ReviewBioEssays : news and reviews in molecular, cellular and developmental biology2026
Mechanisms That Govern Recombinase Fidelity Control During Eukaryotic Homologous Recombination.
Review in BioEssays : news and reviews in molecular, cellular and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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2 authors.
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Abstract
Homologous recombination (HR) is a DNA double-strand break repair pathway that preserves genome integrity by restoring genetic information lost through programmed or spontaneous DNA damage. As a template-directed process, HR identifies homologous DNA sequences to accurately repair broken chromosomes while minimizing inappropriate recombination events. Central to this process are the RecA-family recombinases. Most eukaryotes use Rad51 during mitosis and meiosis and Dmc1 during meiosis to locate and pair homologous DNA sequences. To ensure high-fidelity repair, eukaryotes have evolved regulatory protein networks that control recombinase filament assembly, organization, and strand exchange. Here, we review recent advances in understanding how recombinase filament length, architecture, and dynamics influence the fidelity and outcome of homologous recombination. We discuss their distinct roles in mitotic and meiotic recombination and propose how evolution has shaped filament properties to regulate interactions between donor and recipient DNA templates and promote accurate genome maintenance.
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