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Functional Adaptations of Endogenous Retroviruses to the Drosophila host Reveal Principles of their Evolutionary Diversification

ABSTRACT: Functional Adaptations of Endogenous Retroviruses to the Drosophila host Reveal Principles of their Evolutionary Diversification

PROVIDER: PRJNA1001868 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25506114.fastq.gz	Fastqsanger.gz
	SRR25506115.fastq.gz	Fastqsanger.gz
	SRR25506116.fastq.gz	Fastqsanger.gz
	SRR25506117.fastq.gz	Fastqsanger.gz
	SRR25506118.fastq.gz	Fastqsanger.gz

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Functional Adaptations of Endogenous Retroviruses to the Drosophila host Reveal Principles of their Evolutionary Diversification [PRO-seq]

Project description:Functional Adaptations of Endogenous Retroviruses to the Drosophila host Reveal Principles of their Evolutionary Diversification [PRO-seq]

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Functional Adaptations of Endogenous Retroviruses to the Drosophila host Reveal Principles of their Evolutionary Diversification [RNA-seq]

Project description:Functional Adaptations of Endogenous Retroviruses to the Drosophila host Reveal Principles of their Evolutionary Diversification [RNA-seq]

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Functional Adaptations of Endogenous Retroviruses to the Drosophila host Reveal Principles of their Evolutionary Diversification [sRNA-seq]

Project description:Functional Adaptations of Endogenous Retroviruses to the Drosophila host Reveal Principles of their Evolutionary Diversification [sRNA-seq]

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Functional Adaptations of Endogenous Retroviruses to the Drosophila host Reveal Principles of their Evolutionary Diversification [sRNA-seq]

Project description:Transposable elements profoundly affect the biology and evolution of their hosts, yet their own evolutionary dynamics remain poorly understood. Here, we investigate insect endogenous retroviruses (iERVs), a monophyletic group of LTR retrotransposons that have acquired the trait of infectivity, likely through capture of a Baculovirus envelope gene. In Drosophila ovaries, iERVs with functional envelope have adapted their cis-regulatory sequences to be expressed in any somatic cell type, from where they infect the germline. Strikingly, related retroviruses show distinct expression patterns, indicating niche partitioning. In contrast, all non-infectious iERVs that emerged through secondary envelope-loss are specifically expressed in the germline. Co-evolving with iERVs, the genome-protecting piRNA pathway has assimilated iERV promoter and sequence information into piRNA clusters, underscoring the functional significance of iERV expression in somatic niches. We propose that the evolutionary innovation of cell-to-cell infectivity has triggered the adaptive radiation of iERVs through trait diversification and antagonistic virus-host interactions, processes that likely underpin niche-specific expression of endogenous retroviruses in vertebrates as well.

2023-08-04 | GSE239984 | GEO

Functional Adaptations of Endogenous Retroviruses to the Drosophila host Reveal Principles of their Evolutionary Diversification [PRO-seq]

2023-08-04 | GSE239983 | GEO

Functional Adaptations of Endogenous Retroviruses to the Drosophila host Reveal Principles of their Evolutionary Diversification [RNA-seq]

2023-08-04 | GSE239982 | GEO

Functional Adaptations of Endogenous Retroviruses to the Drosophila host Reveal Principles of their Evolutionary Diversification

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-08-03 | GSE239985 | GEO

TRIM28 silences endogenous retroviruses in neural progenitor cells

Project description:Here we show that in neural progenitor cells (NPCs) TRIM28 silences transcription of two groups of endogenous retroviruses (ERVs): IAP1 and MMERVK10C. Derepression of ERVs in Trim28-deficient NPCs was associated with a loss of H3K9me3 and resulted in transcriptional upregulation and reverse transcription. These findings demonstrate a unique dynamic transcriptional regulation of ERVs in NPCs. Analysis of upregulation of ERVs in Trim28-deficient NPCs

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Project description:Prion-like spreading of protein misfolding is characteristic for neurodegenerative diseases, but the exact mechanisms of intercellular protein aggregate dissemination remain unresolved. Evidence accumulates that endogenous retroviruses, remnants of viral germline infections that are normally epigenetically silenced, become upregulated in neurodegenerative diseases such as amyotrophic lateral sclerosis and tauopathies. Here we uncover that activation of endogenous retroviruses affects prion-like spreading of proteopathic seeds. To identify changes in the proteome of donor cells that might contribute to protein aggregate spreading, we performed mass spectrometry analyses of total cell lysates and donor EV fractions using N2a cells expressing HA epitope-tagged Sup35 NM prion protein at early (P07) and late passages (P16) post cryopreservation. Among the proteins increased in donor cells and EVs upon prolonged culture, we identified mouse endogenous MLV retrovirus proteins to be highly increased.

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The evolutionary capacitor HSP90 buffers the regulatory effects of mammalian endogenous retroviruses.

Project description:The molecular chaperone heat shock protein 90 (HSP90) is thought to buffer genetic variation uncoupling phenotypic outcome from individual genotypes. HSP90 thus acts as an evolutionary capacitor by facilitating an accumulation of natural genetic variation. The molecular mechanism underlying the buffering ability is unclear, and HSP90-contingent genetic variation maps both to coding and non-coding parts of the genome. Our genome-wide data indicate that a compromised chaperoning activity of HSP90 causes derepression of endogenous retroviruses (ERVs) in mouse somatic cells. This results in an upregulation of host genes located in the neighborhood of pre-existing ERVs insertion sites. We provide genetic and biochemical evidence that HSP90 cooperates with KAP1/ SETDB1 histone methyltranferase pathway to repress ERVs. Individual mouse strains have unique integration sites of ERVs in their genomes. Consequently distinct genes are responsive to HSP90 inhibitor in different mouse strains depending on the position of the genes vis-à-vis strain-specific ERV insertion sites. Since ERVs have been exapted to drive novel transcriptional networks during mammalian evolution, HSP90 may have acted as a capacitor by buffering variation caused by ERV in non-coding regions of the genome. Our studies provide the first molecular framework by which HSP90 can mitigate genetic variation in gene-regulatory regions affecting gene expression and phenotypes.

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