Evidence map›Paper›PMID 39005338›Full record

ArticlebioRxiv : the preprint server for biology2024

Insights into non-crossover recombination from long-read sperm sequencing.

Regev Schweiger, Sangjin Lee, Chenxi Zhou, Tsun-Po Yang, Katie Smith, Stacy Li, Rashesh Sanghvi, Matthew Neville, Emily Mitchell, Ayrun Nessa and 6 more

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors.

Regev SchweigerDepartment of Genetics, University of Cambridge, Downing Street, Cambridge CB2 3EH, United Kingdom.ORCID 0000-0003-2450-8901
Sangjin LeeWellcome Sanger Institute, Cancer Ageing and Somatic Mutation, Hinxton, Cambridge CB10 1SA, United Kingdom.
Chenxi ZhouDepartment of Genetics, University of Cambridge, Downing Street, Cambridge CB2 3EH, United Kingdom.ORCID 0000-0002-1735-2630
Tsun-Po YangWellcome Sanger Institute, Cancer Ageing and Somatic Mutation, Hinxton, Cambridge CB10 1SA, United Kingdom.
Katie SmithWellcome Sanger Institute, Cancer Ageing and Somatic Mutation, Hinxton, Cambridge CB10 1SA, United Kingdom.
Stacy LiDepartment of Integrative Biology, University of California Berkeley, Berkeley, USA.
Rashesh SanghviWellcome Sanger Institute, Cancer Ageing and Somatic Mutation, Hinxton, Cambridge CB10 1SA, United Kingdom.
Matthew NevilleWellcome Sanger Institute, Cancer Ageing and Somatic Mutation, Hinxton, Cambridge CB10 1SA, United Kingdom.
Emily MitchellWellcome Sanger Institute, Cancer Ageing and Somatic Mutation, Hinxton, Cambridge CB10 1SA, United Kingdom.
Ayrun NessaKings College London, Department of Twin Research & Genetic Epidemiology, London, United Kingdom.
Sam WadgeKings College London, Department of Twin Research & Genetic Epidemiology, London, United Kingdom.
Kerrin S SmallKings College London, Department of Twin Research & Genetic Epidemiology, London, United Kingdom.
Peter J CampbellWellcome Sanger Institute, Cancer Ageing and Somatic Mutation, Hinxton, Cambridge CB10 1SA, United Kingdom.
Peter H SudmantDepartment of Integrative Biology, University of California Berkeley, Berkeley, USA.ORCID 0000-0002-9573-8248
Raheleh RahbariWellcome Sanger Institute, Cancer Ageing and Somatic Mutation, Hinxton, Cambridge CB10 1SA, United Kingdom.
Richard DurbinDepartment of Genetics, University of Cambridge, Downing Street, Cambridge CB2 3EH, United Kingdom.

Funding

The evolution and diversity of mutation, molecular fidelity, and genome structureR35GM142916 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI Peter Heshedahl Sudmant · 2021 to 2026
$2.5M
NIGMS NIH HHS R35 GM142916Wellcome Trust
6 · The paper itself

Abstract

Meiotic recombination is a fundamental process that generates genetic diversity by creating new combinations of existing alleles. Although human crossovers have been studied at the pedigree, population and single-cell level, the more frequent non-crossover events that lead to gene conversion are harder to study, particularly at the individual level. Here we show that single high-fidelity long sequencing reads from sperm can capture both crossovers and non-crossovers, allowing effectively arbitrary sample sizes for analysis from one male. Using fifteen sperm samples from thirteen donors we demonstrate variation between and within donors for the rates of different types of recombination. Intriguingly, we observe a tendency for non-crossover gene conversions to occur upstream of nearby PRDM9 binding sites, whereas crossover locations have a slight downstream bias. We further provide evidence for two distinct non-crossover processes. One gives rise to the vast majority of non-crossovers with mean conversion tract length under 50bp, which we suggest is an outcome of standard PRDM9-induced meiotic recombination. In contrast ~2% of non-crossovers have much longer mean tract length, and potentially originate from the same process as complex events with more than two haplotype switches, which is not associated with PRDM9 binding sites and is also seen in somatic cells.

Identifiers

PMID39005338
PMCPMC11245106

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Registered trials

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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.