Comprehensive scientific resource on gene conversion mechanisms, meiotic recombination, biased gene conversion, and their implications for genome evolution and human disease.
Genome affected per meiosis
Typical conversion tract
Higher rate than crossover
The molecular processes underlying gene conversion events in meiosis and mitosis
Gene conversion initiates with programmed DSBs by Spo11, followed by 5'-to-3' resection creating single-stranded overhangs that invade homologous templates.
SDSA is the primary non-crossover pathway where the invading strand is displaced after DNA synthesis, leading to gene conversion without crossing over.
Double Holliday junctions can resolve as either crossovers or non-crossovers (gene conversion), depending on the orientation of endonuclease cleavage.
Mismatch repair of heteroduplex DNA during conversion shows a bias toward G:C over A:T base pairs, driving genome-wide GC content evolution.
Conversion tracts typically span 200-2000bp in humans. Tract length and frequency vary by genomic region and correlate with recombination hotspot activity.
Ectopic gene conversion between paralogs can introduce pathogenic variants, as seen in congenital adrenal hyperplasia (CYP21A2/CYP21A1P) and spinal muscular atrophy.
Conversions per meiosis (human)
More frequent than crossovers
GC-biased resolution rate
Recombination hotspots mapped
Recent publications and reviews on gene conversion biology and bioinformatics
An accessible introduction to gene conversion mechanisms, distinguishing allelic from ectopic conversion and explaining their evolutionary significance.
Read ArticleDetailed walkthrough of meiotic gene conversion from DSB initiation through Holliday junction resolution, with molecular diagrams.
Read ArticleReview of latest findings on conversion tract length distribution, detection methods, and implications for understanding genome evolution.
Read ArticleSubmit research data, report errors, or propose collaboration on gene conversion studies.
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