Hayashi, M. He, L. Haplotype structure strongly affects recombination in a maize genetic interval polymorphic for Helitron and retrotransposon insertions. He, Y. Genomic features shaping the landscape of meiotic double-strand break hotspots in maize. Hedrick, P. Sex: differences in mutation, recombination, selection, gene flow, and genetic drift. Evolution 61, — Higgins, J. Genes Dev. Expression and functional analysis of AtMUS81 in Arabidopsis meiosis reveals a role in the second pathway of crossing-over.
Factors underlying restricted crossover localization in barley meiosis. Spatiotemporal asymmetry of the meiotic program underlies the predominantly distal distribution of meiotic crossovers in barley. Plant Cell 24, — Hirota, K. Distinct chromatin modulators regulate the formation of accessible and repressive chromatin at the fission yeast recombination hotspot ade6-M Cell 19, — Howe, F.
Is H3K4me3 instructive for transcription activation? Bioessays 39, 1— Hunter, N. The mismatch repair system contributes to meiotic sterility in an interspecific yeast hybrid. Jackson, J. Jeffreys, A. Reciprocal crossover asymmetry and meiotic drive in a human recombination hot spot. Ji, Y. Homoeologous pairing and recombination in Solanum lycopersicoides monosomic addition and substitution lines of tomato. Johnson, L. Joshi, N. Gradual implementation of the meiotic recombination program via checkpoint pathways controlled by global DSB levels.
Cell 57, — Kauppi, L. Numerical constraints and feedback control of double-strand breaks in mouse meiosis. Keeney, S. Meiosis-specific DNA double-strand breaks are catalyzed by Spo11, a member of a widely conserved protein family. Cell 88, — Kianian, P. High-resolution crossover mapping reveals similarities and differences of male and female recombination in maize.
Kiktev, D. GC content elevates mutation and recombination rates in the yeast Saccharomyces cerevisiae. Kleckner, N. Trends Genet. Knoll, A.
Kon, N. Cytologically integrated physical restriction fragment length polymorphism maps for the barley genome based on translocation breakpoints.
Kurzbauer, M. Lai, J. Genome-wide patterns of genetic variation among elite maize inbred lines. Lam, I. Mechanism and regulation of meiotic recombination initiation. Cold Spring Harb. Nonparadoxical evolutionary stability of the recombination initiation landscape in yeast. Lambing, C. Tackling plant meiosis: from model research to crop improvement. Plant Sci. Lange, J. ATM controls meiotic double-strand-break formation. The landscape of mouse meiotic double-strand break formation, processing, and repair.
Latrille, T. The red queen model of recombination hot-spot evolution: a theoretical investigation. B Biol. Law, J. Establishing, maintaining and modifying DNA methylation patterns in plants and animals. Lawrence, E. Modification of meiotic recombination by natural variation in plants.
Lenormand, T. Recombination difference between sexes: a role for haploid selection. PLoS Biol. Lercher, M. Human SNP variability and mutation rate are higher in regions of high recombination. Li, X. Dissecting meiotic recombination based on tetrad analysis by single-microspore sequencing in maize. Lindroth, A. Lu, P. Analysis of Arabidopsis genome-wide variations before and after meiosis and meiotic recombination by resequencing Landsberg erecta and all four products of a single meiosis.
Lukaszewicz, A. Control of meiotic double-strand-break formation by ATM: local and global views. Cell Cycle 17, — Lynn, A. ZMM proteins during meiosis: crossover artists at work. Chromosome Res. Macaisne, N. Cell Sci. Malagnac, F. Malone, R. Analysis of a recombination hotspot for gene conversion occurring at the HIS2 gene of Saccharomyces cerevisiae. Genetics , 5— Manhart, C. Roles for mismatch repair family proteins in promoting meiotic crossing over.
DNA Repair 38, 84— Marand, A. Meiotic crossovers are associated with open chromatin and enriched with Stowaway transposons in potato. Martini, E. Crossover homeostasis in yeast meiosis. Matic, I. Interspecies gene exchange in bacteria: the role of SOS and mismatch repair systems in evolution of species.
Cell 80, — Mayer, K. A physical, genetic and functional sequence assembly of the barley genome. Melamed-Bessudo, C. Deficiency in DNA methylation increases meiotic crossover rates in euchromatic but not in heterochromatic regions in Arabidopsis.
Mercier, R. Two meiotic crossover classes cohabit in Arabidopsis : one is dependent on MER3 ,whereas the other one is not. The molecular biology of meiosis in plants. Plant Biol. Mets, D. Condensins regulate meiotic DNA break distribution, thus crossover frequency, by controlling chromosome structure. Cell , 73— Mieczkowski, P.
Global analysis of the relationship between the binding of the Bas1p transcription factor and meiosis-specific double-strand DNA breaks in Saccharomyces cerevisiae.
Mirouze, M. Loss of DNA methylation affects the recombination landscape in Arabidopsis. Modliszewski, J. Meiotic recombination gets stressed out: CO frequency is plastic under pressure. Modrich, P. Mismatch repair in replication fidelity, genetic recombination, and cancer biology. Moore, D. Chromosome segregation during meiosis: building an unambivalent bivalent. Morgan, C.
Are the effects of elevated temperature on meiotic recombination and thermotolerance linked via the axis and synaptonemal complex? Myers, S. Drive against hotspot motifs in primates implicates the PRDM9 gene in meiotic recombination. A common sequence motif associated with recombination hot spots and genome instability in humans. Nicolas, A. An initiation site for meiotic gene conversion in the yeast Saccharomyces cerevisiae. Nature , 35— Nilsson-Tillgren, T.
Carlsberg Res. Genetic differences between Saccharomyces carlsbergensis and S. Analysis of chromosome III by single chromosome transfer. Otto, S. The evolutionary enigma of sex. Resolving the paradox of sex and recombination. Pan, J. A hierarchical combination of factors shapes the genome-wide topography of yeast meiotic recombination initiation.
Parvanov, E. Prdm9 controls activation of mammalian recombination hotspots. Science Pawlowski, W. Altered nuclear distribution of recombination protein RAD51 in maize mutants suggests the involvement of RAD51 in meiotic homology recognition. Petes, T. Meiotic recombination hot spots and cold spots. Phillips, D. Quantitative high resolution mapping of HvMLH3 foci in barley pachytene nuclei reveals a strong distal bias.
Pineda-Krch, M. Persistence and loss of meiotic recombination hotspots. Ponting, C. What are the genomic drivers of the rapid evolution of PRDM9?
Pratto, F. Recombination initiation maps of individual human genomes. Rayssiguier, C. The barrier to recombination between Escherichia coli and Salmonella typhimurium is disrupted in mismatch-repair mutants.
Ritz, K. Variation in recombination rate: adaptive or not? Robert, T. Robine, N. Genome-wide redistribution of meiotic double-strand breaks in Saccharomyces cerevisiae. Rocco, V. Sensing of DNA non-homology lowers the initiation of meiotic recombination in yeast. Genes Cells 1, — Rockmill, B. Centromere-proximal crossovers are associated with precocious separation of sister chromatids during meiosis in Saccharomyces cerevisiae. Rodgers-Melnick, E.
Recombination in diverse maize is stable, predictable, and associated with genetic load. Open chromatin reveals the functional maize genome. Rosu, S. Robust crossover assurance and regulated interhomolog access maintain meiotic crossover number. Saintenac, C. Detailed recombination studies along chromosome 3B provide new insights on crossover distribution in wheat Triticum aestivum L.
The recombination landscape in Arabidopsis thaliana F2 populations. Heredity , 1—9. Santos-Rosa, H. Active genes are tri-methylated at K4 of histone H3.
Saze, H. Maintenance of CpG methylation is essential for epigenetic inheritance during plant gametogenesis. Schnable, P. The B73 maize genome: complexity, diversity, and dynamics. Schwacha, A. Interhomolog bias during meiotic recombination: meiotic functions promote a highly differentiated interhomolog-only pathway.
Cell 90, — Serra, H. Massive crossover elevation via combination of HEI10 and recq4a recq4b during Arabidopsis meiosis. Shen, P. Homologous recombination in Escherichia coli : dependence on substrate length and homology. Effect of base mismatches on recombination via the RecBCD pathway. Genomics , — Shen, Y. ZIP4 in homologous chromosome synapsis and crossover formation in rice meiosis. Shilo, S.
DNA crossover motifs associated with epigenetic modifications delineate open chromatin regions in Arabidopsis. Plant Cell 27, — Sidhu, G.
Recombination patterns in maize reveal limits to crossover homeostasis. Simon, L. Structure and function of centromeric and pericentromeric heterochromatin in Arabidopsis thaliana. Simon, M. Quantitative trait loci mapping in five new large recombinant inbred line populations of Arabidopsis thaliana genotyped with consensus single-nucleotide polymorphism markers.
Singhal, S. Stable recombination hotspots in birds. Smeds, L. High-resolution mapping of crossover and non-crossover recombination events by whole-genome re-sequencing of an avian pedigree. Sommermeyer, V. Spp1, a member of the Set1 complex, promotes meiotic DSB formation in promoters by tethering histone H3K4 methylation sites to chromosome axes. Cell 49, 43— Stack, S.
Crossing over as assessed by late recombination nodules is related to the pattern of synapsis and the distribution of early recombination nodules in maize. Steiner, W. Meiotic DNA breaks at the S. Cell 9, — Stewart, M. Changing partners: moving from non- homologous to homologous centromere pairing in meiosis. Stroud, H. Comprehensive analysis of silencing mutants reveals complex regulation of the Arabidopsis methylome. Sturtevant, A. The linear arrangement of six sex-linked factors in Drosophila, as shown by their mode of association.
Sun, L. Landscaping crossover interference across a genome. Trends Plant Sci. Sun, Y. Deep genome-wide measurement of meiotic gene conversion using tetrad analysis in Arabidopsis thaliana. Symington, L. Expansions and contractions of the genetic map relative to the physical map of yeast chromosome III.
Tam, S. Effects of suppressing the DNA mismatch repair system on homeologous recombination in tomato. Thacker, D. Homologue engagement controls meiotic DNA break number and distribution. The Arabidopsis Genome Initiative Analysis of the genome sequence of the flowering plant Arabidopsis thaliana.
Tiemann-Boege, I. The consequences of sequence erosion in the evolution of recombination hotspots. Tischfield, S. Scale matters. The spatial correlation of yeast meiotic DNA breaks with histone H3 trimethylation is driven largely by independent colocalization at promoters. Cell Cycle 11, — Tomato Genome Consortium The tomato genome sequence provides insights into fleshy fruit evolution. Underwood, C. Varas, J. Analysis of the relationships between DNA double-strand breaks, synaptonemal complex and crossovers using the Atfas mutant.
Vervoort, M. Evolution of Prdm genes in animals: insights from comparative genomics. Villeneuve, A. Whence meiosis? Vizir, I. Sex difference in recombination frequency in Arabidopsis. Heredity 65, — Vongs, A. Arabidopsis thaliana DNA methylation mutants. Vrielynck, N. Wahls, W. Discrete DNA sites regulate global distribution of meiotic recombination. Wang, S. Meiotic crossover patterns: obligatory crossover, interference and homeostasis in a single process. Cell Cycle 14, — Wang, Y.
Meiotic recombination: mixing it up in plants. White, M. Transcription factors are required for the meiotic recombination hotspot at the HIS4 locus in Saccharomyces cerevisiae. Wijnker, E. The genomic landscape of meiotic crossovers and gene conversions in Arabidopsis thaliana. Hanley Rd, Suite St. Louis, MO Subject optional. Email address: Your name:. Example Question 1 : Understanding Crossing Over.
Possible Answers: Metaphase I. Correct answer: Prophase I. Explanation : During prophase I homologous chromosomes will line up with one another, forming tetrads. Report an Error.
What is the evolutionary purpose of cells that undergo crossing over? Possible Answers: To produce gametes that are genetically identical. Correct answer: To increase genetic diversity. Explanation : Crossing over is a process that happens between homologous chromosomes in order to increase genetic diversity. Example Question 3 : Understanding Crossing Over. During which step of cell division does crossing over occur? Possible Answers: Metaphase II.
Explanation : When chromatids "cross over," homologous chromosomes trade pieces of genetic material, resulting in novel combinations of alleles, though the same genes are still present. Example Question 4 : Understanding Crossing Over. What structures exchange genetic material during crossing over?
Possible Answers: Egg and sperm chromosomes. Correct answer: Nonsister chromatids. Explanation : During crossing over, homologous chromosomes come together in order to form a tetrad. Example Question 5 : Understanding Crossing Over. Crossover of homologous chromosomes in meiosis occurs during which phase? Possible Answers: Prophase II of meiosis. Correct answer: Prophase I of meiosis.
Explanation : The crossing over of homologous chromosomes occurs in prophase I of meiosis. Example Question 6 : Understanding Crossing Over. During crossing over, two homologous chromosomes pair to form which of the following choices? Possible Answers: Tetrad. Correct answer: Tetrad. Explanation : The tetrad, which divides into non-sister chromatids, exchanges genetic information in order to make the genetic pool more variant, and result in combinations of phenotypic traits that can occur outside of linked genotypic coding.
Example Question 7 : Understanding Crossing Over. Chromosomal crossover occurs in which phase of meiosis? Possible Answers: Anaphase II. Explanation : During prophase I, homologous chromosomes pair with each other and exchange genetic material in a process called chromosomal crossover.
Example Question 8 : Understanding Crossing Over. For example, much theory has been developed to explain the evolutionary advantage of recombination, but this theory does not address quantitative differences among individuals or variation at different genomic scales [ 17 ]. Variation in recombination may be explained by variation in the sexual system and the evolutionary consequences of different reproductive modes.
For example, selfing and inbreeding species may benefit from high rates of recombination because it can increase genetic diversity and allelic shuffling, and there is some evidence to support this [ 4 ]. However, the transition to obligate asexuality may result in suppression of recombination, because asexuals often have modified meiosis and because recombination can erode heterozygosity in asexuals [ 18 ].
To investigate how recombination rate varies between sexual and asexual species, Haag et al. In their focal sexual species, they report one of the shortest linkage maps known, and propose that the observed low recombination rates in some sexual species may favour sex—asex transitions or, alternatively, may be a consequence of it. The generality of this finding has yet to be tested and Haag et al. One notable counter example is observed in Daphnia , a genus that contains both sexual and asexual parthenogenetic species.
In cyclically parthenogenic species for which linkage maps have been made, we observe a very high recombination rate per megabase compared to other crustaceans [ 4 ]. These apparent contradictory results demonstrate that we need more recombination data in a greater ranges of species in order to begin to address long-standing theories on the evolution of recombination.
A notable pattern to emerge from empirical data is the observation that the distribution of recombination events is distinctly non-random across the genome. Variation is observed at many genomic scales: between chromosomes, between megabase regions within chromosomes and across regions spanning only a few kilobases. Between closely related species, there is often more variation in the distribution of recombination events compared to the total frequency of these events, suggesting that the rate at which recombination evolves is likely to depend on the genomic scale [ 4 , 17 ].
Variable rates of recombination between chromosomes have long been recognized, with sex chromosomes representing the most well-known example of this phenomenon as non-recombining sex chromosomes have evolved multiple times across taxa. The repeatability with which sex chromosomes have evolved suppressed recombination makes them excellent models to investigate how selection drives regional suppression of recombination and to identify proximate mechanisms [ 16 ].
In her contribution, Charlesworth [ 16 ] reviews the proximate and ultimate mechanisms driving suppression of recombination in sex chromosomes and provides recommendations of how to study this in divergent systems that differ in the age of their sex-linked regions.
Estimates of recombination at the fine genomic scale can provide information about how recombination influences or is influenced by genetic elements and neighbouring DNA sequence. Recombination is often higher in sequence regions with high gene density and GC content and lower in sequence regions that are enriched for simple repeats and transposable elements TE. Although these patterns are known from a wide range of eukaryotes, the proximate and ultimate mechanisms driving these correlations are poorly understood.
To begin to address this problem, Kent et al. TEs accumulate in regions of low recombination , but TEs can also modify the local recombination rate when the host genomes epigenetically silence TEs, and this often results in suppressed recombination [ 19 ]. Kent et al. Another commonly observed pattern in sequence data is a positive correlation between recombination rate and nucleotide diversity.
This relationship can be driven by the mutagenic effects of recombination [ 8 ], but it can also be the result of purifying selection acting on a deleterious mutation, and in doing so reducing genetic diversity at neighbouring, genetically liked loci a process referred to as background selection BGS [ 12 ]. This size of the region that experiences a loss in diversity is determined by the strength of selection increasing with increasing selection and the local recombination rate larger in regions of low recombination.
Comeron [ 12 ] reviews the concepts behind BGS, and argues that studies that attempt to investigate evidence for selection in the genome using patterns of nucleotide diversity should use a null model that incorporates BGS. With this approach, we can better determine baseline levels of diversity across the genome and identify the regions experiencing different forms of selection [ 12 ].
A pervasive pattern to emerge from accumulating fine-scale recombination data is that in many species, recombination is localized to small genomic regions referred to as hotspots.
Hotspots are present in a wide range of species, but absent from some well-known model species such as Caenorhabditis elegans [ 20 ] and Drosophila [ 21 ]. Progress in understanding the molecular mechanisms controlling hotspot position and activity has fuelled exciting empirical and theoretical work.
Tiemann-Boege et al. Repair of DSBs often introduces changes into the sequence—either via mutations or via biased gene conversion, and in many cases, the allele that initiates the DSB active allele is converted to an inactive allele—turning hotspots cold [ 8 , 15 ]. One mechanism controlling hotspot activity in several mammals is PRDM9, a zinc-finger binding protein that recognizes and binds to sequence motifs, initiating a DSB. Investigation of this trans -acting factor has provided a great deal of insight into how and why hotspot activity varies between species [ 22 ].
The rapid turnover of hotspots controlled by PRDM9 can also drive reproductive isolation between mouse strains [ 8 ] and PRDM9 was originally described as a speciation gene [ 7 ]. The self-destructive nature of PRDM9-directed hotspots creates rapid evolutionary dynamics—when an active allele is converted to an inactive allele and recombination rate declines, selection will favour new PRDM9 alleles in order to restore the optimal level of recombination for the species [ 15 ].
To model these rapid dynamics, Latrille et al. Importantly, their analyses demonstrate that for low-scaled mutation rates i. By contrast, at higher scaled mutation rates, a population of PRDM9 alleles can exist, each binding unique motifs in the genome [ 15 ].
Variation in recombination is not solely due to genetic factors: a multitude of environmental factors both extrinsic and intrinsic have been found to alter recombination frequency and distribution. Experimental work in Drosophila melanogaster has been instrumental in the development of this field and Stevison et al.
The authors also reflect on the lessons learnt and provide recommendations for future empirical research, which they successfully implement in a related species D. Alves et al. One hypothesis proposed to explain increased aneuploidy in older females is that recombination frequency or distribution changes with age; however, Alves and coauthors argue that this is unlikely because the effects of maternal age on recombination are not consistent or strong enough to drive the patterns of aneuploidy observed [ 7 ].
While there are many environmental cues known to influence recombination, temperature and condition are perhaps the most well known. Morgan et al. As proteins responsible for the formation of those structures during meiosis are in general across eukaryotes prone to aggregation and hence are particularly temperature-sensitive, this could explain why temperature often has a relatively consistent effect on recombination across taxa [ 5 ].
The second important environmental cue to influence recombination is condition. An organism in poor condition or in a poor environment may benefit from shuffling its genome, as its haplotype is poorly matched to the current environment, and there is some empirical evidence to support this [ 14 ].
Previous theoretical work suggests that condition-dependent recombination seems to emerge most readily in models of haploid rather than diploid selection, and that recombination rate plasticity is unlikely unless, for example, maternal effects are assumed. Rybnikov et al. Their model demonstrates that in the case where recombination rates within a group of selected loci are determined by an unlinked locus, alleles at the locus conferring condition-dependent recombination can readily invade a population with a fixed recombination rate.
These modelling results agree with theoretical studies that indicate that in diploids, direct effects—where the locus determining recombination influences recombination between itself and the group of selected loci—are unlikely to lead to plasticity in recombination rate.
0コメント