“…Even though the FOXH1 gene is involved in lipid metabolism, FOXO1 ( FOX family gene) is an insulin-sensitive DNA binding transcription factor that can alter the synthesis or stability of the MAF1 protein. The MAF1 gene ( MAF1 homolog, negative regulator of RNA polymerase III) is a protein coding that is important to the regulation of mammalian intracellular lipids [34,35]. The MAF family member proteins regulate tissue-specific gene expression and cell differentiation in a wide variety of tissues.…”
Simple SummaryMilk fat content and fatty acid composition are key traits for the dairy industry, as they directly influence consumer acceptance of dairy products and are associated with the chemical-physical characteristics of milk. In order to genetically improve milk fat composition, it is important to understand the biological mechanisms behind the phenotypic variability observed in these traits. In this study, we used a genomic dataset for 6692 animals and over 770,000 genetic markers distributed across the genome. We compared different statistical approaches to better identify the genes associated with milk fatty acid composition in Holstein cattle. Our results suggest that the DGAT1 gene accounts for most of the variability in milk fatty acid composition, and that the PLBD1 and MGST1 genes are important additional candidate genes in Holstein cattle.AbstractThe identification of genomic regions and candidate genes associated with milk fatty acids contributes to better understand the underlying biology of these traits and enables breeders to modify milk fat composition through genetic selection. The main objectives of this study were: (1) to perform genome-wide association analyses for five groups of milk fatty acids in Holstein cattle using a high-density (777K) SNP panel; and (2) to compare the results of GWAS accounting (or not) for the DGAT1 gene effect as a covariate in the statistical model. The five groups of milk fatty acids analyzed were: (1) saturated (SFA); (2) unsaturated (UFA); (3) short-chain (SCFA); (4) medium-chain (MCFA); and (5) long-chain (LCFA) fatty acids. When DGAT1 was not fitted as a covariate in the model, significant SNPs and candidate genes were identified on BTA5, BTA6, BTA14, BTA16, and BTA19. When fitting the DGAT1 gene in the model, only the MGST1 and PLBD1 genes were identified. Thus, this study suggests that the DGAT1 gene accounts for most of the variability in milk fatty acid composition and the PLBD1 and MGST1 genes are important additional candidate genes in Holstein cattle.
“…Even though the FOXH1 gene is involved in lipid metabolism, FOXO1 ( FOX family gene) is an insulin-sensitive DNA binding transcription factor that can alter the synthesis or stability of the MAF1 protein. The MAF1 gene ( MAF1 homolog, negative regulator of RNA polymerase III) is a protein coding that is important to the regulation of mammalian intracellular lipids [34,35]. The MAF family member proteins regulate tissue-specific gene expression and cell differentiation in a wide variety of tissues.…”
Simple SummaryMilk fat content and fatty acid composition are key traits for the dairy industry, as they directly influence consumer acceptance of dairy products and are associated with the chemical-physical characteristics of milk. In order to genetically improve milk fat composition, it is important to understand the biological mechanisms behind the phenotypic variability observed in these traits. In this study, we used a genomic dataset for 6692 animals and over 770,000 genetic markers distributed across the genome. We compared different statistical approaches to better identify the genes associated with milk fatty acid composition in Holstein cattle. Our results suggest that the DGAT1 gene accounts for most of the variability in milk fatty acid composition, and that the PLBD1 and MGST1 genes are important additional candidate genes in Holstein cattle.AbstractThe identification of genomic regions and candidate genes associated with milk fatty acids contributes to better understand the underlying biology of these traits and enables breeders to modify milk fat composition through genetic selection. The main objectives of this study were: (1) to perform genome-wide association analyses for five groups of milk fatty acids in Holstein cattle using a high-density (777K) SNP panel; and (2) to compare the results of GWAS accounting (or not) for the DGAT1 gene effect as a covariate in the statistical model. The five groups of milk fatty acids analyzed were: (1) saturated (SFA); (2) unsaturated (UFA); (3) short-chain (SCFA); (4) medium-chain (MCFA); and (5) long-chain (LCFA) fatty acids. When DGAT1 was not fitted as a covariate in the model, significant SNPs and candidate genes were identified on BTA5, BTA6, BTA14, BTA16, and BTA19. When fitting the DGAT1 gene in the model, only the MGST1 and PLBD1 genes were identified. Thus, this study suggests that the DGAT1 gene accounts for most of the variability in milk fatty acid composition and the PLBD1 and MGST1 genes are important additional candidate genes in Holstein cattle.
“…MAF1 is a transcriptional repressor. Recent research has shown that it represses the expression of both pol III-dependent genes and certain RNA pol II-dependent genes that play a crucial part in oncogenesis, [ 31 ] and is important for the regulation of intracellular lipids [ 31 , 32 ]. It is likely that MAF1 has a diversity of physiological functions, but knowledge of its roles is still limited [ 33 ].…”
BackgroundThe biological mechanisms underlying frailty in older people are poorly understood. There is some evidence to suggest that DNA methylation patterns may be altered in frail individuals.MethodsParticipants were 791 people aged 70 years from the Lothian Birth Cohort 1936. DNA methylation was measured in whole blood. Biological age was estimated using two measures of DNA methylation-based age acceleration-extrinsic and intrinsic epigenetic age acceleration. We carried out an epigenome-wide association study of physical frailty, as defined by the Fried phenotype. Multinomial logistic regression was used to calculate relative risk ratios for being physically frail or pre-frail according to epigenetic age acceleration.ResultsThere was a single significant (P = 1.16 × 10–7) association in the epigenome-wide association study comparing frail versus not frail. The same CpG was not significant when comparing pre-frail versus not frail. Greater extrinsic epigenetic age acceleration was associated with an increased risk of being physically frail, but not of being pre-frail. For a year increase in extrinsic epigenetic age acceleration, age- and sex-adjusted relative risk ratios (95% CI) for being physically frail or pre-frail were 1.06 (1.02, 1.10) and 1.02 (1.00, 1.04), respectively. After further adjustment for smoking and chronic disease, the association with physical frailty remained significant. Intrinsic epigenetic age acceleration was not associated with physical frailty status.ConclusionsPeople who are biologically older, as indexed by greater extrinsic epigenetic age acceleration, are more likely to be physically frail. Future research will need to investigate whether epigenetic age acceleration plays a causal role in the onset of physical frailty.Electronic supplementary materialThe online version of this article (10.1186/s13148-018-0538-4) contains supplementary material, which is available to authorized users.
“…The Maf1 protein (a repressor of RNA polymerase III) is a part of the target of rapamycin complex 1 (TORC1) pathway that responds to stress caused by nutrient deprivation in S. cerevisiae and mammals (Loewith and Hall, 2011 ). Maf1 represses transcription of highly abundant tRNAs and ribosomal RNAs through its function as a regulator of RNA polymerase III (Upadhya et al ., 2002 ; Boguta, 2013 ; Moir and Willis, 2015 ). In nutrient-rich conditions, Maf1 remains inactive due to phosphorylation (Pluta et al ., 2001 ; Shor et al ., 2010 ), while under starvation conditions, it is de-phosphorylated and the activated protein binds and inhibits RNA polymerase III (Vannini et al ., 2010 ).…”
Section: Upstream Orfs In
Plasmodium Falciparummentioning
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