ReviewCurrent opinion in genetics & development2018
The Retrotransposon storm and the dangers of a Collyer's genome.
Review in Current opinion in genetics & development, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed.
- Temporal and spatial niche partitioning in a retrotransposon community of the Drosophila melanogaster genome.Nucleic acids research · 2025Article
- An endogenous retroviral element co-opts an upstream regulatory sequence to achieve somatic expression and mobility.Nucleic acids research · 2025Article
- TDP-43 pathology in Drosophila induces glial-cell type specific toxicity that can be ameliorated by knock-down of SF2/SRSF1.PLoS genetics · 2023Article
- What do we mean by "aging"? Questions and perspectives revealed by studies in Drosophila.Mechanisms of ageing and development · 2023Article
- TDP-43 pathology inbioRxiv : the preprint server for biology · 2023Article
- Confounding factors in profiling of locus-specific human endogenous retrovirus (HERV) transcript signatures in primary T cells using multi-study-derived datasets.BMC medical genomics · 2023Article
- Endogenous retroviruses and TDP-43 proteinopathy form a sustaining feedback driving intercellular spread of Drosophila neurodegeneration.Nature communications · 2023Article
- Transposon control as a checkpoint for tissue regeneration.Development (Cambridge, England) · 2022Article
- An early proinflammatory transcriptional response to tau pathology is age-specific and foreshadows reduced tau burden.Brain pathology (Zurich, Switzerland) · 2022Article
- Transcription start site signal profiling improves transposable element RNA expression analysis at locus-level.Frontiers in genetics · 2022Article
- L1 Retrotransposons: A Potential Endogenous Regulator for Schizophrenia.Frontiers in genetics · 2022Review
- Endogenous retroviruses in the origins and treatment of cancer.Genome biology · 2021Review
- Unraveling the features of somatic transposition in the Drosophila intestine.The EMBO journal · 2021Article
- Intercellular viral spread and intracellular transposition of Drosophila gypsy.PLoS genetics · 2021Article
- Somatic piRNAs and Transposons are Differentially Expressed Coincident with Skeletal Muscle Atrophy and Programmed Cell Death.Frontiers in genetics · 2021Article
- The Gypsy Endogenous Retrovirus Drives Non-Cell-Autonomous Propagation in a Drosophila TDP-43 Model of Neurodegeneration.Current biology : CB · 2019Article
- Host-transposon interactions: conflict, cooperation, and cooption.Genes & development · 2019Review
- Article
- L1 retrotransposition in the soma: a field jumping ahead.Mobile DNA · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
Abstract
Like the famous Collyer's mansion in NY, our genomes have accumulated vast quantities of sequences that have been referred to as 'junk DNA,' much of which consists of retrotransposons (RTEs). A recent literature establishes the phenomenology that many RTEs become expressed at progressively higher levels during the course of normal aging. This seems to reflect gradual loss of heterochromatin in old age. In addition, RTEs appear to be precociously expressed in brains of younger animals that are experiencing neurodegenerative decline. Although it is difficult to distinguish cause from consequence, several recent studies support the contention that RTE expression, and even perhaps transposition, causally contribute to both the normal deterioration seen with age and to the precipitous decline in some neurodegenerative disorders. This may reflect a two hit model in which normal age-dependent loss of heterochromatin synergizes with a disruption to posttranscriptional silencing of RTEs caused by genetic and environmental stress.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.