Clustering of Drosophila melanogaster immune genes in interplay with recombination rate.

<h4>Background</h4>Gene 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 c...

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Autor principal:	K Mathias Wegner
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2008
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/bd3e73cfe182484e882ab1151f78ff01
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spelling	oai:doaj.org-article:bd3e73cfe182484e882ab1151f78ff012021-11-25T06:11:22ZClustering of Drosophila melanogaster immune genes in interplay with recombination rate.1932-620310.1371/journal.pone.0002835https://doaj.org/article/bd3e73cfe182484e882ab1151f78ff012008-07-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/18665272/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Gene 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.<h4>Principal findings</h4>Immune 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).<h4>Conclusions</h4>Epistatically 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.K Mathias WegnerPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 3, Iss 7, p e2835 (2008)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q K Mathias Wegner Clustering of Drosophila melanogaster immune genes in interplay with recombination rate.
description	<h4>Background</h4>Gene 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.<h4>Principal findings</h4>Immune 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).<h4>Conclusions</h4>Epistatically 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.
format	article
author	K Mathias Wegner
author_facet	K Mathias Wegner
author_sort	K Mathias Wegner
title	Clustering of Drosophila melanogaster immune genes in interplay with recombination rate.
title_short	Clustering of Drosophila melanogaster immune genes in interplay with recombination rate.
title_full	Clustering of Drosophila melanogaster immune genes in interplay with recombination rate.
title_fullStr	Clustering of Drosophila melanogaster immune genes in interplay with recombination rate.
title_full_unstemmed	Clustering of Drosophila melanogaster immune genes in interplay with recombination rate.
title_sort	clustering of drosophila melanogaster immune genes in interplay with recombination rate.
publisher	Public Library of Science (PLoS)
publishDate	2008
url	https://doaj.org/article/bd3e73cfe182484e882ab1151f78ff01
work_keys_str_mv	AT kmathiaswegner clusteringofdrosophilamelanogasterimmunegenesininterplaywithrecombinationrate
_version_	1718414066878251008

Clustering of Drosophila melanogaster immune genes in interplay with recombination rate.

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