The DNA-binding protein CST associates with the cohesin complex and promotes chromosome cohesion.
Autor: | Schuck PL; Department of Biological Sciences, University of South Carolina, Columbia, South Carolina, USA., Ball LE; Department of Cell and Molecular Pharmacology, Medical University of South Carolina, Charleston, South Carolina, USA., Stewart JA; Department of Biological Sciences, University of South Carolina, Columbia, South Carolina, USA. Electronic address: jason.stewart@sc.edu. |
---|---|
Jazyk: | angličtina |
Zdroj: | The Journal of biological chemistry [J Biol Chem] 2021 Sep; Vol. 297 (3), pp. 101026. Date of Electronic Publication: 2021 Jul 30. |
DOI: | 10.1016/j.jbc.2021.101026 |
Abstrakt: | Sister chromatid cohesion (SCC), the pairing of sister chromatids after DNA replication until mitosis, is established by loading of the cohesin complex on newly replicated chromatids. Cohesin must then be maintained until mitosis to prevent segregation defects and aneuploidy. However, how SCC is established and maintained until mitosis remains incompletely understood, and emerging evidence suggests that replication stress may lead to premature SCC loss. Here, we report that the ssDNA-binding protein CTC1-STN1-TEN1 (CST) aids in SCC. CST primarily functions in telomere length regulation but also has known roles in replication restart and DNA repair. After depletion of CST subunits, we observed an increase in the complete loss of SCC. In addition, we determined that CST associates with the cohesin complex. Unexpectedly, we did not find evidence of altered cohesin loading or mitotic progression in the absence of CST; however, we did find that treatment with various replication inhibitors increased the association between CST and cohesin. Because replication stress was recently shown to induce SCC loss, we hypothesized that CST may be required to maintain or remodel SCC after DNA replication fork stalling. In agreement with this idea, SCC loss was greatly increased in CST-depleted cells after exogenous replication stress. Based on our findings, we propose that CST aids in the maintenance of SCC at stalled replication forks to prevent premature cohesion loss. Competing Interests: Conflict of interest The authors declare that they have no conflicts of interest with the contents of this article. (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.) |
Databáze: | MEDLINE |
Externí odkaz: |