Structural variation and DNA methylation shape the centromere-proximal meiotic crossover landscape in Arabidopsis
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ABSTRACT:
PROVIDER: PRJEB71632 | ENA |
REPOSITORIES: ENA
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Project description:Nanopore Sequencing and assembly of Col-0 carrying seed coat expressed GFP and RFP transgenes flanking the centromere of chromosome 3 (CTL 3.9) - additionally, DNA methylation was derived using deepsignal-plant using these reads.
2024-01-20 | E-MTAB-13686 | biostudies-arrayexpress
Project description:BackgroundCentromeres load kinetochore complexes onto chromosomes, which mediate spindle attachment and allow segregation during cell division. Although centromeres perform a conserved cellular function, their underlying DNA sequences are highly divergent within and between species. Despite variability in DNA sequence, centromeres are also universally suppressed for meiotic crossover recombination, across eukaryotes. However, the genetic and epigenetic factors responsible for suppression of centromeric crossovers remain to be completely defined.ResultsTo explore the centromere-proximal meiotic recombination landscape, we map 14,397 crossovers against fully assembled Arabidopsis thaliana (A. thaliana) genomes. A. thaliana centromeres comprise megabase satellite repeat arrays that load nucleosomes containing the CENH3 histone variant. Each chromosome contains a structurally polymorphic region of ~3-4 megabases, which lack crossovers and include the satellite arrays. This polymorphic region is flanked by ~1-2 megabase low-recombination zones. These recombination-suppressed regions are enriched for Gypsy/Ty3 retrotransposons, and additionally contain expressed genes with high genetic diversity that initiate meiotic recombination, yet do not crossover. We map crossovers at high-resolution in proximity to CEN3, which resolves punctate centromere-proximal hotspots that overlap gene islands embedded in heterochromatin. Centromeres are densely DNA methylated and the recombination landscape is remodelled in DNA methylation mutants. We observe that the centromeric low-recombining zones decrease and increase crossovers in CG (met1) and non-CG (cmt3) mutants, respectively, whereas the core non-recombining zones remain suppressed.ConclusionOur work relates the genetic and epigenetic organization of A. thaliana centromeres and flanking pericentromeric heterochromatin to the zones of crossover suppression that surround the CENH3-occupied satellite repeat arrays.
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Project description:Meiotic crossover formation requires the stabilization of early recombination intermediates by a set of proteins and occurs within the environment of the chromosome axis, a structure important for the regulation of meiotic recombination events. The molecular mechanisms underlying and connecting crossover recombination and axis localization are elusive. Here, we identified the ZZS (Zip2–Zip4–Spo16) complex, required for crossover formation, which carries two distinct activities: one provided by Zip4, which acts as hub through physical interactions with components of the chromosome axis and the crossover machinery, and the other carried by Zip2 and Spo16, which preferentially bind branched DNA molecules in vitro. We found that Zip2 and Spo16 share structural similarities to the structure-specific XPF–ERCC1 nuclease, although it lacks endonuclease activity. The XPF domain of Zip2 is required for crossover formation, suggesting that, together with Spo16, it has a noncatalytic DNA recognition function. Our results suggest that the ZZS complex shepherds recombination intermediates toward crossovers as a dynamic structural module that connects recombination events to the chromosome axis. The identification of the ZZS complex improves our understanding of the various activities required for crossover implementation and is likely applicable to other organisms, including mammals.
2018-02-14 | GSE103877 | GEO
Project description:Programmed DNA double-strand breaks (DSBs) initiate meiotic recombination and their subsequent repair culminates in crossover (CO) formation. COs result from the asymmetric cleavage of double-Holliday junction (dHJ) intermediates, that requires the MutLγ endonuclease and a non-catalytic function of Exo1, an activity essential for fertility but at risk of generating unwanted chromosome rearrangements. Here we show how crossover formation by MutLγ is activated at the right time and at the right place. MutLγ forms a constitutive complex with Exo1, and in meiotic cells transiently contacts the upstream MutSγ (Msh4-Msh5) heterodimer. MutLγ associates with DSB hotspots only once recombination intermediates have been stabilized and engaged in the crossover repair pathway. MutLγ-Exo1 is recruited to DSB hotspots independently of the polo-like Cdc5 kinase, but to activate dHJ resolution, Cdc5 is recruited to the recombination intermediates and interacts individually with both MutLγ and Exo1, suggesting their direct modification. in vivo, MutLγ occupancy is restrained on recombination intermediates, and MutLγ associates with the vast majority of DSB hotspots, but at a lower frequency in centromeres, consistent with a strategy to reduce at-risk crossover events in these regions, and in late replicating regions. Our data highlight the tight temporal and spatial control of the activity of this constitutive, potentially harmful, nuclease.
2020-01-15 | GSE133108 | GEO
Project description:Programmed DNA double-strand breaks (DSBs) initiate meiotic recombination and their subsequent repair culminates in crossover (CO) formation. COs result from the asymmetric cleavage of double-Holliday junction (dHJ) intermediates, that requires the MutLγ complex together with a non-catalytic function of Exo1, an activity essential for fertility but at risk of generating unwanted chromosome rearrangements. Here we show how crossover formation by MutLγ is activated at the right time and at the right place. MutLγ forms a constitutive complex with Exo1, and in meiotic cells transiently contacts the upstream MutSγ (Msh4-Msh5) heterodimer. MutLγ associates with DSB hotspots at a late step in the recombinational repair, once recombination intermediates have been stabilized and engaged in the crossover repair pathway. MutLγ-Exo1 is recruited to DSB hotspots independently of the polo-like Cdc5 kinase, but to activate dHJ resolution, Cdc5 is recruited to the recombination intermediates and interacts individually with both MutLγ and Exo1, suggesting their direct modification. in vivo, MutLγ occupancy is restrained on recombination intermediates, and genome-wide, MutLγ associates with the vast majority of DSB hotspots, but at a lower frequency in centromeres, consistent with a strategy to reduce at-risk crossover events in these regions, and in late replicating regions. Our data highlight the highly temporally and spatially control of the activity of this constitutive, potentially harmful, nuclease
2019-12-01 | GSE132850 | GEO
Project description:Meiotic crossover landscape within RAC1 disease resistance gene
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Project description:Centromere Pairing Enables Correct Segregation of Meiotic Chromosomes
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Project description:Using microarrays to genotype the parental origin of progeny resulting from a cross between S96 and YJM789 yeast strains, we mapped the distribution of crossovers that occurred during meiosis. Knowledge of the crossover distribution allowed us to assess changes in crossover control in wild type and mutant strains. The S96 strain is a S288 derivative and thus its DNA sequence has high homology to the oligo sequences used to create the S98 Affymetrix Gene chip. The YJM789 strain is ~ 0.6% divergent from S288. Keywords: wild type and mutant analysis
2008-09-16 | GSE12170 | GEO
Project description:During meiosis, crossover recombination is essential to link homologous chromosomes and drive faithful chromosome segregation. Crossover recombination is non-random across the genome, and centromere-proximal crossovers are associated with an increased risk of aneuploidy, including Trisomy 21 in humans. Here, we identify the conserved Ctf19/CCAN kinetochore sub-complex as a major factor that minimizes potentially deleterious centromere-proximal crossovers in budding yeast. We uncover multi-layered suppression of pericentromeric recombination by the Ctf19 complex, operating across distinct chromosomal distances. The Ctf19 complex prevents meiotic DNA break formation, the initiating event of recombination, proximal to the centromere. The Ctf19 complex independently drives the enrichment of cohesin throughout the broader pericentromere to suppress crossovers, but not DNA breaks. This non-canonical role of the kinetochore in defining a chromosome domain that is refractory to crossovers adds a new layer of functionality by which the kinetochore prevents the incidence of chromosome segregation errors that generate aneuploid gametes.
2015-12-15 | GSE72683 | GEO
Project description:Meiotic crossover recombination is triggered by the formation of programmed double strand breaks (DSBs) catalyzed by the conserved Spo11 protein. Only a subset of these DSBs are repaired as crossovers, promoted by a group of eight evolutionarily conserved proteins, named ZMM. The synaptonemal complex (SC) that assembles between homologous chromosomes is composed of two axial elements, from which chromatin loops emanate, held together by a central region, composed of the central element and a transverse filament protein. In budding yeast, crossover formation is functionally linked to the formation of the SC, but the underlying mechanism is unknown. Here we found that the SC central element protein, Ecm11, mainly localizes on both DSB sites and sites that attach chromatin loops to the chromosome axis, in a way that strictly requires the ZMM protein Zip4. We further show that Zip4 directly interacts with Ecm11 and that point mutants that specifically abolish the Zip4-Ecm11 interaction loose Ecm11 binding to chromosomes and exhibit defective SC assembly. Interestingly, SC assembly can be partially rescued by artificially tethering interaction-defective Ecm11 to Zip4. This direct connection that ensures SC assembly from CO sites could be a way for the meiotic cell to shut down further DSB formation once enough recombination sites have been selected for crossovers, thereby preventing excess crossovers. Finally, we found that the mammalian ortholog of Zip4, TEX11, interacts with the SC central element TEX12, raising the possibility that this may be a general mechanism.
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