Origin of the polycomb repressive complex 2 and gene silencing by an E(z) homolog in the unicellular alga Chlamydomonas

Scott Shaver, J. Armando Casas-Mollano, Ronald L. Cerny, Heriberto Cerutti

Research output: Contribution to journalArticlepeer-review

107 Scopus citations


Polycomb group proteins play an essential role in the maintenance of cell identity and the regulation of development in both animals and plants. The polycomb Repressive complex 2 (PRC2) is involved in the establishment of transcriptionally silent chromatin states, in part through its ability to methylate lysine 27 of histone H3 by the Enhancer of zeste [E(z)] subunit. The absence of PRC2 in unicellular model fungi and its function in the repression of genes vital for the development of higher eukaryotes led to the proposal that this complex may have evolved together with the emergence of multicellularity. however, we report here on the widespread presence of PRC2 core subunits in unicellular eukaryotes from the Opisthokonta, chromalveolata and archaeplastida supergroups. To gain insight on the role of PRC2 in single celled organisms, we characterized an E(z) homolog, EZH, in the green alga Chlamydomonas reinhardtii. RNAi-mediated suppression of EZH led to defects in the silencing of transgenes and retrotransposons as well as to a global increase in histone post-translational modifications associated with transcriptional activity, such as trimethylation of histone H3 lysine 4 and acetylation of histone H4. On the basis of the parsimony principle, our findings suggest that PRC2 appeared early in eukaryotic evolution, even perhaps in the last unicellular common ancestor of eukaryotes. One of the ancestral roles of PCR2 may have been in defense responses against intragenomic parasites such as transposable elements, prior to being co-opted for lineage specific functions like developmental regulation in multicellular eukaryotes.

Original languageEnglish (US)
Pages (from-to)301-312
Number of pages12
Issue number4
StatePublished - May 16 2010
Externally publishedYes

Bibliographical note

Funding Information:
We thank members of the Cerutti lab for critical reading of the manuscript. This work was supported in part by grants from the National Institutes of Health and the National Science Foundation (to H.C.). We also acknowledge the support of the Nebraska EPSCoR program.


  • Chromatin
  • Enhancer of zeste
  • Gene silencing
  • H3K27 methylation
  • Polycomb


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