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A developmentally programmed splicing failure attenuates the DNA damage response during mammalian zygotic genome activation

ABSTRACT: A developmentally programmed splicing failure attenuates the DNA damage response during mammalian zygotic genome activation

PROVIDER: PRJNA685191 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13253500_1.fastq.gz	Fastqsanger.gz
	SRR13253500_2.fastq.gz	Fastqsanger.gz
	SRR13253501_1.fastq.gz	Fastqsanger.gz
	SRR13253501_2.fastq.gz	Fastqsanger.gz
	SRR13253502_1.fastq.gz	Fastqsanger.gz

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A developmentally programmed splicing failure attenuates the DNA damage response during mammalian zygotic genome activation

Project description:The transition from maternal to embryonic transcriptional control is a crucial step in embryogenesis. However, how alternative splicing is regulated during this process and how it contributes to early development is unknown. Using transcriptomic data from pre-implantation stages of human, mouse and cow, we show that the stage of zygotic genome activation (ZGA) exhibits the highest levels of exon skipping diversity reported for any cell or tissue type. Interestingly, much of this exon skipping is temporary, leads to disruptive non-canonical isoforms, and occurs in genes enriched for DNA damage response in the three species. We identified two core spliceosomal components, Snrpb and Snrpd2, as regulators of these patterns. These genes have low maternal expression at the time of ZGA and increase sharply thereafter. Consistently, microinjection of Snrpb/d2 mRNA into mouse zygotes reduces the levels of temporary exon skipping at ZGA, and leads to an increase in etoposide-induced DNA damage response. Altogether, our results suggest that mammalian embryos undergo an evolutionarily conserved and developmentally programmed specific splicing failure at the time of genome activation that attenuates cellular responses to DNA damage at these early stages.

2022-04-27 | GSE163205 | GEO

A developmentally programmed splicing failure contributes to DNA damage response attenuation during mammalian zygotic genome activation.

Project description:Transition from maternal to embryonic transcriptional control is crucial for embryogenesis. However, alternative splicing regulation during this process remains understudied. Using transcriptomic data from human, mouse, and cow preimplantation development, we show that the stage of zygotic genome activation (ZGA) exhibits the highest levels of exon skipping diversity reported for any cell or tissue type. Much of this exon skipping is temporary, leads to disruptive noncanonical isoforms, and occurs in genes enriched for DNA damage response in the three species. Two core spliceosomal components, Snrpb and Snrpd2, regulate these patterns. These genes have low maternal expression at ZGA and increase sharply thereafter. Microinjection of Snrpb/d2 messenger RNA into mouse zygotes reduces the levels of exon skipping at ZGA and leads to increased p53-mediated DNA damage response. We propose that mammalian embryos undergo an evolutionarily conserved, developmentally programmed splicing failure at ZGA that contributes to the attenuation of cellular responses to DNA damage.

| S-EPMC9007516 | biostudies-literature

Huangxueyishen formular attenuates Chronic renal failure by promoting activation of p38/MAPK signaling pathway

Project description:To investigated the possible mechanism of HXYS attenuates chronic renal failure in rat via proteomic methods.

2023-06-30 | PXD043416 |

Deletion of NuRD component Mta2 in nephron progenitor cells causes developmentally programmed FSGS

Project description:Deletion of NuRD component Mta2 in nephron progenitor cells causes developmentally programmed FSGS

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Microarray analysis of developmentally programmed hepatic steatosis in Undernourishment in utero mouse model

Project description:Microarray analysis of developmentally programmed hepatic steatosis in Undernourishment in utero mouse model

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Deletion of NuRD component Mta2 in nephron progenitor cells causes developmentally programmed FSGS [2month.ChIPseq]

Project description:Deletion of NuRD component Mta2 in nephron progenitor cells causes developmentally programmed FSGS [2month.ChIPseq]

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Deletion of NuRD component Mta2 in nephron progenitor cells causes developmentally programmed FSGS [2month.RNAseq]

Project description:Deletion of NuRD component Mta2 in nephron progenitor cells causes developmentally programmed FSGS [2month.RNAseq]

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Developmentally programmed tankyrase activity upregulates β-catenin and licenses progression of embryonic genome activation

Project description:Developmentally programmed tankyrase activity upregulates β-catenin and licenses progression of embryonic genome activation

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Programmed cell senescence during embryonic development

Project description:Cellular senescence disables the proliferation of damaged cells and it is relevant for cancer and aging. Here, we show that cellular senescence occurs during mammalian embryonic development. Specifically, we have focused on the mouse regressing mesonephros and the endolymphatic sac of the inner ear. Senescence is characterized by SAM-NM-2G activity, heterochromatinization, and proliferative arrest. Mechanistically, developmentally-programmed senescence at the mesonephros and endolymphatic sac is strictly dependent on p21, but independent of DNA damage, p53 or other cell cycle inhibitors, and it is regulated by the TGFM-NM-2/SMAD and PI3K/FOXO pathways. Developmentally-programmed senescence is followed by macrophage infiltration and clearance of senescent cells. Abrogation of senescence by p21 deletion is only partially compensated by apoptosis and originates detectable developmental abnormalities. Importantly, high levels of p21 are also associated to the regressing mesonephros and endolymphatic sac in human embryos. These findings place cellular senescence as a relevant morphogenic process during embryonic development. We microdissected mesonephric tubules from senescent (WT) and non-senescent (p21-null) embryos to get information about this new senescence that occurs during embryogenesis.

2013-11-14 | E-GEOD-49108 | biostudies-arrayexpress

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