ArticleMolecular and cellular biology1993
Unusual mutation clusters provide insight into class I gene conversion mechanisms.
Article in Molecular and cellular biology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Regulatory T cells and co-evolution of allele-specific MHC recognition by the TCR.Scandinavian journal of immunology · 2020Review
- Concerted and birth-and-death evolution of multigene families.Annual review of genetics · 2005Review
- Frequent segmental sequence exchanges and rapid gene duplication characterize the MHC class I genes in lemurs.Immunogenetics · 2003Article
- Discrimination of MHC-derived odors by untrained mice is consistent with divergence in peptide-binding region residues.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Single and coincident intragenic mutations attributable to gene conversion in a human cell line.Genetics · 1997Article
- Fabry disease: thirty-five mutations in the alpha-galactosidase A gene in patients with classic and variant phenotypes.Molecular medicine (Cambridge, Mass.) · 1997Article
- A complex major histocompatibility complex D locus variant generated by an unusual recombination mechanism in mice.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genetic diversity among the K and D alleles of the mouse major histocompatibility complex is generated by gene conversion among members of the class I multigene family. The majority of known class I mutants contain clusters of nucleotide changes that can be traced to linked family members. However, the details of the gene conversion mechanism are not known. The bm3 and bm23 mutations represent exceptions to the usual pattern and provide insight into intermediates generated during the gene conversion process. Both of these variants contain clusters of five nucleotide substitutions, but they differ from the classic conversion mutants in the important respect that no donor gene for either mutation could be identified in the parental genome. Nevertheless, both mutation clusters are composed of individual mutations that do exist within the parent. Therefore, they are not random and appear to be templated. Significantly, the bm3 and bm23 mutation clusters are divided into overlapping regions that match class I genes which have functioned as donor genes in other characterized gene conversion events. The unusual structure of the mutation clusters indicates an underlying gene conversion mechanism that can generate mutation clusters as a result of the interaction of three genes in a single genetic event. The unusual mutation clusters are consistent with a hypothetical gene conversion model involving extrachromosomal intermediates.
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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.