期刊
NEW PHYTOLOGIST
卷 229, 期 6, 页码 3208-3220出版社
WILEY
DOI: 10.1111/nph.17129
关键词
cell differentiation; microalgae; Phaeodactylum tricornutum; polycomb
资金
- CNRS
- region of Pays de la Loire (ConnecTalent EPIALG project)
- ERC Advanced Award 'Diatomite, the French Government'Investissements d'Avenir' programmes MEMO LIFE [ANR-10-LABX-54]
- PSL* Research University [ANR-1253 11-IDEX-0001-02]
- Chinese Scholarship Council [CSC-201604910722]
- International PhD fellowship from the MEMO LIFE Program
- Epicycle ANR project [ANR-19-CE20-0028-02]
The PRC2 complex plays a crucial role in gene silencing and cell development in multicellular organisms, and recent studies have shown its existence and importance in unicellular species, particularly in microalgae. This discovery emphasizes the significance of PRC2 in cell differentiation in unicellular organisms, extending its ancestral function beyond current understanding of its evolutionary context.
In multicellular organisms, Polycomb Repressive Complex2 (PRC2) is known to deposit tri-methylation of lysine 27 of histone H3 (H3K27me3) to establish and maintain gene silencing, critical for developmentally regulated processes. The PRC2 complex is absent in both widely studied model yeasts, which initially suggested that PRC2 arose with the emergence of multicellularity. However, its discovery in several unicellular species including microalgae questions its role in unicellular eukaryotes. Here, we use Phaeodactylum tricornutum enhancer of zeste E(z) knockouts and show that P. tricornutum E(z) is responsible for di- and tri-methylation of lysine 27 of histone H3. H3K27me3 depletion abolishes cell morphology in P. tricornutum providing evidence for its role in cell differentiation. Genome-wide profiling of H3K27me3 in fusiform and triradiate cells further revealed genes that may specify cell identity. These results suggest a role for PRC2 and its associated mark in cell differentiation in unicellular species, and highlight their ancestral function in a broader evolutionary context than currently is appreciated.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据