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<p>The in vivo mechanism, <i>cis</i>-acting roadblocks, and biological functions of DNA loop extrusion by eukaryotic SMC complexes remain incompletely defined. Here, we identify condensin-dependent Hi-C contact stripes at the recombination enhancer (<i>RE</i>) and at <i>rDNA</i> in <i>S. cerevisiae</i>. The <i>RE</i> is an autonomous condensin loading site only active in <i>MAT</i>a cells from which oriented, unidirectional loop extrusion proceeds with an estimated processivity ~150–250 kb and a density ~0.04–0.18 that varies across the cell cycle. Centromeres, replication forks, and highly transcribed RNA PolII-dependent genes represent roadblocks for condensin. Cohesin is not an obstacle for condensin, while Top2 promotes its loop extrusion activity. A DNA double-strand break (DSB) at <i>MAT</i> blocks loop extrusion, resulting in the establishment of a ~170 kb-long <i>RE</i>-<i>MAT</i> loop. The <i>RE</i> and the DSB are required and sufficient to form this site-specific loop, which promotes <i>RE</i>-proximal homology identification in the early stages of recombinational DNA break-repair. We propose that juxtaposition of the broken <i>MAT</i>a site and its target <i>HML</i>α donor is the relevant structure by which condensin promotes a-to-α mating-type switching.</p>

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Condensin loop extrusion properties, roadblocks, and role in homology search during recombination in S. cerevisiae

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月23日

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  • Vinciane Piveteau,
  • Chloé Dupont,
  • Hossein Salari,
  • Agnès Dumont,
  • Jérôme Savocco,
  • Daniel Jost,
  • Aurèle Piazza

摘要

The in vivo mechanism, cis-acting roadblocks, and biological functions of DNA loop extrusion by eukaryotic SMC complexes remain incompletely defined. Here, we identify condensin-dependent Hi-C contact stripes at the recombination enhancer (RE) and at rDNA in S. cerevisiae. The RE is an autonomous condensin loading site only active in MATa cells from which oriented, unidirectional loop extrusion proceeds with an estimated processivity ~150–250 kb and a density ~0.04–0.18 that varies across the cell cycle. Centromeres, replication forks, and highly transcribed RNA PolII-dependent genes represent roadblocks for condensin. Cohesin is not an obstacle for condensin, while Top2 promotes its loop extrusion activity. A DNA double-strand break (DSB) at MAT blocks loop extrusion, resulting in the establishment of a ~170 kb-long RE-MAT loop. The RE and the DSB are required and sufficient to form this site-specific loop, which promotes RE-proximal homology identification in the early stages of recombinational DNA break-repair. We propose that juxtaposition of the broken MATa site and its target HMLα donor is the relevant structure by which condensin promotes a-to-α mating-type switching.