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Early life provision of 12-HETE by neutrophils imprints self-renewing capacity on alveolar macrophages

ABSTRACT: Early life provision of 12-HETE by neutrophils imprints self-renewing capacity on alveolar macrophages

PROVIDER: PRJNA894158 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22032000_1.fastq.gz	Fastqsanger.gz
	SRR22032000_2.fastq.gz	Fastqsanger.gz
	SRR22032001_1.fastq.gz	Fastqsanger.gz
	SRR22032001_2.fastq.gz	Fastqsanger.gz
	SRR22032002_1.fastq.gz	Fastqsanger.gz

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Early life provision of 12-HETE by neutrophils imprints self-renewing capacity on alveolar macrophages

Project description:Early life provision of 12-HETE by neutrophils imprints self-renewing capacity on alveolar macrophages

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Early life provision of 12-HETE by neutrophils imprints self-renewing capacity on alveolar macrophages

Project description:The goal of this study is to determine the role of the 12/15-lipoxygenase pathway in the development and maintenance of alveolar macrophages.

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Early life provision of 12-HETE by neutrophils imprints self-renewing capacity on alveolar macrophages

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Transgenerational inheritance of acquired memory and epigenetic imprints through maternal gametes

Project description:Transgenerational inheritance of acquired traits/characteristics from ancestors is believed to play important roles in evolution, as well as health problems/symptoms not due to “classical genetic inheritance”. However, the central enigma, such as how the acquired transgenerational characteristics are developed, and how the acquired traits are transmitted from generations to generations of offspring, largely remained veiled. In this study, we used C elegans as a model system and provide evidence that the dynamic of H3K27me3 as a hallmark and regulator for the gut-mediated transgenerational inheritance of acquired traits. Further, we demonstrate that yolk proteins guide the establishment of the acquired epigenetic imprints in soma, as well as determines the transgenerational inheritance of epigenetic imprints and subsequent acquired behavior in offspring by maternal provision. Taken together, our findings support that yolk proteins both function as a systemic “non-nuclear factor” for establishing the somatic epigenetic imprints and as a “cargo” to transmit acquired epigenetic information to the subsequent generations through oocytes.

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Antigen exposure reshapes chromatin architecture in central memory CD8+ T cells and imprints enhanced recall capacity

Project description:Antigen exposure reshapes chromatin architecture in central memory CD8+ T cells and imprints enhanced recall capacity

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Project description:Antigen exposure reshapes chromatin architecture in central memory CD8+ T cells and imprints enhanced recall capacity [CUT&RUN]

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Antigen exposure reshapes chromatin architecture in central memory CD8+ T cells and imprints enhanced recall capacity [ATAC-seq]

Project description:Antigen exposure reshapes chromatin architecture in central memory CD8+ T cells and imprints enhanced recall capacity [ATAC-seq]

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Antigen exposure reshapes chromatin architecture in central memory CD8+ T cells and imprints enhanced recall capacity [RNA-seq]

Project description:Antigen exposure reshapes chromatin architecture in central memory CD8+ T cells and imprints enhanced recall capacity [RNA-seq]

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Restrictive and extensively self-renewing erythroblast

Project description:Transcription profiles of self renewing erythroblast cultures isolated from both the restricted and extensively self-renewing phases of growth. The samples are paired.

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Project description:Genome-wide DNA demethylation, including the erasure of genome imprints, in primordial germ cells (PGCs), is critical as a first step for creating the totipotent epigenome in the germ line. Here, we provide evidence that contrary to the prevailing model involving active DNA demethylation, imprint erasure in mouse PGCs occurs in a manner consistent with replication-coupled passive DNA demethylation: PGCs erase imprints during their rapid proliferation with little de novo as well as maintenance DNA methylation potential and no major chromatin alterations. Our findings necessitate the re-evaluation of and provide novel insights into the mechanism of genome-wide DNA demethylation in PGCs. We performed expression analysis of primordial germ cells (PGCs) at embryonic days 10.5-13.5. Because the number of PGCs available at these stages were low, cDNAs were amplified by the method that we previously published (Kurimoto et al. 2006, NAR 34: e42 (PMID 16547197)). To include analysis of PGC gene expression at E9.5, we re-normalized the data from our E9.5 PGC samples (GSM744103, GSM744104) from our previous publication (Hayashi et al., 2011, Cell 146: 519-32 (PMD 21820164)) together with the data from this submission.

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