Hypo-methylated Igf2r gene locus marks phthalate-mediated trans-generational inheritance of murine allergic phenotypes
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE102745 | GEO | 2020/12/08
REPOSITORIES: GEO
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Project description:Familial risk in hypertensive renal disease has stimulated a search for genetic variation contributing to this risk. The current phase of population genetic studies has sought to associate genetic variation with disease in large populations by testing genotypes at a large number of common genetic variations in the genome, expecting that common genetic variants contributing to renal disease risk will be identified. These genome-wide association studies (GWAS) have been productive and are a clear technical success. It is also clear that narrowly defined loci and genes containing variation contributing to disease risk have been identified. Further extension and refinement of these GWAS are likely to extend this success. However, it is also clear that few if any variants with substantial effects accounting for the greatest part of heritability will be uncovered by GWAS. This raises an interesting biological question regarding where the remaining heritable risk may be located. One result of the progress of GWAS is likely to be a renewed interest in mechanisms by which related individuals can share and transmit traits independently of Mendelian inheritance. This paper reviews current progress in this area and considers other mechanisms by which familial aggregation of risk for renal disease may arise.
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Project description:Biotic stress can induce plastic changes in fitness-relevant plant traits. Recently, it has been shown that such changes can be transmitted to subsequent generations. However, the occurrence and extent of transmission across different types of traits is still unexplored. Here, we assessed the emergence and transmission of herbivory-induced changes in Brassica rapa and their impact on interactions with insects. We analysed changes in morphology and reproductive traits as well as in flower and leaf volatile emission during two generations with leaf herbivory by Mamestra brassicae and Pieris brassicae and two subsequent generations without herbivory. Herbivory induced changes in all trait types, increasing attractiveness of the plants to the parasitoid wasp Cotesia glomerata and decreasing visitation by the pollinator Bombus terrestris, a potential trade-off. While changes in floral and leaf volatiles disappeared in the first generation after herbivory, some changes in morphology and reproductive traits were still measurable two generations after herbivory. However, neither parasitoids nor pollinators further discriminated between groups with different past treatments. Our results suggest that transmission of herbivore-induced changes occurs preferentially in resource-limited traits connected to plant growth and reproduction. The lack of alterations in plant-insect interactions was likely due to the transient nature of volatile changes.
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Project description:This SuperSeries is composed of the SubSeries listed below.
2017-07-01 | GSE97238 | GEO
Project description:Animals respond to dietary changes by adapting their metabolism to available nutrients through insulin and insulin-like growth factor signalling. Restricting calorie intake generally extends life and health span, but Drosophila fed non-ideal sugars such as galactose are stressed and have shorter life spans. Here, we report that although these flies have shorter life spans, their offspring show significant life extension if switched to a normal sugar (glucose) diet. We define this as TGH or trans-generational hormesis, a beneficial effect that comes from a mild stress. We trace the effects to changes in stress responses in parents, ROS production, effects on lipid metabolism, and changes in chromatin and gene expression. We find that this mechanism is similar to what happens to the long lived Indy mutants on normal food, but surprisingly find that Indy is required for life span extension for galactose fed flies. Indy mutant flies grown on galactose do not live longer as do their siblings grown on glucose, rather overexpression of Indy rescues lifespan for galactose reared flies. We define a process where sugar metabolism can generate epigenetic changes that are inherited by offspring, providing a mechanism for how transgenerational nutrient sensitivities are passed on.
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Project description:Animals respond to dietary changes by adapting their metabolism to available nutrients through insulin and insulin-like growth factor signalling. Restricting calorie intake generally extends life and health span, but Drosophila fed non-ideal sugars such as galactose are stressed and have shorter life spans. Here, we report that although these flies have shorter life spans, their offspring show significant life extension if switched to a normal sugar (glucose) diet. We define this as TGH or trans-generational hormesis, a beneficial effect that comes from a mild stress. We trace the effects to changes in stress responses in parents, ROS production, effects on lipid metabolism, and changes in chromatin and gene expression. We find that this mechanism is similar to what happens to the long lived Indy mutants on normal food, but surprisingly find that Indy is required for life span extension for galactose fed flies. Indy mutant flies grown on galactose do not live longer as do their siblings grown on glucose, rather overexpression of Indy rescues lifespan for galactose reared flies. We define a process where sugar metabolism can generate epigenetic changes that are inherited by offspring, providing a mechanism for how transgenerational nutrient sensitivities are passed on.
2017-07-01 | GSE97162 | GEO
Project description:Trans-generational epigenetic inheritance (TEI), which functionally intersects RNA with histone modification, recently forced a reinterpretation of the interplay between gene expression and selective pressures. Our groups integrate genetic, genomic, dynamic imaging, biochemistry and proteomic technologies to provide a functional mechanistic understanding of the interplay of TEI and the RNA interference (RNAi) phenomena in the nematode C. elegans. We discovered a family of proteins (the nuclear Argonaute-interacting proteins or NIPs), which controls the strength, inheritance and gene target specificity of nuclear RNAi. Loss of NIP-1 and NIP-2 in the soma leads to an enhancement of nuclear RNAi activities without affecting cytoplasmic RNAi. Loss of NIP-3 in the germline disables TEI and leads to a profoundly impaired response to transposable genomic elements (viral-like sequences). The genome of nip-3 mutants becomes de-stabilized; spontaneous visible mutations arise at high frequency due to an unbridled mobilization of a subset of transposable elements. Surprisingly, silencing of a distinct subset of transposable elements is coincidentally enhanced. Finally, expression imaging revealed an eminent role for the maturing male germline in TEI. This data supports a model wherein NIPs determine the potency and stability of TEI by gating and sorting small RNAs (which provide specificity) towards germline and somatic nuclear RNAi and epigenetic machineries. Our work further implies that this molecular machinery evolved to atone an animal’s epigenetic memory to preserve a species’ integrity in face of genetic pathogens.
2020-03-09 | GSE126377 | GEO
Project description:Di (2-ethylhexyl) phthalate (DEHP) is a common plasticizer. Studies have revealed that DEHP exposure can cause liver damage. Green tea is one of the most popular beverages in China. Green tea polyphenols (GTPs) have been proven to have therapeutic effects on organ damage induced by heavy metal exposure. However, few study report on GTP relieving DEHP-induced liver damage.
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Project description:Di(2-ethylhexyl) phthalate (DEHP) is a commonly used plasticizer and known endocrine disrupting chemical, which causes transgenerational reproductive toxicity in female rodents. However, the mechanisms of action underlying the transgenerational toxicity of DEHP are not understood. Therefore, this study determined the effects of prenatal and ancestral DEHP exposure on various ovarian pathways in the F1, F2, and F3 generations of mice. Pregnant CD-1 dams were orally exposed to corn oil (vehicle control) or DEHP (20 μg/kg/day-750 mg/kg/day) from gestation day 10.5 until birth. At postnatal day 21 for all generations, ovaries were removed for gene expression analysis of various ovarian pathways and for 5-methyl cytosine (5-mC) quantification. In the F1 generation, prenatal DEHP exposure disrupted the expression of cell cycle regulators, the expression of peroxisome-proliferator activating receptors, and the percentage of 5-mC compared to control. In the F2 generation, exposure to DEHP decreased the expression of steroidogenic enzymes, apoptosis factors, and ten-eleven translocation compared to controls. It also dysregulated the expression of phosphoinositide 3-kinase (PI3K) factors. In the F3 generation, ancestral DEHP exposure decreased the expression of steroidogenic enzymes, PI3K factors, cell cycle regulators, apoptosis factors, Esr2, DNA methylation mediators, and the percentage of 5-mC compared to controls. Overall, the data show that prenatal and ancestral DEHP exposure greatly suppress gene expression of pathways required for folliculogenesis and steroidogenesis in the ovary in a transgenerational manner and that gene expression may be influenced by DNA methylation. These results provide insight into some of the mechanisms of DEHP-mediated toxicity in the ovary across generations.
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Project description:Trans-Generational Hormesis and the Inheritance of Aging Resistance
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Project description:This SuperSeries is composed of the following subset Series: GSE21640: Gene expression analysis of cardiomyocytes treated with a clinically relevant concentration of DEHP (50 ug/mL) GSE21641: Dose-dependent gene expression analysis of cardiomyocytes treated with DEHP (1-50 ug/mL) Refer to individual Series
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