ArticleeLife2023
What AlphaFold tells us about cohesin's retention on and release from chromosomes.
Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 13 citations in OpenAlex.
- Nested TAD hierarchy defines cohesion zones on replicated chromosomes.The EMBO journal · 2026Article
- Cohesin release-factor Wapl modulates axis and chromatin structure to promote conjunction and separation of meiotic chromosomes.Cell reports · 2026Article
- Cohesin cofactor dosage sets the rate of loop extrusion, rendering genome folding tunable yet vulnerable to genetic disruption.Molecular cell · 2026Article
- Organization of replicated chromosomes by DNA loops and sister chromatid cohesion.Nature reviews. Molecular cell biology · 2026Review
- The physical chemistry of interphase loop extrusion.Cell genomics · 2026Article
- Sororin locks the DNA-exit gate of cohesin to preserve sister-chromatid cohesion.Nature communications · 2026Article
- The Use of the Homobifunctional Crosslinker BMOE to Investigate Cohesin Function by Measuring Protein-Protein and Protein-DNA Interactions.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Crosstalk between cohesins and axis proteins determines meiotic chromosome architecture in Sordaria macrospora.PLoS genetics · 2025Article
- Dosage sensitivity of the loop extrusion rate confers tunability to genome folding while creating vulnerability to genetic disruption.bioRxiv : the preprint server for biology · 2025Article
- A chromatin-remodeling-independent role for ATRX in protecting centromeric cohesion.The EMBO journal · 2025Article
- Cohesin in 3D: development, differentiation, and disease.Genes & development · 2025Review
- Article
- Requirement of Nek2a and cyclin A2 for Wapl-dependent removal of cohesin from prophase chromatin.The EMBO journal · 2024Article
- Helical coiled nucleosome chromosome architectures during cell cycle progression.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Molecular mechanism and functional significance of Wapl interaction with the Cohesin complex.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- From interaction networks to interfaces, scanning intrinsically disordered regions using AlphaFold2.Nature communications · 2024Article
- The intrinsically disordered tail of ESCO1 binds DNA in a charge-dependent manner.bioRxiv : the preprint server for biology · 2023Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
Cohesin is a trimeric complex containing a pair of SMC proteins (Smc1 and Smc3) whose ATPase domains at the end of long coiled coils (CC) are interconnected by Scc1. During interphase, it organizes chromosomal DNA topology by extruding loops in a manner dependent on Scc1's association with two large hook-shaped proteins called SA (yeast: Scc3) and Nipbl (Scc2). The latter's replacement by Pds5 recruits Wapl, which induces release from chromatin via a process requiring dissociation of Scc1's N-terminal domain (NTD) from Smc3. If blocked by Esco (Eco)-mediated Smc3 acetylation, cohesin containing Pds5 merely maintains pre-existing loops, but a third fate occurs during DNA replication, when Pds5-containing cohesin associates with Sororin and forms structures that hold sister DNAs together. How Wapl induces and Sororin blocks release has hitherto remained mysterious. In the 20 years since their discovery, not a single testable hypothesis has been proposed as to their role. Here, AlphaFold 2 (AF) three-dimensional protein structure predictions lead us to propose formation of a quarternary complex between Wapl, SA, Pds5, and Scc1's NTD, in which the latter is juxtaposed with (and subsequently sequestered by) a highly conserved cleft within Wapl's C-terminal domain. AF also reveals how Scc1's dissociation from Smc3 arises from a distortion of Smc3's CC induced by engagement of SMC ATPase domains, how Esco acetyl transferases are recruited to Smc3 by Pds5, and how Sororin prevents release by binding to the Smc3/Scc1 interface. Our hypotheses explain the phenotypes of numerous existing mutations and are highly testable.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.