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Soma-to-Germline miRNA inheritance via Yolk Promotes Stress Resilience in Progeny [mRNA]

ABSTRACT: Soma-to-Germline miRNA inheritance via Yolk Promotes Stress Resilience in Progeny [mRNA]

PROVIDER: PRJNA1086515 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28292579.fastq.gz	Fastqsanger.gz
	SRR28292580.fastq.gz	Fastqsanger.gz
	SRR28292581.fastq.gz	Fastqsanger.gz
	SRR28292582.fastq.gz	Fastqsanger.gz
	SRR28292583.fastq.gz	Fastqsanger.gz

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Inheritance of miRNAs via Yolk Promotes Stress Resilience in Progeny

Project description:At the onset of reproduction, oviparous animals synthesize large amounts of yolk in somatic tissues to provide lipids and other nutrients to their progeny. However, whether the yolk transports other types of molecules, such as RNAs with gene regulatory functions, remains largely unexplored. Here, we have biochemically purified the yolk granules in the nematode Caenorhabditis elegans and show they contain microRNAs (miRNAs). We provide evidence that the yolk transports such miRNAs from the mother’s intestine to the embryos via the lipoprotein yolk receptor RME-2. These yolk-enriched miRNAs inherited by the embryos regulate the transcriptomes of developing larvae. Moreover, environmental stresses and maternal age modulate the transfer of yolk-enriched miRNAs, contributing to stress resilience benefits to progeny. This discovery establishes a novel paradigm in intergenerational gene regulation, where the gut-germline axis orchestrates the transmission of environmental cues through yolk-enriched miRNAs. Our work reveals a new mechanism underlying the soma-to-germline transfer of epigenetic information in animals.

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Inheritance of miRNAs via Yolk Promotes Stress Resilience in Progeny [small RNA]

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Inheritance of miRNAs via Yolk Promotes Stress Resilience in Progeny [small RNA]

Project description:Inheritance of miRNAs via Yolk Promotes Stress Resilience in Progeny [small RNA]

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Soma-to-Germline miRNA inheritance via Yolk Promotes Stress Resilience in Progeny

Project description:Identification of proteins present in purified yolk granules from C. elegans RME-2 degron strain, before internalisation in oocytes.

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Transcriptome comparisons of "expandable hemangioblasts" (eHBs) and their progeny to control cells

Project description:We examined the transcriptomes of murine "expandable hemangioblasts" (eHBs) and their blood and endothelial progeny, comparing them to the transcriptomes of murine embryonic stem (ES) cells, primary murine endothelial cells isolated from E11.5 yolk sacs or embryos, and E14.5 fetal liver hematopoietic stem cells.

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Project description:Colibacillosis caused by avian pathogenic Escherichia coli (APEC) is a major disease syndrome in poultry with the yolk sac infection recognized as a leading factor contributing to embryonic mortality. Yolk sac is the initial site of infection, however its contribution in embryonic mortality at molecular level has remained unexplored. To address this critical gap, we conducted RNA sequencing (RNA-seq) to analyze the comprehensive in vivo transcriptomic profiles of yolk sac and embryonic liver from APEC-infected embryos, comparing dead embryos with those that survived and mock-infected controls, to uncover key differences in host responses in multiple scenarios. Our results revealed that dead embryos displayed significant pro-inflammatory cytokine activity and cellular senescence, disrupted lipid and energy metabolism, and compromised antioxidative defenses, particularly in the yolk sac. In contrast, surviving embryos exhibited a regulated inflammatory response, enhanced mitochondrial activity, robust antioxidative responses and tissue repair mechanisms, which likely underpinned its resilience. Notably, yolk sac showed positive correlation (r = 0.531) with the embryonic liver, but demonstrated more severe inflammation and metabolic dysregulation, thereby highlighting its heightened vulnerability. Furthermore, reactive oxygen species (ROS) levels, the balance of the inflammatory response, and yolk sac integrity are crucial determinants of embryonic survival, with mitochondrial dysfunction serving as a key regulator of host immune and metabolic adaptation. The insights provide a deeper understanding of the previously overlooked role of yolk sac compared to liver during APEC infection, offering potential avenues for improving host resilience and mitigating economic losses in poultry.

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