ArticlePloS one2008
Clustering of Drosophila melanogaster immune genes in interplay with recombination rate.
Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Heterochromatic silencing of immune-related genes in glia is required for BBB integrity and normal lifespan in drosophila.Aging cell · 2023Article
- Selection for Plastic, Pathogen-Inducible Recombination in a Red Queen Model with Diploid Antagonists.Pathogens (Basel, Switzerland) · 2021Article
- Gene buddies: linked balanced polymorphisms reinforce each other even in the absence of epistasis.PeerJ · 2018Article
- Antagonistic experimental coevolution with a parasite increases host recombination frequency.BMC evolutionary biology · 2012Article
- Support for multiple classes of local expression clusters in Drosophila melanogaster, but no evidence for gene order conservation.Genome biology · 2011Article
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1 author.
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Abstract
backgroundGene order in eukaryotic chromosomes is not random and has been linked to coordination of gene expression, chromatin structure and also recombination rate. The evolution of recombination rate is especially relevant for genes involved in immunity because host-parasite co-evolution could select for increased recombination rate (Red Queen hypothesis). To identify patterns left by the intimate interaction between hosts and parasites, I analysed the genomic parameters of the immune genes from 24 gene families/groups of Drosophila melanogaster. PRINCIPAL
findingsImmune genes that directly interact with the pathogen (i.e. recognition and effector genes) clustered in regions of higher recombination rates. Out of these, clustered effector genes were transcribed fastest indicating that transcriptional control might be one major cause for cluster formation. The relative position of clusters to each other, on the other hand, cannot be explained by transcriptional control per se. Drosophila immune genes that show epistatic interactions can be found at an average distance of 15.44+/-2.98 cM, which is considerably closer than genes that do not interact (30.64+/-1.95 cM).
conclusionsEpistatically interacting genes rarely belong to the same cluster, which supports recent models of optimal recombination rates between interacting genes in antagonistic host-parasite co-evolution. These patterns suggest that formation of local clusters might be a result of transcriptional control, but that in the condensed genome of D. melanogaster relative position of these clusters may be a result of selection for optimal rather than maximal recombination rates between these clusters.
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