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      Arabidopsis meiotic crossover hotspots overlap with H2A.Z nucleosomes at gene promoters

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          Abstract

          PRDM9 directs human meiotic crossover hotspots to intergenic sequence motifs, whereas budding yeast hotspots overlap low nucleosome density regions in gene promoters. To investigate hotspots in plants, which lack PRDM9, we used coalescent analysis of Arabidopsis genetic variation. Crossovers increase towards gene promoters and terminators, and hotspots are associated with active chromatin modifications, including H2A.Z, histone H3K4 me3, low nucleosome density and low DNA methylation. Hotspot-enriched A-rich and CTT-repeat DNA motifs occur upstream and downstream of transcriptional start respectively. Crossovers are asymmetric around promoters and highest over CTT-motifs and H2A.Z-nucleosomes. Pollen-typing, segregation and cytogenetic analysis show decreased crossovers in the arp6 H2A.Z deposition mutant, at multiple scales. During meiosis H2A.Z and DMC1/RAD51 recombinases form overlapping chromosomal foci. As arp6 reduces DMC1/RAD51 foci, H2A.Z may promote formation or processing of meiotic DNA double-strand breaks. We propose that gene chromatin ancestrally designates hotspots within eukaryotes and PRDM9 is a derived state within vertebrates.

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          Shotgun bisulphite sequencing of the Arabidopsis genome reveals DNA methylation patterning.

          Shawn Cokus, Suhua Feng, Xiaoyu Zhang … (2008)
          Cytosine DNA methylation is important in regulating gene expression and in silencing transposons and other repetitive sequences. Recent genomic studies in Arabidopsis thaliana have revealed that many endogenous genes are methylated either within their promoters or within their transcribed regions, and that gene methylation is highly correlated with transcription levels. However, plants have different types of methylation controlled by different genetic pathways, and detailed information on the methylation status of each cytosine in any given genome is lacking. To this end, we generated a map at single-base-pair resolution of methylated cytosines for Arabidopsis, by combining bisulphite treatment of genomic DNA with ultra-high-throughput sequencing using the Illumina 1G Genome Analyser and Solexa sequencing technology. This approach, termed BS-Seq, unlike previous microarray-based methods, allows one to sensitively measure cytosine methylation on a genome-wide scale within specific sequence contexts. Here we describe methylation on previously inaccessible components of the genome and analyse the DNA methylation sequence composition and distribution. We also describe the effect of various DNA methylation mutants on genome-wide methylation patterns, and demonstrate that our newly developed library construction and computational methods can be applied to large genomes such as that of mouse.
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            Whole-genome sequencing of multiple Arabidopsis thaliana populations.

            Jun Cao, Korbinian Schneeberger, Stephan Ossowski … (2011)
            The plant Arabidopsis thaliana occurs naturally in many different habitats throughout Eurasia. As a foundation for identifying genetic variation contributing to adaptation to diverse environments, a 1001 Genomes Project to sequence geographically diverse A. thaliana strains has been initiated. Here we present the first phase of this project, based on population-scale sequencing of 80 strains drawn from eight regions throughout the species' native range. We describe the majority of common small-scale polymorphisms as well as many larger insertions and deletions in the A. thaliana pan-genome, their effects on gene function, and the patterns of local and global linkage among these variants. The action of processes other than spontaneous mutation is identified by comparing the spectrum of mutations that have accumulated since A. thaliana diverged from its closest relative 10 million years ago with the spectrum observed in the laboratory. Recent species-wide selective sweeps are rare, and potentially deleterious mutations are more common in marginal populations.
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              The fine-scale structure of recombination rate variation in the human genome.

              Gilean McVean, Simon Myers, Sarah Hunt … (2004)
              The nature and scale of recombination rate variation are largely unknown for most species. In humans, pedigree analysis has documented variation at the chromosomal level, and sperm studies have identified specific hotspots in which crossing-over events cluster. To address whether this picture is representative of the genome as a whole, we have developed and validated a method for estimating recombination rates from patterns of genetic variation. From extensive single-nucleotide polymorphism surveys in European and African populations, we find evidence for extreme local rate variation spanning four orders in magnitude, in which 50% of all recombination events take place in less than 10% of the sequence. We demonstrate that recombination hotspots are a ubiquitous feature of the human genome, occurring on average every 200 kilobases or less, but recombination occurs preferentially outside genes.
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                Author and article information

                Journal
                Journal ID (nlm-journal-id): 9216904
                Journal ID (pubmed-jr-id): 2419
                Journal ID (nlm-ta): Nat Genet
                Journal ID (iso-abbrev): Nat. Genet.
                Title: Nature genetics
                ISSN (Print): 1061-4036
                ISSN (Electronic): 1546-1718
                Publication date Nihms-submitted: 28 August 2013
                Publication date (Electronic): 22 September 2013
                Publication date (Print): November 2013
                Publication date PMC-release: 01 May 2014
                Volume: 45
                Issue: 11
                Electronic Location Identifier: 10.1038/ng.2766
                Affiliations
                [1 ]Department of Plant Sciences, Downing Street, University of Cambridge, Cambridge, CB2 3EA, United Kingdom
                [2 ]Wellcome Trust Centre for Human Genetics, Roosevelt Drive, University of Oxford, Oxford, OX3 7BN, United Kingdom
                [3 ]School of Biosciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT, United Kingdom
                [4 ]Department of Biotechnology, Adam Mickiewicz University, Umultowska 89, Poznan, Poland
                [5 ]Department of Biology and the Carolina Center for Genome Sciences, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, 27599, USA
                [6 ]Lineberger Comprehensive Cancer Center, The University of North Carolina School of Medicine, Chapel Hill, North Carolina, 27599, USA
                Author notes
                [* ]Correspondence to: irh25@ 123456cam.ac.uk

                AUTHOR CONTRIBUTIONS

                KC, JDH, NEY, PAZ performed experiments. KC, JDH, NEY, PAZ, GPC, FCHF and IRH designed experiments. XZ, KAK, OV, TJH, GM and IRH designed and performed computational and statistical analysis. KC, XZ, KAK, OV, JDH, NEY, TJH, PAZ, GPC, FCHF, GM and IRH wrote the paper.

                [†]

                Equal contribution.

                Article
                Manuscript ID: EMS54625
                DOI: 10.1038/ng.2766
                PMC ID: 3812125
                PubMed ID: 24056716
                SO-VID: a77ec7ab-4800-4a95-b245-633a3be9c9b1
                License:

                Users may view, print, copy, download and text and data- mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms

                History
                Funding
                Funded by: Wellcome Trust :
                Award ID: 090532 || WT
                Categories
                Subject: Article

                ScienceOpen disciplines: Genetics
                Data availability:
                ScienceOpen disciplines: Genetics

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