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Related Concept Videos

Retrovirus Life Cycles01:10

Retrovirus Life Cycles

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Retroviruses have a single-stranded RNA genome that undergoes a special form of replication. Once the retrovirus has entered the host cell, an enzyme called reverse transcriptase synthesizes double-stranded DNA from the retroviral RNA genome. This DNA copy of the genome is then integrated into the host’s genome inside the nucleus via an enzyme called integrase. Consequently, the retroviral genome is transcribed into RNA whenever the host’s genome is transcribed, allowing the...
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Retroviruses02:33

Retroviruses

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Retroviruses and retrotransposons both insert copies of their genetic elements into the genome of the host cell. Thus, the viral genes are passed on when the host genome is replicated or translated. A typical retroviral DNA sequence contains 3-4 genes that encode the different proteins required for its structural assembly and function as a molecular parasite. This DNA is transcribed into a single mRNA, which is very similar in structure to conventional mRNAs, i.e., it is capped at the 5’...
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siRNA - Small Interfering RNAs02:30

siRNA - Small Interfering RNAs

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Small interfering RNAs, or siRNAs, are short regulatory RNA molecules that can silence genes post-transcriptionally, as well as the transcriptional level in some cases. siRNAs are important for protecting cells against viral infections and silencing transposable genetic elements.
In the cytoplasm, siRNA is processed from a double-stranded RNA, which comes from either endogenous DNA transcription or exogenous sources like a virus. This double-stranded RNA is then cleaved by the...
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Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

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Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
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Replicative Cell Senescence02:15

Replicative Cell Senescence

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Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
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Non-LTR Retrotransposons03:18

Non-LTR Retrotransposons

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As the name suggests, non-LTR retrotransposons lack the long terminal repeats characteristic of the LTR retrotransposons. Additionally, both LTR and non-LTR retrotransposons use distinct mechanisms of mobilization. Non-LTR retrotransposons are further divided into two classes - Long interspersed nuclear elements (LINEs) and short interspersed nuclear elements (SINEs), both of which occur abundantly in most mammals, including humans. Some of the active non-LTR retrotransposons in humans are L1...
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  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Transcription Of Endogenous Retroviruses In Senescent Cells Contributes To The Accumulation Of Double-stranded Rnas That Trigger An Anti-viral Response That Reinforces Senescence.
  1. Home
  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Transcription Of Endogenous Retroviruses In Senescent Cells Contributes To The Accumulation Of Double-stranded Rnas That Trigger An Anti-viral Response That Reinforces Senescence.

Related Experiment Video

Techniques to Induce and Quantify Cellular Senescence
06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

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Transcription of endogenous retroviruses in senescent cells contributes to the accumulation of double-stranded RNAs that trigger an anti-viral response that reinforces senescence.

Eros Di Giorgio1, Liliana Ranzino2, Vanessa Tolotto2

  • 1Laboratory of Biochemistry, Department of Medicine, Università degli Studi di Udine, p.le Kolbe 4, 33100, Udine, Italy.

Cell Death & Disease
|February 21, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

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A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence
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A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence

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Measurement of Protein Turnover Rates in Senescent and Non-Dividing Cultured Cells with Metabolic Labeling and Mass Spectrometry
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Measurement of Protein Turnover Rates in Senescent and Non-Dividing Cultured Cells with Metabolic Labeling and Mass Spectrometry

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Related Experiment Videos

Techniques to Induce and Quantify Cellular Senescence
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Techniques to Induce and Quantify Cellular Senescence

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A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence
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A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence

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Measurement of Protein Turnover Rates in Senescent and Non-Dividing Cultured Cells with Metabolic Labeling and Mass Spectrometry
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Measurement of Protein Turnover Rates in Senescent and Non-Dividing Cultured Cells with Metabolic Labeling and Mass Spectrometry

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Cellular senescence involves an epigenetic switch that upregulates endogenous retroviruses (ERVs). These ERVs trigger an antiviral response, maintaining the senescence-associated growth arrest and altering the cellular microenvironment.

Area of Science:

  • Epigenetics
  • Cellular Biology
  • Virology

Background:

  • Cellular senescence is a state of irreversible growth arrest.
  • Epigenetic modifications play a crucial role in regulating gene expression during senescence.
  • Endogenous retroviruses (ERVs) are typically silenced in healthy cells.

Purpose of the Study:

  • To investigate the role of ERVs in cellular senescence.
  • To identify specific ERVs upregulated during senescence.
  • To elucidate the mechanism by which ERVs contribute to senescence maintenance.

Main Methods:

  • Analysis of ERV transcription in proliferating and senescent cells.
  • Investigation of epigenetic modifications, including H3K27me3, in senescent cells.
  • Assessment of the dsRNA accumulation and antiviral signaling pathways (IFIH1-MAVS) in senescence.

Main Results:

  • A subset of ERVs is epigenetically silenced in proliferating cells but upregulated during replicative and oncogene-induced senescence.
  • HDAC4 depletion or RAS/Akt activation leads to ERV upregulation.
  • Removal of H3K27me3 is implicated in ERV transcription during senescence.
  • Upregulated ERVs lead to dsRNA accumulation, activating the IFIH1-MAVS antiviral pathway.
  • MAVS signaling contributes to senescence-associated growth arrest and microenvironment modulation.

Conclusions:

  • ERVs are epigenetically regulated during senescence and contribute to its maintenance.
  • The ERV-dsRNA-IFIH1-MAVS axis is a key pathway in senescence.
  • This pathway actively shapes the senescent microenvironment and enforces growth arrest.