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Retrotransposons and the global shutdown of homeostatic innate immunity in the tumor cells by oncolytic parvovirus H-1PV

ABSTRACT: Retrotransposons and the global shutdown of homeostatic innate immunity in the tumor cells by oncolytic parvovirus H-1PV

PROVIDER: PRJNA672945 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12925260.fastq.gz	Fastqsanger.gz
	SRR12925261.fastq.gz	Fastqsanger.gz
	SRR12925262.fastq.gz	Fastqsanger.gz
	SRR12925263.fastq.gz	Fastqsanger.gz
	SRR12925264.fastq.gz	Fastqsanger.gz

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Human Retrotransposons and the Global Shutdown of Homeostatic Innate Immunity by Oncolytic Parvovirus H-1PV in Pancreatic Cancer.

Project description:Although the oncolytic parvovirus H-1PV has entered clinical trials, predicting therapeutic success remains challenging. We investigated whether the antiviral state in tumor cells determines the parvoviral oncolytic efficacy. The interferon/interferon-stimulated genes (IFN/ISG)-circuit and its major configurator, human endogenous retroviruses (HERVs), were evaluated using qRT-PCR, ELISA, Western blot, and RNA-Seq techniques. In pancreatic cancer cell lines, H-1PV caused a late global shutdown of innate immunity, whereby the concomitant inhibition of HERVs and IFN/ISGs was co-regulatory rather than causative. The growth-inhibitory IC50 doses correlated with the power of suppression but not with absolute ISG levels. Moreover, H-1PV was not sensitive to exogenous IFN despite upregulated antiviral ISGs. Such resistance questioned the biological necessity of the oncotropic ISG-shutdown, which instead might represent a surrogate marker for personalized oncolytic efficacy. The disabled antiviral homeostasis may modify the activity of other viruses, as demonstrated by the reemergence of endogenous AluY-retrotransposons. This way of suppression may compromise the interferogenicity of drugs having gemcitabine-like mechanisms of action. This shortcoming in immunogenic cell death induction is however amendable by immune cells which release IFN in response to H-1PV.

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Retrotransposons and the global shutdown of homeostatic innate immunity in the tumor cells by oncolytic parvovirus H-1PV

Project description:RNAseq-based comparison of H-1PV infected vs. non-infected cells revealed global suppression of antiviral innate immunity in the PDAC cells (AsPC1, MiaPaca2 and T3M4 taken at 48hpi) and global stimulation – in the healthy donor PBMCs (taken at 24hpi).

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Lysosomal catabolic activity governs the exit of the murine totipotent 2-cell state by silencing early-embryonic retrotransposons [RNA-seq]

Project description:During the development in mouse early embryos, a subset of retrotransposons and genes are transiently expressed in the totipotent 2-cell embryos. These 2-cell-embryo-asscoiated (referred to as 2C) transcripts rapidly shut down their expression beyond the late 2-cell stage of embryos, and this timely shutdown governs the embryo to exit from the 2-cell stage. However, mechanisms regulating this wave of shutdown are not fully understood. In this study, we established a novel connection between lysosomal catabolic activity and 2C transcripts in regulating the exit of totipotent 2-cell state by using both in vitro 2-cell-like cells model and mouse embryos. Our results showed that the activation of lysosomal catabolism in mouse embryos governed the embryo to exit from the 2-cell state by suppressing the expression of 2C transcripts. Mechanistically, we found that lysosomal catabolic activity modulated 2C transcripts by inactivating transcriptional factors Tfe3/Tfeb and abolishing their transcriptional activation on 2C retrotransposons, MERVL/MT2-Mm. Collectively, our study elucidates the function of lysosomal activity in orchestrating transcriptomic landscape and early development in mouse embryos and reveals an unanticipated layer of transcriptional control on early-embryonic retrotransposons from lysosomal signaling.

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Lysosomal catabolic activity governs the exit of the murine totipotent 2-cell state by silencing early-embryonic retrotransposons [CUT&Tag]

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Direct cell-to-cell transmission of retrotransposons

Project description:Transposable elements are abundant in host genomes but are generally considered to be confined to the cell in which they are expressed, with the notable exception of endogenous retroviruses. Here, we identify a group of LTR retrotransposons that infect the germline from somatic cells within the Drosophila ovary, despite lacking the fusogenic Envelope protein typically required for retroviral entry. Instead, these elements encode a short transmembrane protein, sORF2, with structural features reminiscent of viral cell-cell fusogens. Through genetics, imaging, and electron microscopy, we show that sORF2 localizes to invasive somatic protrusions, enabling the direct transfer of retrotransposon capsids into the oocyte. Remarkably, sORF2-like proteins are widespread among insect retrotransposons and also occur in piscine nackednaviruses and avian picornaviruses. These findings reveal a noncanonical, Envelope-independent transmission mechanism shared by retrotransposons and non-enveloped viruses, offering important insights into host-pathogen evolution and soma-germline interactions.

2025-03-21 | PXD061763 | Pride

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