PUBLICATION

Parental vitamin deficiency affects the embryonic gene expression of immune-, lipid transport- and apolipoprotein genes

Authors
Skjaerven, K.H., Jakt, L.M., Dahl, J.A., Espe, M., Aanes, H., Hamre, K., Fernandes, J.M.
ID
ZDB-PUB-161013-2
Date
2016
Source
Scientific Reports   6: 34535 (Journal)
Registered Authors
Fernandes, Jorge
Keywords
Embryology, Environmental impact, Gastrulation
MeSH Terms
  • Animals
  • Apolipoproteins*/biosynthesis
  • Apolipoproteins*/immunology
  • Avitaminosis/embryology
  • Avitaminosis/immunology
  • Female
  • Gene Expression Regulation, Developmental*
  • Lipid Metabolism/immunology*
  • Male
  • Zebrafish*/embryology
  • Zebrafish*/immunology
  • Zebrafish Proteins*/biosynthesis
  • Zebrafish Proteins*/immunology
PubMed
27731423 Full text @ Sci. Rep.
Abstract
World Health Organization is concerned for parental vitamin deficiency and its effect on offspring health. This study examines the effect of a marginally dietary-induced parental one carbon (1-C) micronutrient deficiency on embryonic gene expression using zebrafish. Metabolic profiling revealed a reduced 1-C cycle efficiency in F0 generation. Parental deficiency reduced the fecundity and a total of 364 genes were differentially expressed in the F1 embryos. The upregulated genes (53%) in the deficient group were enriched in biological processes such as immune response and blood coagulation. Several genes encoding enzymes essential for the 1-C cycle and for lipid transport (especially apolipoproteins) were aberrantly expressed. We show that a parental diet deficient in micronutrients disturbs the expression in descendant embryos of genes associated with overall health, and result in inherited aberrations in the 1-C cycle and lipid metabolism. This emphasises the importance of parental micronutrient status for the health of the offspring.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping