ArticleGenetics2005
Persistence and loss of meiotic recombination hotspots.
Article in Genetics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed.
- On the origin of PRDM9-guided recombination hotspots.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Down the Penrose stairs, or how selection for fewer recombination hotspots maintains their existence.eLife · 2023Article
- PRDM9, a driver of the genetic map.PLoS genetics · 2018Review
- Where to Cross Over? Defining Crossover Sites in Plants.Frontiers in genetics · 2018Review
- Hotspots for Initiation of Meiotic Recombination.Frontiers in genetics · 2018Review
- Genomic and chromatin features shaping meiotic double-strand break formation and repair in mice.Cell cycle (Georgetown, Tex.) · 2017Article
- Repeated losses of PRDM9-directed recombination despite the conservation of PRDM9 across vertebrates.eLife · 2017Article
- Nonparadoxical evolutionary stability of the recombination initiation landscape in yeast.Science (New York, N.Y.) · 2015Article
- Antagonistic Coevolution Drives Whack-a-Mole Sensitivity in Gene Regulatory Networks.PLoS computational biology · 2015Article
- Specific modifications of histone tails, but not DNA methylation, mirror the temporal variation of mammalian recombination hotspots.Genome biology and evolution · 2014Article
- Mouse tetrad analysis provides insights into recombination mechanisms and hotspot evolutionary dynamics.Nature genetics · 2014Article
- Article
- Natural competence and the evolution of DNA uptake specificity.Journal of bacteriology · 2014Review
- Self-organization of meiotic recombination initiation: general principles and molecular pathways.Annual review of genetics · 2014Review
- Distribution of recombination hotspots in the human genome--a comparison of computer simulations with real data.PloS one · 2013Article
- Preaching about the converted: how meiotic gene conversion influences genomic diversity.Annals of the New York Academy of Sciences · 2012Review
- Epigenetic functions enriched in transcription factors binding to mouse recombination hotspots.Proteome science · 2012Article
- DNA sequence-mediated, evolutionarily rapid redistribution of meiotic recombination hotspots.Genetics · 2011Article
- GC-biased evolution near human accelerated regions.PLoS genetics · 2010Article
- Conservation of recombination hotspots in yeast.Proceedings of the National Academy of Sciences of the United States of America · 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The contradiction between the long-term persistence of the chromosomal hotspots that initiate meiotic recombination and the self-destructive mechanism by which they act strongly suggests that our understanding of recombination is incomplete. This "hotspot paradox" has been reinforced by the finding that biased gene conversion also removes active hotspots from human sperm. To investigate the requirements for hotspot persistence, we developed a detailed computer simulation model of their activity and its evolutionary consequences. With this model, unopposed hotspot activity could drive strong hotspots from 50% representation to extinction within 70 generations. Although the crossing over that hotspots cause can increase population fitness, this benefit was always too small to slow the loss of hotspots. Hotspots could not be maintained by plausible rates of de novo mutation, nor by crossover interference, which alters the frequency and/or spacing of crossovers. Competition among hotspots for activity-limiting factors also did not prevent their extinction, although the rate of hotspot loss was slowed. Key factors were the probability that the initiating hotspot allele is destroyed and the nonmeiotic contributions hotspots make to fitness. Experimental investigation of these deserves high priority, because until the paradox is resolved all components of the mechanism are open to doubt.
Indexed as
Identifiers
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.