiota influence feed efficiency.How ever,the associations between gut microbiota and host genetics,as well as their combined contributions to feed efficiency in laying hens during the late laying period,remain largely unclear.Methods In total,686 laying hens were used for whole-genome resequencing and liver transcriptome sequencing.16S rRNA gene sequencing was conducted on gut chyme(duodenum,jejunum,ileum,and cecum)and fecal samples from 705 individuals.Bioinformatic analysis was performed by integrating the genome,transcriptome,and microbiome to screen for key genetic variations,genes,and gut microbiota associated with feed efficiency.Results The heritability of feed conversion ratio(FCR)and residual feed intake(RFI)was determined to be 0.28and 0.48,respectively.The ileal and fecal microbiota accounted for 15%and 10%of the FCR variance,while the jejunal,cecal,and fecal microbiota accounted for 20%,11%and 10%of the RFI variance.Through SMR analysis based on summary data from liver eQTL mapping and GWAS,we further identified four protein-coding genes,SUCLA2,TNFSF13B,SERTM1,and MARVELD3,that influence feed efficiency in laying hens.The SUCLA2 and TNFSFI 3B genes were significantly associated with SNP 1:25664581 and SNP rs312433097,respectively.SERTM1 showed significant associations with rs730958360 and 1:33542680 and is a potential causal gene associated with the abundance of Corynebacteriaceae in feces.MARVELD3 was significantly associated with the 1:135348198 and was significantly correlated with the abundance of Enterococcus in ileum.Specifically,a lower abundance of Enterococcus in ileum and a higher abundance of Corynebacteriaceae in feces were associated with better feed efficiency.Conclusions This study confirms that both host genetics and gut microbiota can drive variations in feed efficiency.A small portion of the gut microbiota often interacts with host genes,collectively enhancing feed efficiency.Therefore,targeting both the gut microbiota and host genetic variation by supporting more efficient taxa and selective breeding could improve feed efficiency in laying hens during the late laying period.
基金funded in part by grants from the National Natural Science Foundation of China (No.31930105)National Key Research and Development Program of China (2022YFF1000204)China Agriculture Research Systems (CARS-40)。
文摘Background Hepatic steatosis is a prevalent manifestation of fatty liver, that has detrimental effect on the health and productivity of laying hens, resulting in economic losses to the poultry industry. Here, we aimed to systematically investigate the genetic regulatory mechanisms of hepatic steatosis in laying hens.Methods Ninety individuals with the most prominent characteristics were selected from 686 laying hens according to the accumulation of lipid droplets in the liver, and were graded into three groups, including the control, mild hepatic steatosis and severe hepatic steatosis groups. A combination of transcriptome, proteome, acetylome and lipidome analyses, along with bioinformatics analysis were used to screen the key biological processes, modifications and lipids associated with hepatic steatosis.Results The rationality of the hepatic steatosis grouping was verified through liver biochemical assays and RNA-seq. Hepatic steatosis was characterized by increased lipid deposition and multiple metabolic abnormalities. Integration of proteome and acetylome revealed that differentially expressed proteins(DEPs) interacted with differentially acetylated proteins(DAPs) and were involved in maintaining the metabolic balance in the liver. Acetylation alterations mainly occurred in the progression from mild to severe hepatic steatosis, i.e., the enzymes in the fatty acid oxidation and bile acid synthesis pathways were significantly less acetylated in severe hepatic steatosis group than that in mild group(P < 0.05). Lipidomics detected a variety of sphingolipids(SPs) and glycerophospholipids(GPs) were negatively correlated with hepatic steatosis(r ≤-0.5, P < 0.05). Furthermore, the severity of hepatic steatosis was associated with a decrease in cholesterol and bile acid synthesis and an increase in exogenous cholesterol transport.Conclusions In addition to acquiring a global and thorough picture of hepatic steatosis in laying hens, we were able to reveal the role of acetylation in hepatic steatosis and depict the changes in hepatic cholesterol metabolism. The findings provides a wealth of information to facilitate a deeper understanding of the pathophysiology of fatty liver and contributes to the development of therapeutic strategies.
