The cohesin modifier ESCO2 is stable during DNA replication

Cohesion between sister chromatids by the cohesin protein complex ensures accurate chromosome segregation and enables recombinational DNA repair. Sister chromatid cohesion is promoted by acetylation of the SMC3 subunit of cohesin by the ESCO2 acetyltransferase, inhibiting cohesin release from chroma...

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Bibliographic Details
Published in:Chromosome research 2023-01, Vol.31 (1), p.6-6, Article 6
Main Authors: Jevitt, Allison M., Rankin, Brooke D., Chen, Jingrong, Rankin, Susannah
Format: Article
Language:English
Subjects:
Acetylation
Acetyltransferase
Acetyltransferases - metabolism
Animal Genetics and Genomics
Biomedical and Life Sciences
Cell Biology
Cell cycle
Cell Cycle Proteins - metabolism
Cell lines
Cell-free system
Chromatids
Chromatids - metabolism
Chromatin
Chromosomal Proteins, Non-Histone - metabolism
Chromosome Segregation
Chromosomes
Cohesin
Cohesins
Deoxyribonucleic acid
DNA
DNA biosynthesis
DNA damage
DNA repair
DNA Replication
Flow cytometry
Human Genetics
Life Sciences
Plant Genetics and Genomics
Proteins
Replication
S phase
Sister chromatids
Somatic cells
Yeast
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Summary:Cohesion between sister chromatids by the cohesin protein complex ensures accurate chromosome segregation and enables recombinational DNA repair. Sister chromatid cohesion is promoted by acetylation of the SMC3 subunit of cohesin by the ESCO2 acetyltransferase, inhibiting cohesin release from chromatin. The interaction of ESCO2 with the DNA replication machinery, in part through PCNA-interacting protein (PIP) motifs in ESCO2, is required for full cohesion establishment. Recent reports have suggested that Cul4-dependent degradation regulates the level of ESCO2 protein following replication. To follow up on these observations, we have characterized ESCO2 stability in Xenopus egg extracts, a cell-free system that recapitulates cohesion establishment in vitro. We found that ESCO2 was stable during DNA replication in this system. Indeed, further challenging the system by inducing DNA damage signaling or increasing the number of nuclei undergoing DNA replication had no significant impact on the stability of ESCO2. In transgenic somatic cell lines, we also did not see evidence of GFP-ESCO2 degradation during S phase of the cell cycle using both flow cytometry and live-cell imaging. We conclude that ESCO2 is stable during DNA replication in both embryonic and somatic cells.
ISSN:1573-6849
0967-3849
1573-6849
DOI:10.1007/s10577-023-09711-1