ArticleGenetics2008
End joining at Caenorhabditis elegans telomeres.
Article in Genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 30 citations in OpenAlex.
- Telomerase-independent survival leads to a mosaic of complex subtelomere rearrangements inGenome research · 2023Article
- Nematode chromosomes.Genetics · 2022Review
- Heterologous synapsis in C. elegans is regulated by meiotic double-strand breaks and crossovers.Chromosoma · 2021Article
- The double-stranded DNA-binding proteins TEBP-1 and TEBP-2 form a telomeric complex with POT-1.Nature communications · 2021Article
- Long-read sequencing and de novo genome assemblies reveal complex chromosome end structures caused by telomere dysfunction at the single nucleotide level.Nucleic acids research · 2021Article
- Germ granule dysfunction is a hallmark and mirror of Piwi mutant sterility.Nature communications · 2021Article
- Article
- Binding of anGenetics · 2019Article
- CENP-A and topoisomerase-II antagonistically affect chromosome length.The Journal of cell biology · 2017Article
- C. elegans whole-genome sequencing reveals mutational signatures related to carcinogens and DNA repair deficiency.Genome research · 2014Article
- Synthetic cytotoxicity: digenic interactions with TEL1/ATM mutations reveal sensitivity to low doses of camptothecin.Genetics · 2014Article
- The shelterin protein POT-1 anchors Caenorhabditis elegans telomeres through SUN-1 at the nuclear periphery.The Journal of cell biology · 2013Article
- Spontaneous telomere to telomere fusions occur in unperturbed fission yeast cells.Nucleic acids research · 2013Article
- Caenorhabditis elegans POT-1 and POT-2 repress telomere maintenance pathways.G3 (Bethesda, Md.) · 2013Article
- Article
- Caenorhabditis elegans POT-2 telomere protein represses a mode of alternative lengthening of telomeres with normal telomere lengths.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- DNA synthesis generates terminal duplications that seal end-to-end chromosome fusions.Science (New York, N.Y.) · 2011Article
- An MLL/COMPASS subunit functions in the C. elegans dosage compensation complex to target X chromosomes for transcriptional regulation of gene expression.Genes & development · 2011Article
- Non-homologous end joining plays a key role in transgene concatemer formation in transgenic zebrafish embryos.International journal of biological sciences · 2010Article
- Telomere disruption results in non-random formation of de novo dicentric chromosomes involving acrocentric human chromosomes.PLoS genetics · 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
5 authors at 1 institution in 1 country.
Funding
Abstract
Critically shortened telomeres can be subjected to DNA repair events that generate end-to-end chromosome fusions. The resulting dicentric chromosomes can enter breakage-fusion-bridge cycles, thereby impeding elucidation of the structures of the initial fusion events and a mechanistic understanding of their genesis. Current models for the molecular basis of fusion of critically shortened, uncapped telomeres rely on PCR assays that typically capture fusion breakpoints created by direct ligation of chromosome ends. Here we use independent approaches that rely on distinctive features of Caenorhabditis elegans to study the frequency of direct end-to-end chromosome fusion in telomerase mutants: (1) holocentric chromosomes that allow for genetic isolation of stable end-to-end fusions and (2) unique subtelomeric sequences that allow for thorough PCR analysis of samples of genomic DNA harboring multiple end-to-end fusions. Surprisingly, only a minority of end-to-end fusion events resulted from direct end joining with no additional genome rearrangements. We also demonstrate that deficiency for the C. elegans Ku DNA repair heterodimer does not affect telomere length or cause synthetic effects in the absence of telomerase.
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.