Project description:Increasing evidence indicates that paternal dietary conditions influence the metabolic disorders of offspring. Previous studies suggested the involvement of epigenetic regulation for such phenomena, but the mechanism remains elusive. To reveal the molecular function of stress-dependent epigenetic regulator ATF7 in paternal inheritance of dietry effect on offpring phenotype, we analyzed ATF7-binding profiles in testicular germ cells by ChIP-seq, DNA methylation profiles in sperm by TGBS, small RNA expression profiles in HRCS by RNA-seq, and whole expression profiles in offspring liver by expression array analysis, using wild-type and ATF7 heterozygous mutant mice fed with control diet or low-protein diet. We performed expression array analysis to identidy genes which expressions are affected by paternal diet and ATF7 mutation.
Project description:Liver tissue samples were harvested from offspring sired by conventionally-raised male mice or dysbiotic sire, and profiled for genome changes using whole genome sequencing. F1 offspring samples were collected from six independent mating, and gDNA was extracted from offspring liver at postnatal day P17.
Project description:Investigation of whole genome gene expression level changes in kidney, brain, liver and spleen of the offspring of CBA/Ca and BALB/c male mice exposed to 1 Gy of acute X-rays The pattern of gene expression of a number of circadian rhythm genes in the offspring of irradiated males is compromised
Project description:Investigation of whole genome gene expression level changes in kidney, brain, liver and spleen of the offspring of CBA/Ca and BALB/c male mice exposed to 1 Gy of acute X-rays The pattern of gene expression of a number of circadian rhythm genes in the offspring of irradiated males is compromised A twenty-two 12x135K chip study using total RNA extracted from kidney, brain, liver and spleen of control CBA/Ca and BALB/c male mice and the first-generation offspring of male mice exposed to 1 Gy of acute X-rays. The expression of 42,575 genes was measured with two-fold technical redundancy.
Project description:Based on the developmental origin of health of disease hypothesis, we previously showed that prenatal 70% maternal food restriction (FR30) predisposes the offspring to development of pathologies in adulthood. In the present study, we focused on the liver gene expression profile of standard and high fat (HF)-fed FR30 adult offspring.
Project description:one-carbon metabolism in the liver plays a critical role in placental and fetal growth. Impaired functioning of one-carbon metabolism is associated with increased homocysteine (Hcy) levels. In this study, we applied a comprehensive proteomic approach to identify differential expression of proteins related to one-carbon metabolism in the livers of rat offspring as an effect of maternal food restriction during gestation. We determined that betaine-homocysteine S-methyltransferase 1 (BHMT1), methylenetetrahydrofolate dehydrogenase 1 (MTHFD1), and ATP synthase subunit beta mitochondrial (ATP5B) expression levels were significantly reduced in the livers of rat offspring exposed to maternal food restriction during gestation compared with in the offspring of rats fed a normal diet (p<0.05).
Project description:Maternal chromium restriction may disturb susceptibility in offspring. Liver from maternal chromium diet has 264 up- and 199 down- regulated genes, compared to control. Especially, Insulin signaling pathway and WNT pathway were affected.
Project description:Transcriptional profiling of rainbow trout liver and muscle cells comparing small fish with large fish within a population of neomale offspring. Small vs. large-fish liver and muscle cells from neomale offspring. Biological replicates: 4 small replicates, 4 large replicates.
Project description:Gestational diabetes mellitus (GDM) has long-term effects on the offspring health. Among these chronic diseases, inflammatory profiles play important roles in their development. Assessment for inflammatory status of GDM offspring is limited. Thus, the single cell RNA sequencing (scRNA-seq) was conducted to delineate the inflammatory characteristics of offspring with intrauterine hyperglycemia (IHG). scRNA-seq analysis of mice liver revealed myeloid polarization and multiple lineages developmental retardationwas identified in IHG offspring. Proinflammatory potential of myeloid cells seemed to be deeply imprinted in the liver of adult offspring with IHG.