ArticleGenome research2009
Diverse cis factors controlling Alu retrotransposition: what causes Alu elements to die?
Article in Genome research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
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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.
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Who cites it
56 citing papers in PubMed, 104 citations in OpenAlex.
- Diverse short tandem repeat sequences influence gene regulation in human populations.Genome biology · 2025Article
- Identification of a minimal Alu domain required for retrotransposition.Nucleic acids research · 2025Article
- lncRNA BC200 is processed into a stable Alu monomer.RNA (New York, N.Y.) · 2024Article
- Causes and Consequences of Varying Transposable Element Activity: An Evolutionary Perspective.Annual review of genomics and human genetics · 2024Review
- Variable patterns of retrotransposition in different HeLa strains provide mechanistic insights into SINE RNA mobilization processes.Nucleic acids research · 2024Article
- Navigating the brain and aging: exploring the impact of transposable elements from health to disease.Frontiers in cell and developmental biology · 2024Review
- Article
- Human Retrotransposons and Effective Computational Detection Methods for Next-Generation Sequencing Data.Life (Basel, Switzerland) · 2022Review
- Tail Wags Dog's SINE: Retropositional Mechanisms of Can SINE Depend on Its A-Tail Structure.Biology · 2022Article
- The genetic and molecular features of the intronic pentanucleotide repeat expansion in spinocerebellar ataxia type 10.Frontiers in genetics · 2022Review
- Alu RNA and their roles in human disease states.RNA biology · 2021Article
- Diversity of short interspersed nuclear elements (SINEs) in lepidopteran insects and evidence of horizontal SINE transfer between baculovirus and lepidopteran hosts.BMC genomics · 2021Article
- Pedigree-based estimation of human mobile element retrotransposition rates.Genome research · 2019Article
- Article
- A computational reconstruction ofMobile DNA · 2018Article
- Selective elimination of long INterspersed element-1 expressing tumour cells by targeted expression of the HSV-TK suicide gene.Oncotarget · 2017Article
- Papio Baboon Species Indicative Alu Elements.Genome biology and evolution · 2017Article
- Discovery of rare, diagnosticMobile DNA · 2017Article
- Discovery of a new repeat family in the Callithrix jacchus genome.Genome research · 2016Article
- Roles for retrotransposon insertions in human disease.Mobile DNA · 2016Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The human genome contains nearly 1.1 million Alu elements comprising roughly 11% of its total DNA content. Alu elements use a copy and paste retrotransposition mechanism that can result in de novo disease insertion alleles. There are nearly 900,000 old Alu elements from subfamilies S and J that appear to be almost completely inactive, and about 200,000 from subfamily Y or younger, which include a few thousand copies of the Ya5 subfamily which makes up the majority of current activity. Given the much higher copy number of the older Alu subfamilies, it is not known why all of the active Alu elements belong to the younger subfamilies. We present a systematic analysis evaluating the observed sequence variation in the different sections of an Alu element on retrotransposition. The length of the longest number of uninterrupted adenines in the A-tail, the degree of A-tail heterogeneity, the length of the 3' unique end after the A-tail and before the RNA polymerase III terminator, and random mutations found in the right monomer all modulate the retrotransposition efficiency. These changes occur over different evolutionary time frames. The combined impact of sequence changes in all of these regions explains why young Alus are currently causing disease through retrotransposition, and the old Alus have lost their ability to retrotranspose. We present a predictive model to evaluate the retrotransposition capability of individual Alu elements and successfully applied it to identify the first putative source element for a disease-causing Alu insertion in a patient with cystic fibrosis.
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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.