Cohesin Complex Promotes Transcriptional Termination between Convergent Genes in S. pombe

Gullerová, Monika; Proudfoot, Nick J.

doi:10.1016/j.cell.2008.02.040

Cited by 193 publications

(228 citation statements)

References 31 publications

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“…The data suggest that transcription prevents the accumulation of functional cohesin complexes on the URA3 excision cassettes. The results are consistent with previous reports of transcription altering the distribution of cohesin on chromatin (15,16,(20)(21)(22)40).…”

Section: Resultssupporting

confidence: 83%

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Binding, sliding, and function of cohesin during transcriptional activation

Borrie

Campor

Joshi

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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The ring-shaped cohesin complex orchestrates long-range DNA interactions to mediate sister chromatid cohesion and other aspects of chromosome structure and function. In the yeast Saccharomyces cerevisiae, the complex binds discrete sites along chromosomes, including positions within and around genes. Transcriptional activity redistributes the complex to the 3′ ends of convergently oriented gene pairs. Despite the wealth of information about where cohesin binds, little is known about cohesion at individual chromosomal binding sites and how transcription affects cohesion when cohesin complexes redistribute. In this study, we generated extrachromosomal DNA circles to study cohesion in response to transcriptional induction of a model gene, URA3. Functional cohesin complexes loaded onto the locus via a poly(dA:dT) tract in the gene promoter and mediated cohesion before induction. Upon transcription, the fate of these complexes depended on whether the DNA was circular or not. When gene activation occurred before DNA circularization, cohesion was lost. When activation occurred after DNA circularization, cohesion persisted. The presence of a convergently oriented gene also prevented transcription-driven loss of functional cohesin complexes, at least in M phase-arrested cells. The results are consistent with cohesin binding chromatin in a topological embrace and with transcription mobilizing functional complexes by sliding them along DNA.T he protein complex known as cohesin organizes eukaryotic genomes into structures that segregate faithfully between dividing cells. The complex was first discovered for its role in mediating sister chromatid cohesion, but it is now known to participate in numerous aspects of chromosome biology (1, 2). Cohesin is clinically relevant because mutations in subunits of the complex or in factors that load and activate the complex lead to developmental disorders such as Cornelia de Lange syndrome, Roberts syndrome, and Warsaw breakage syndrome (3, 4).Cohesin is a ring-shaped complex composed of four subunits named Smc1, Smc3, Scc3, and Mcd1/Scc1 in budding yeast. The complex is thought to embrace DNA topologically with chromatin fibers passing through a central open channel (5-7). A substantial body of work supports a model in which cohesion arises from single cohesin complexes that embrace both sister chromatids [the double embrace model (6)]. Whether the central channel is large enough to accommodate both chromatids has recently been brought into question (8). In addition, the behavior of cohesin has not always been consistent with a double embrace by single complexes (for examples, see refs. 9-11). These situations usually involve a perturbation that causes loss of cohesion but not a loss of cohesin binding from chromatin. Such results force consideration of alternative models in which cohesin complexes embrace only one chromatid topologically and interact with other cohesin complexes or chromatin features to mediate cohesion (9,11,12).Cohesin binds densely in centromeric regions of chromos...

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Section: Resultssupporting

confidence: 83%

“…Work with representative RNA polymerase II genes showed that transcription causes cohesin to move from initial positions on ORFs, often leading to enrichment at downstream regions (15,16,(20)(21)(22). Mobilization by an advancing RNA polymerase has been invoked to account for the redistribution.…”

mentioning

confidence: 99%

Binding, sliding, and function of cohesin during transcriptional activation

Borrie

Campor

Joshi

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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“…In addition, it is possible that chromatin remodeling factors facilitate the recruitment of factors that are directly involved in termination. This is illustrated by a recent study in S. pombe showing that Swi6 (human HP1) recruits cohesin to the intergenic region of convergent genes, which forces RNAPII to terminate by blocking RNAPII elongation (Gullerova and Proudfoot 2008). While ChIP analysis in HeLa cells showed an association of several proteins involved in chromatin remodeling with the entire transcription unit, including the region downstream from the poly(A) site (Venkataraman et al 2005), detailed studies of the possible role of chromatin remodeling factors in mammalian termination are necessary to better understand the exact function and generality of chromatin in termination.…”

Section: Rnapii Termination and Chromatin Remodeling Factorsmentioning

confidence: 98%

Transcription termination by nuclear RNA polymerases

Richard

Manley²

2009

Genes Dev.

291

326

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Gene transcription in the cell nucleus is a complex and highly regulated process. Transcription in eukaryotes requires three distinct RNA polymerases, each of which employs its own mechanisms for initiation, elongation, and termination. Termination mechanisms vary considerably, ranging from relatively simple to exceptionally complex. In this review, we describe the present state of knowledge on how each of the three RNA polymerases terminates and how mechanisms are conserved, or vary, from yeast to human.

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“…Fission yeast cohesin has an important function in regulating transcriptional termination of convergently transcribed genes. 41 In fact, cohesin is loaded in the termination region of these genes already in G 1 . Therefore, it is conceivable that some cohesin protection mechanism is in place.…”

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confidence: 99%