A chromatin-independent role of Polycomb-like 1 to stabilize p53 and promote cellular quiescence

Polycomb-like proteins 1-3 (PCL1-3) are substoichiometric components of the Polycomb-repressive complex 2 (PRC2) that are essential for association of the complex with chromatin. However, it remains unclear why three proteins with such apparent functional redundancy exist in mammals. Here we charact...

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Published inGenes & development Vol. 29; no. 21; pp. 2231 - 2243
Main Authors Brien, Gerard L, Healy, Evan, Jerman, Emilia, Conway, Eric, Fadda, Elisa, O'Donovan, Darragh, Krivtsov, Andrei V, Rice, Alan M, Kearney, Conor J, Flaus, Andrew, McDade, Simon S, Martin, Seamus J, McLysaght, Aoife, O'Connell, David J, Armstrong, Scott A, Bracken, Adrian P
Format Journal Article
LanguageEnglish
Published United States Cold Spring Harbor Laboratory Press 01.11.2015
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Abstract Polycomb-like proteins 1-3 (PCL1-3) are substoichiometric components of the Polycomb-repressive complex 2 (PRC2) that are essential for association of the complex with chromatin. However, it remains unclear why three proteins with such apparent functional redundancy exist in mammals. Here we characterize their divergent roles in both positively and negatively regulating cellular proliferation. We show that while PCL2 and PCL3 are E2F-regulated genes expressed in proliferating cells, PCL1 is a p53 target gene predominantly expressed in quiescent cells. Ectopic expression of any PCL protein recruits PRC2 to repress the INK4A gene; however, only PCL2 and PCL3 confer an INK4A-dependent proliferative advantage. Remarkably, PCL1 has evolved a PRC2- and chromatin-independent function to negatively regulate proliferation. We show that PCL1 binds to and stabilizes p53 to induce cellular quiescence. Moreover, depletion of PCL1 phenocopies the defects in maintaining cellular quiescence associated with p53 loss. This newly evolved function is achieved by the binding of the PCL1 N-terminal PHD domain to the C-terminal domain of p53 through two unique serine residues, which were acquired during recent vertebrate evolution. This study illustrates the functional bifurcation of PCL proteins, which act in both a chromatin-dependent and a chromatin-independent manner to regulate the INK4A and p53 pathways.
AbstractList Polycomb-like proteins 1–3 (PCL1–3) are substoichiometric components of the Polycomb-repressive complex 2 (PRC2) that are essential for association of the complex with chromatin. However, it remains unclear why three proteins with such apparent functional redundancy exist in mammals. Here we characterize their divergent roles in both positively and negatively regulating cellular proliferation. We show that while PCL2 and PCL3 are E2F-regulated genes expressed in proliferating cells, PCL1 is a p53 target gene predominantly expressed in quiescent cells. Ectopic expression of any PCL protein recruits PRC2 to repress the INK4A gene; however, only PCL2 and PCL3 confer an INK4A -dependent proliferative advantage. Remarkably, PCL1 has evolved a PRC2- and chromatin-independent function to negatively regulate proliferation. We show that PCL1 binds to and stabilizes p53 to induce cellular quiescence. Moreover, depletion of PCL1 phenocopies the defects in maintaining cellular quiescence associated with p53 loss. This newly evolved function is achieved by the binding of the PCL1 N-terminal PHD domain to the C-terminal domain of p53 through two unique serine residues, which were acquired during recent vertebrate evolution. This study illustrates the functional bifurcation of PCL proteins, which act in both a chromatin-dependent and a chromatin-independent manner to regulate the INK4A and p53 pathways.
Polycomb-like proteins 1-3 (PCL1-3) are substoichiometric components of the Polycomb-repressive complex 2 (PRC2) that are essential for association of the complex with chromatin. However, it remains unclear why three proteins with such apparent functional redundancy exist in mammals. Here we characterize their divergent roles in both positively and negatively regulating cellular proliferation. We show that while PCL2 and PCL3 are E2F-regulated genes expressed in proliferating cells, PCL1 is a p53 target gene predominantly expressed in quiescent cells. Ectopic expression of any PCL protein recruits PRC2 to repress the INK4A gene; however, only PCL2 and PCL3 confer an INK4A-dependent proliferative advantage. Remarkably, PCL1 has evolved a PRC2- and chromatin-independent function to negatively regulate proliferation. We show that PCL1 binds to and stabilizes p53 to induce cellular quiescence. Moreover, depletion of PCL1 phenocopies the defects in maintaining cellular quiescence associated with p53 loss. This newly evolved function is achieved by the binding of the PCL1 N-terminal PHD domain to the C-terminal domain of p53 through two unique serine residues, which were acquired during recent vertebrate evolution. This study illustrates the functional bifurcation of PCL proteins, which act in both a chromatin-dependent and a chromatin-independent manner to regulate the INK4A and p53 pathways.
Brien et al. show that while Polycomb-like proteins PCL2 and PCL3 are E2F-regulated genes expressed in proliferating cells, PCL1 is a p53 target gene predominantly expressed in quiescent cells. PCL1 binds to and stabilizes p53 to block cellular proliferation, and depletion of PCL1 phenocopies the defects in maintaining cellular quiescence associated with p53 loss. Polycomb-like proteins 1–3 (PCL1–3) are substoichiometric components of the Polycomb-repressive complex 2 (PRC2) that are essential for association of the complex with chromatin. However, it remains unclear why three proteins with such apparent functional redundancy exist in mammals. Here we characterize their divergent roles in both positively and negatively regulating cellular proliferation. We show that while PCL2 and PCL3 are E2F-regulated genes expressed in proliferating cells, PCL1 is a p53 target gene predominantly expressed in quiescent cells. Ectopic expression of any PCL protein recruits PRC2 to repress the INK4A gene; however, only PCL2 and PCL3 confer an INK4A -dependent proliferative advantage. Remarkably, PCL1 has evolved a PRC2- and chromatin-independent function to negatively regulate proliferation. We show that PCL1 binds to and stabilizes p53 to induce cellular quiescence. Moreover, depletion of PCL1 phenocopies the defects in maintaining cellular quiescence associated with p53 loss. This newly evolved function is achieved by the binding of the PCL1 N-terminal PHD domain to the C-terminal domain of p53 through two unique serine residues, which were acquired during recent vertebrate evolution. This study illustrates the functional bifurcation of PCL proteins, which act in both a chromatin-dependent and a chromatin-independent manner to regulate the INK4A and p53 pathways.
Author Bracken, Adrian P
Krivtsov, Andrei V
Flaus, Andrew
Armstrong, Scott A
Healy, Evan
Jerman, Emilia
O'Connell, David J
Conway, Eric
Kearney, Conor J
McLysaght, Aoife
Fadda, Elisa
Rice, Alan M
Brien, Gerard L
O'Donovan, Darragh
Martin, Seamus J
McDade, Simon S
AuthorAffiliation 5 Centre for Chromosome Biology, School of Life Sciences, National University of Ireland Galway, Galway, Ireland
6 Centre for Cancer Research and Cell Biology, Queen's University Belfast, Belfast BT9 7BL, United Kingdom
3 The Conway Institute, University College Dublin, Dublin 4, Ireland
2 Department of Chemistry, National University of Ireland, Maynooth, Ireland
1 Smurfit Institute of Genetics, Trinity College Dublin, Dublin 2, Ireland
4 Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA
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Issue 21
Keywords PHD reader domain
cellular senescence
Polycomb-like
neofunctionalization
cellular quiescence
p53
Language English
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Snippet Polycomb-like proteins 1-3 (PCL1-3) are substoichiometric components of the Polycomb-repressive complex 2 (PRC2) that are essential for association of the...
Polycomb-like proteins 1–3 (PCL1–3) are substoichiometric components of the Polycomb-repressive complex 2 (PRC2) that are essential for association of the...
Brien et al. show that while Polycomb-like proteins PCL2 and PCL3 are E2F-regulated genes expressed in proliferating cells, PCL1 is a p53 target gene...
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StartPage 2231
SubjectTerms Animals
Cell Proliferation - genetics
Cells, Cultured
Chromatin - metabolism
Cyclin-Dependent Kinase Inhibitor p16 - genetics
Cyclin-Dependent Kinase Inhibitor p16 - metabolism
DNA-Binding Proteins - genetics
DNA-Binding Proteins - metabolism
E2F Transcription Factors - metabolism
Gene Expression Regulation, Neoplastic
Humans
Mice
Polycomb-Group Proteins - genetics
Polycomb-Group Proteins - metabolism
Protein Binding
Protein Stability
Protein Structure, Tertiary - genetics
Research Paper
Transcription Factors - metabolism
Tumor Suppressor Protein p53 - metabolism
Title A chromatin-independent role of Polycomb-like 1 to stabilize p53 and promote cellular quiescence
URI https://www.ncbi.nlm.nih.gov/pubmed/26494712
https://search.proquest.com/docview/1731784099
https://search.proquest.com/docview/1773834401
https://pubmed.ncbi.nlm.nih.gov/PMC4647557
Volume 29
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