ArticleGenetics2007
The dynamics of the roo transposable element in mutation-accumulation lines and segregating populations of Drosophila melanogaster.
Article in Genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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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
6 citing papers in PubMed.
- qPCR as a Selective Tool for Cytogenetics.Plants (Basel, Switzerland) · 2022Article
- Review
- A unique cluster ofMobile DNA · 2019Article
- Low Genetic Quality Alters Key Dimensions of the Mutational Spectrum.PLoS biology · 2016Article
- Sequencing of pooled DNA samples (Pool-Seq) uncovers complex dynamics of transposable element insertions in Drosophila melanogaster.PLoS genetics · 2012Article
- LTR retroelements in the genome of Daphnia pulex.BMC genomics · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We estimated the number of copies for the long terminal repeat (LTR) retrotransposable element roo in a set of long-standing Drosophila melanogaster mutation-accumulation full-sib lines and in two large laboratory populations maintained with effective population size approximately 500, all of them derived from the same isogenic origin. Estimates were based on real-time quantitative PCR and in situ hybridization. Considering previous estimates of roo copy numbers obtained at earlier stages of the experiment, the results imply a strong acceleration of the insertion rate in the accumulation lines. The detected acceleration is consistent with a model where only one (maybe a few) of the approximately 70 roo copies in the ancestral isogenic genome was active and each active copy caused new insertions with a relatively high rate ( approximately 10(-2)), with new inserts being active copies themselves. In the two laboratory populations, however, a stabilized copy number or no accelerated insertion was found. Our estimate of the average deleterious viability effects per accumulated insert [E(s) < 0.003] is too small to account for the latter finding, and we discuss the mechanisms that could contain copy number.
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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.