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Models of Recombination

Models of Recombination. Fogel and Hurst. 1967. Meiotic gene conversion in yeast tetrads and the theory of recombination. Genetics. 57: 455-481. His. arg. 7. +. +. +. 1. +. thr. Nos. of tetrads in which the His+ strand participates in a crossover. Events leading to His+.

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Models of Recombination

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  1. Models of Recombination

  2. Fogel and Hurst. 1967. Meiotic gene conversion in yeast tetrads and the theory of recombination. Genetics. 57: 455-481. His arg 7 + + + 1 + thr

  3. Nos. of tetrads in which the His+ strand participates in a crossover Events leading to His+ tetrads w. crossovers in: Nos. of tetrads 70 - None Reciprocal crossing over between sites 7 and 1 2 5 Region I 0 0 Region II 1 1 Regions I & II 220 - None 138 141 Region I Conversion of site 7 to + 84 60 Region II 7 7 Regions I & II 23 - None 3 3 Region I Conversion of site 1 to + 49 49 Region II 0 0 Regions I & II

  4. Summary: gene conversion: • Replacement of one allele by another on a non-sister chromatid, leading to “abnormal” segregation ratios in tetrads. • In about half the cases in which gene conversion occurs, there is also full (i.e., reciprocal crossing over between flanking markers. The conversion site itself must be involved in the process of crossing over. • Models of recombination must account for gene conversion and its association with crossing over as observed in yeast tetrads.

  5. Models of recombination • Initiation by nicking of DNA • Exchange of single nucleotide strands between chromatids (DNA duplexes), which creates heteroduplexed areas. • Mismatch repair of heteroduplexes or not. • Resolution of the intermediate (reciprocal recomnination for flanking makers, or not).

  6. The Holliday model (c) strand exchange takes place between the chromatids (d) ligation occurs yielding two completely intact DNA molecules (a) pair of chromatids (b) a single strand cut is made in each chromatid

  7. (e) Branch migration occurs, giving regions of heteroduplex DNA (f) Resolution of the Holliday junction gives two DNA molecules with heteroduplex DNA. Depending upon how the Holliday junction is resolved, we either observe no exchange of flanking markers (left) or an exchange of flanking markers (right)

  8. If the heteroduplex is repaired, the result is either a chromatid conversion or a normal chromatid, depending on which allele is removed. If the heteroduplex is not repaired, then when the resulting DNA replicates, one daughter DNA molecular is +, while the other DNA molecular is m. The result is a half-chromatid conversion wherein only half the chromatid is converted.

  9. Summary of the Holliday model • Single-strand DNA nick on both chromatids. • Strand exchange generates the Holliday junction.

  10. A Modification of the Holliday Model:The Meselson-Radding model • A single DNA strand is nicked. • Strand displacement (invasions) and subsequent DNA synthesis generates the Holliday junction

  11. The Meselson-Radding model

  12. The Meselson-Radding model

  13. Double-Strand Break-Repair model • A single double-strand break is generated in one chromatid (DNA molecule) • Strand displacement (invasion) and subsequent DNA synthesis generates the Holliday junction.

  14. Double-Strand Break-Repair model

  15. Double-Strand Break-Repair model

  16. Proc. Natl. Acad. Sci. USA Vol. 94, pp. 5213-5218, May 1997 Genetics Clustering of meiotic double-strand breaks on yeast chromosome III Frédéric Baudat and Alain Nicolas* Institut Curie, Section de Recherche, Centre National de la Recherche Scientifique, Unité Mixte deRecherche 144, Compartimentation et Dynamique Cellulaires, 26 rue d'Ulm, 75248 Paris Cedex 05, France

  17. ABSTRACT In the yeast Saccharomyces cerevisiae, meiotic recombination is initiated by transient DNA double-strand breaks (DSBs) that are repaired by interaction of the broken chromosome with its homologue. To identify a large number of DSB sites and gain insight into the control of DSB formation at both the local and the whole chromosomal levels, we have determined at high resolution the distribution of meiotic DSBs along the 340 kb of chromosome III. We have found 76 DSB regions, mostly located in intergenic promoter-containing intervals. The frequency of DSBs varies at least 50-fold from one region to another. The global distribution of DSB regions along chromosome III is nonrandom, defining large (39-105 kb) chromosomal domains, both hot and cold. The distribution of these localized DSBs indicates that they are likely to initiate most crossovers along chromosome III, but some discrepancies remain to be explained.

  18. Figure 2. Location and amount of meiotic DSBs on chromosome III.

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