Acute condensin depletion causes genome decompaction without altering the level of global gene expression in<i>Saccharomyces cerevisiae</i>

Paul, Matthew R.; Markowitz, Tovah E.; Hochwagen, Andreas; Ercan, Sevinç

doi:10.1101/195487

Cited by 4 publications

(2 citation statements)

References 79 publications

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“…Loss of these interactions in the DCC mutant is consistent with the effect of removing SMC complexes in other contexts. Loss of cohesin loading in mouse cells and loss of condensin in yeast both result in reduced interactions at distances below 200 kb (Paul et al, 2018;Schwarzer et al, 2017).…”

Section: Tads and Transcriptionmentioning

confidence: 99%

X Chromosome Domain Architecture Regulates Caenorhabditis elegans Lifespan but Not Dosage Compensation

et al. 2019

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Section: Tads and Transcriptionmentioning

confidence: 99%

X Chromosome Domain Architecture Regulates Caenorhabditis elegans Lifespan but Not Dosage Compensation

et al. 2019

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“…While in vitro and in silico experiments suggest similar molecular activities for condensins and cohesin, it is less clear how condensin binding and movement on eukaryotic chromosomes are regulated in vivo [7]. In yeast, condensin regulates chromosomal interactions across the ribosomal DNA and form gene loops involved in repression of the quiescent genome [22][23][24]. However, since yeast chromosomes support much smaller interaction domains and lack clear TAD boundaries, how condensin binding regulates larger eukaryotic genomes remains unknown.…”

Section: Introductionmentioning

confidence: 99%

Condensin DC loads and spreads from recruitment sites to create loop-anchored TADs inC. elegans

Jimenez

Kim

Ragipani

et al. 2021

Preprint

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Condensins are molecular motors that compact DNA for chromosome segregation and gene regulation. In vitro experiments have begun to elucidate the mechanics of condensin function but how condensin loading and translocation along DNA controls eukaryotic chromosome structure in vivo remains poorly understood. To address this question, we took advantage of a specialized condensin, which organizes the 3D conformation of X chromosomes to mediate dosage compensation (DC) in C. elegans. Condensin DC is recruited and spreads from a small number of recruitment elements on the X chromosome (rex). We found that ectopic insertion of rex sites on an autosome leads to bidirectional spreading of the complex over hundreds of kilobases. On the X chromosome, strong rex sites contain multiple copies of a 12-bp sequence motif and act as TAD borders. Inserting a strong rex and ectopically recruiting the complex on the X chromosome or an autosome creates a loop-anchored TAD. Unlike the CTCF system, which controls TAD formation by cohesin, direction of the 12-bp motif does not control the specificity of loops. In an X;V fusion chromosome, condensin DC linearly spreads into V and increases 3D DNA contacts, but fails to form TADs in the absence of rex sites. Finally, we provide in vivo evidence for the loop extrusion hypothesis by targeting multiple dCas9-Suntag complexes to an X chromosome repeat region. Consistent with linear translocation along DNA, condensin DC accumulates at the block site. Together, our results support a model whereby strong rex sites act as insulation elements through recruitment and bidirectional spreading of condensin DC molecules and form loop-anchored TADs.

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Persistent DNA-break potential near telomeres increases initiation of meiotic recombination on short chromosomes

Subramanian

Zhu

Markowitz

et al. 2017

Preprint

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SUMMARYFaithful meiotic chromosome inheritance and fertility relies on the stimulation of meiotic crossover recombination by potentially genotoxic DNA double-strand breaks (DSBs). To avoid excessive damage, feedback mechanisms down-regulate DSBs on chromosomes that have successfully initiated crossover repair. In Saccharomyces cerevisiae, this regulation requires the removal of the conserved DSB-promoting protein Hop1/HORMAD during chromosome synapsis. Here, we identify privileged domains spanning roughly 100 Kb near all telomeres that escape this regulation and continue to break in pachynema, well after chromosomes are fully synapsed. These telomere-adjacent regions (TARs) retain Hop1 despite normal synapsis, indicating that synapsis is necessary but not sufficient for Hop1 removal. TAR establishment requires the disassemblase Pch2/TRIP13, which preferentially removes Hop1 from telomeredistant sequences. Importantly, the uniform size of TARs between chromosomes contributes to disproportionately high DSB and repair signals on small chromosomes in pachynema, suggesting that TARs partially underlie the curiously high recombination rate of small chromosomes.

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Acute condensin depletion causes genome decompaction without altering the level of global gene expression inSaccharomyces cerevisiae

Cited by 4 publications

References 79 publications

X Chromosome Domain Architecture Regulates Caenorhabditis elegans Lifespan but Not Dosage Compensation

X Chromosome Domain Architecture Regulates Caenorhabditis elegans Lifespan but Not Dosage Compensation

Condensin DC loads and spreads from recruitment sites to create loop-anchored TADs inC. elegans

Persistent DNA-break potential near telomeres increases initiation of meiotic recombination on short chromosomes

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