ArticleG3 (Bethesda, Md.)2015
Chromoanasynthetic Genomic Rearrangement Identified in a N-Ethyl-N-Nitrosourea (ENU) Mutagenesis Screen in Caenorhabditis elegans.
Article in G3 (Bethesda, Md.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Chromosomal Instability and Chromoanagenesis as Forces for Genomic Evolution.Methods in molecular biology (Clifton, N.J.) · 2025Review
- Single variant, yet "double trouble": TSC and KBG syndrome because of a large de novo inversion.Life science alliance · 2024Article
- Deciphering complex genome rearrangements in C. elegans using short-read whole genome sequencing.Scientific reports · 2021Article
- Chromothripsis-Explosion in Genetic Science.Cells · 2021Review
- Article
- A spontaneous complex structural variant in rcan-1 increases exploratory behavior and laboratory fitness of Caenorhabditis elegans.PLoS genetics · 2020Article
- Requirement for translocon-associated protein (TRAP) α in insulin biogenesis.Science advances · 2019Article
- CRISPR/Cas9 Methodology for the Generation of Knockout Deletions inG3 (Bethesda, Md.) · 2019Article
- Chromoanagenesis: cataclysms behind complex chromosomal rearrangements.Molecular cytogenetics · 2019Review
- Mutational and transcriptional landscape of spontaneous gene duplications and deletions inProceedings of the National Academy of Sciences of the United States of America · 2018Article
- N-Ethyl-N-Nitrosourea (ENU) Mutagenesis Reveals an Intronic Residue Critical for Caenorhabditis elegans 3' Splice Site Function in Vivo.G3 (Bethesda, Md.) · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Chromoanasynthesis is a recently discovered phenomenon in humans with congenital diseases that is characterized by complex genomic rearrangements (CGRs) resulting from aberrant repair of catastrophic chromosomal damage. How these CGRs are induced is not known. Here, we describe the structure and function of dpDp667, a causative CGR that emerged from a Caenorhabditis elegans dauer suppressor screen in which animals were treated with the point mutagen N-ethyl-N-nitrosourea (ENU). dpDp667 comprises nearly 3 Mb of sequence on the right arm of the X chromosome, contains three duplications and one triplication, and is devoid of deletions. Sequences from three out of the four breakpoint junctions in dpDp667 reveal microhomologies that are hallmarks of chromoanasynthetic CGRs. Our findings suggest that environmental insults and physiological processes that cause point mutations may give rise to chromoanasynthetic rearrangements associated with congenital disease. The relatively subtle phenotype of animals harboring dpDp667 suggests that the prevalence of CGRs in the genomes of mutant and/or phenotypically unremarkable animals may be grossly underestimated.
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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.