ArticlePLoS genetics2008
Segmental duplications arise from Pol32-dependent repair of broken forks through two alternative replication-based mechanisms.
Article in PLoS genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 papers.
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Who cites it
135 citing papers in PubMed, 213 citations in OpenAlex.
- Switch from canonical to recombination-dependent DNA synthesis by M-CDK phosphorylation of DNA Polα.The EMBO journal · 2026Article
- Segmental duplications and supernumerary chromosomes drive antifungal drug resistance in Candida auris.Nature communications · 2026Article
- Beyond inversions and deletions: the evolutionary and functional insights from translocations, fissions, and fusions in animal genomes.Heredity · 2026Review
- Mutations and structural variants arising during double-strand break repair.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Interplay Between Ribosomal Gene Deficiency and Calorie Restriction in Shaping Yeast Biosynthetic Capacity.Cells · 2025Article
- Genotyping sequence-resolved copy number variation using pangenomes reveals paralog-specific global diversity and expression divergence of duplicated genes.Nature genetics · 2025Article
- Mechanisms and genomic implications of break-induced replication.Nature structural & molecular biology · 2025Review
- A transient mutational burst occurs during yeast colony development.Molecular systems biology · 2025Article
- High-quality genome assembly and comparative analysis reveal extensive genomic variation inMicrobial genomics · 2025Article
- RPA and Rad27 limit templated and inverted insertions at DNA breaks.Nucleic acids research · 2025Article
- The Evolutionary Potential of Chromoanagenesis.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Mechanisms of tandem duplication in the cancer genome.DNA repair · 2025Review
- Structural and Mechanistic Diversity of Constitutional Chromoanagenesis.Methods in molecular biology (Clifton, N.J.) · 2025Article
- POLD3 as Controller of Replicative DNA Repair.International journal of molecular sciences · 2024Review
- Stressed? Break-induced replication comes to the rescue!DNA repair · 2024Review
- Duplications and Retrogenes Are Numerous and Widespread in Modern Canine Genomic Assemblies.Genome biology and evolution · 2024Article
- Gross Chromosomal Rearrangement at Centromeres.Biomolecules · 2023Review
- Telomerase-independent survival leads to a mosaic of complex subtelomere rearrangements inGenome research · 2023Article
- Delineation of two multi-invasion-induced rearrangement pathways that differently affect genome stability.Genes & development · 2023Article
- Delineation of two multi-invasion-induced rearrangement pathways that differently affect genome stability.bioRxiv : the preprint server for biology · 2023Article
75 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The propensity of segmental duplications (SDs) to promote genomic instability is of increasing interest since their involvement in numerous human genomic diseases and cancers was revealed. However, the mechanism(s) responsible for their appearance remain mostly speculative. Here, we show that in budding yeast, replication accidents, which are most likely transformed into broken forks, play a causal role in the formation of SDs. The Pol32 subunit of the major replicative polymerase Poldelta is required for all SD formation, demonstrating that SDs result from untimely DNA synthesis rather than from unequal crossing-over. Although Pol32 is known to be required for classical (Rad52-dependant) break-induced replication, only half of the SDs can be attributed to this mechanism. The remaining SDs are generated through a Rad52-independent mechanism of template switching between microsatellites or microhomologous sequences. This new mechanism, named microhomology/microsatellite-induced replication (MMIR), differs from all known DNA double-strand break repair pathways, as MMIR-mediated duplications still occur in the combined absence of homologous recombination, microhomology-mediated, and nonhomologous end joining machineries. The interplay between these two replication-based pathways explains important features of higher eukaryotic genomes, such as the strong, but not strict, association between SDs and transposable elements, as well as the frequent formation of oncogenic fusion genes generating protein innovations at SD junctions.
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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.