Lipid metabolic disarray in young and adult mice offspring's liver is induced by saturated fatty acids (SFA) but prevented by alpha linolenic acid (ALA, 18:3 3) in the maternal diet during pregnancy and lactation. The aim of the present study was to analyse the impact of maternal dietary ALA on the liver gene expression in the new-born offspring in comparison to a SFA diet. Methods: C57Bl6/J dams were fed with diets normal in calories but rich in ALA or SFA before mating and during pregnancy. Pups were sacrificed at birth and liver parameters were assessed. Gene expression was characterized by microarray analysis and validated by real time qPCR. Results: ALA compared to SFA in maternal diets during pregnancy, increased polyunsaturated fatty acids while differentially modified fatty acid desaturase activities in offspring liver. Overall, 474 and 662 genes from born pups liver, were differentially regulated by ALA and SFA compared to control diet (p<0.05; Fold change 2), respectively. Notably, Per3 was up-regulated by ALA whereas down-regulated by SFA, compared to control diet. Conclusions: ALA and SFA enriched diets differentially affect gene expression pattern in the offsprings liver. ALA in particular, upregulates genes associated to low adiposity.
Maternal Diet Enriched with α-Linolenic or Saturated Fatty Acids Differentially Regulates Gene Expression in the Liver of Mouse Offspring.
Specimen part, Disease, Treatment
View SamplesEffect of high grain protein locus on barley grain protein accumulation. Gene expression levels were analysed in Karl, a low grain protein variety with its near-isogenic line 10_11(has high grain protein locus, chromosome 6)using Barley1 22k affymetrix chip. ****[PLEXdb(http://www.plexdb.org) has submitted this series at GEO on behalf of the original contributor, Aravind Jukanti. The equivalent experiment is BB53 at PLEXdb.]
Comparative transcriptome profiling of near-isogenic barley (Hordeum vulgare) lines differing in the allelic state of a major grain protein content locus identifies genes with possible roles in leaf senescence and nitrogen reallocation.
Age, Specimen part
View SamplesExpression levels of the RNA-binding protein Quaking (QKI) are low in monocytes of early, human atherosclerotic lesions, but abundant in macrophages of advanced plaques. Specific depletion of QKI protein impaired monocyte adhesion, migration, differentiation into macrophages, and foam cell formation in vitro and in vivo. RNA-seq and microarray analysis of human monocyte and macrophage transcriptomes, including those of a unique QKI haploinsufficient patient, revealed striking changes in QKI-dependent mRNA levels and splicing of RNA transcripts. Overall design: RNA-seq analysis of primary monocytes and macrophages from a QKI haploinsufficient patient and their (control) sibling.
Quaking promotes monocyte differentiation into pro-atherogenic macrophages by controlling pre-mRNA splicing and gene expression.
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