Intestine-to-germline transmission of epigenetic information transgenerationally ensures systemic stress resistance in C. elegans
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PROVIDER: PRJNA490709 | ENA |
REPOSITORIES: ENA
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Project description:Epigenetic states are metastable and changed throughout life, and their changes play a major role in the regulation of organismal homeostasis, including stress resistance. However, the mechanisms coordinating epigenetic states and systemic stress resistance across tissues remain largely unknown. Here, we identify the intestine-to-germline communication of epigenetic states, which enhances stress resistance transgenerationally in C. elegans. We firstly show that the alteration in epigenetic states by deficiency of the histone H3K4me3 modifier ASH-2 in the intestine or germline increases organismal oxidative stress resistance, which is abrogated by knockdown of the H3K4 demethylase RBR-2 in the same tissue. Remarkably, the increase in stress resistance induced by ASH-2 deficiency in the intestine is abrogated by RBR-2 knockdown in the germline, suggesting the existence of inter-tissue transmission of epigenetic information from intestine to germline. Simultaneously, this intestine-to-germline communication in the parental generation transgenerationally provides the increase in stress resistance of the descendants for over two generations. Further analyses reveal that the inter-tissue communication requires the insulin/IGF-1 signaling effector DAF-16/FOXO in the intestine and is mediated, at least in part, by transcriptional regulation of F08F1.3, one of the intestinal ASH-2 target genes. These results unveil the novel intestine-to-germline communication of epigenetic information that provides the transgenerational regulation of organismal stress resistance. To further investigate the molecular mechanisms underlying intestine-to-germline communication, we sought the gene expression changes in the intestine ash-2 knockdown worms.
2020-09-03 | GSE119917 | GEO
Project description:It is unknown whether the activity of the nervous system can be inherited. In Caenorhabditis elegans nematodes, parental responses can transmit heritable small RNAs that regulate gene expression transgenerationally. In this study we show that a neuronal process can impact the next generations. Neurons-specific synthesis of RDE-4-dependent small RNAs regulates germline amplified endogenous siRNAs and germline gene expression for multiple generations. Further, the production of small RNAs in neurons controls the chemotaxis behavior of the progeny for at least three generations via the germline Argonaute HRDE-1. Among the targets of these small RNAs we identified the conserved gene saeg-2, which is transgenerationally downregulated in the germline. Silencing of saeg-2 following neuronal small RNA biogenesis is required for chemotaxis under stress. Thus, we propose a small RNA-based mechanism for communication of neuronal processes transgenerationally.
2019-06-05 | GSE124049 | GEO
Project description:RNA sequencing of N2 worms. Heterochromatic repetitive DNA transmits environmentally-acquired information for up-to fourteen generations in C. elegans
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Project description:Neuronal Small RNAs Control Behavior Transgenerationally
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Project description:The host-microbiota relationship has evolved to shape mammalian physiology, including immunity, metabolism, and development. Germ-free models are widely used to study microbial effects on host processes such as immunity. Here, we find that both germ-free and T cell-deficient mice exhibit a robust sebum secretion defect persisting across multiple generations despite microbial colonization and T cell repletion. These phenotypes are inherited by progeny conceived during in vitro fertilization using germ-free sperm and eggs, demonstrating that non-genetic information in the gametes is required for microbial-dependent phenotypic transmission. Accordingly, gene expression in early embryos derived from gametes from germ-free or T-cell deficient mice are strikingly and similarly altered. Our findings demonstrate that microbial and immune-dependent regulation of non-genetic information in the gametes can transmit inherited phenotypes transgenerationally in mice. This mechanism could rapidly generate phenotypic diversity to enhance host adaptation to environmental perturbations.
2024-03-24 | GSE240797 | GEO
Project description:Composting biotechnology information Genome sequencing
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Project description:Hormesis is a biological phenomenon, whereby exposure to low levels of toxic agents or conditions increases organismal viability. It thus represents a beneficial aspect of adaptive responses to harmful environmental stimuli. Here we show that hormesis effects induced in the parental generation can be passed on to the descendants in Caenorhabditis elegans. Animals subjected to various stressors during developmental stages exhibit increased resistance to oxidative stress and proteotoxicity. The increased resistance is transmitted to the subsequent generations grown under unstressed conditions through epigenetic alterations. Our analysis reveal that the insulin/insulin-like growth factor (IGF) signalling effector DAF-16/FOXO and the heat-shock factor HSF-1 in the parental somatic cells mediate the formation of epigenetic memory, which is maintained through the histone H3 lysine 4 trimethylase complex in the germline across generations. The elicitation of memory requires the transcription factor SKN-1/Nrf in somatic tissues. We propose that germ-to-soma communication across generations is an essential framework for the transgenerational inheritance of acquired traits, which provides the offspring with survival advantages to deal with environmental perturbation.
| S-EPMC5227915 | biostudies-literature
Project description:A number of environmental factors (e.g. toxicants) have been shown to promote the epigenetic transgenerational inheritance of disease and phenotypic variation. Transgenerational inheritance requires the germline transmission of altered epigenetic information between generations in the absence of direct environmental exposures. The primary periods for epigenetic programming of the germline is associated with primordial germ cell development and during fetal gonadal sex determination. The current study examined the actions of an agricultural fungicide vinclozolin on gestating female (F0 generation) progeny in regards to the primordial germ cell (PGC) epigenetic reprogramming of the F3 generation (i.e. great-grandchildren). The F3 generation primordial germ cell transcriptome and epigenome (DNA methylation) was altered transgenerationally. Interestingly, the differential DNA methylation regions (DMR) and altered transcriptomes were distinct between the onset of gonadal sex determination at embryonic day 13 (E13) and after cord formation in the testis at embryonic day 16 (E16). A larger number of DMR and transcriptional alterations were observed in the E13 PGC than E16 germ cells. Observations demonstrate an altered transgenerational epigenetic reprogramming and function of the primordial germ cells and subsequent male germline is a component of vinclozolin induced epigenetic transgenerational inheritance of disease. Insights into the molecular control of germline transmitted epigenetic inheritance are provided. The combined observations demonstrate ancestral exposure of a gestating female during fetal gonadal sex determination can promote transgenerational alterations in the primordial germ cell and subsequent male germline epigenetic and transcriptional programming. This altered germline programming leads to the epigenetic transgenerational inheritance of disease and phenotypic variation. Observations support the role of the primordial germ cell programming in the molecular mechanism involved and provides insights into the molecular mechanisms that control the epigenetic transgenerational inheritance phenomena. Results suggest a cascade of epigenetic and transcriptional events during germ cell development is needed to obtain the mature germline epigenome that is then transmitted transgenerationally. RNA samples from PGC of 2 F3-control lineage groups were compared to PGC of 2 F3-vinclozolin lineage groups for two embryonic age E13 and E16
2013-01-17 | E-GEOD-43559 | biostudies-arrayexpress