Establishing the body plan of a multicellular organism relies on precisely orchestrated cell divisions coupled with pattern formation. In animals, cell proliferation and embryonic patterning are regulated by Polycomb group (PcG) proteins that form various multisubunit complexes (Grossniklaus and Paro, 2014). The evolutionary conserved Polycomb Repressive Complex 2 (PRC2) trimethylates histone H3 at lysine 27 (H3K27me3) and comes in different flavors in the model plant Arabidopsis thaliana (Forderer et al., 2016; Grossniklaus and Paro, 2014). The histone methyltransferase MEDEA (MEA) is part of the FERTILIZATION INDEPENDENT SEED (FIS)-PRC2 required for seed development4. Although embryos derived from mea mutant egg cells show morphological abnormalities (Grossniklaus et al., 1998), defects in the development of the placenta-like endosperm are considered the main cause of seed abortion (Kinoshita et al., 1999; Scott et al., 1998), and a role of FIS-PRC2 in embryonic patterning was dismissed (Bouyer et al., 2011; Leroy et al., 2007). Here, we demonstrate that endosperm lacking MEA activity sustains normal embryo development and that embryos derived from mea mutant eggs abort even in presence of a wild-type endosperm because MEA is required for embryonic patterning and cell lineage determination. We show that, similar to PcG proteins in mammals, MEA regulates embryonic growth by repressing the transcription of core cell cycle components. Our work demonstrates that Arabidopsis embryogenesis is under epigenetic control of maternally expressed PcG proteins, revealing that PRC2 was independently recruited to control embryonic cell proliferation and patterning in animals and plants.

中文翻译：

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Polycomb组蛋白MEDEA控制拟南芥中的细胞增殖和胚胎模式

建立多细胞生物的身体计划依赖于精确协调的细胞分裂以及模式形成。在动物中，细胞增殖和胚胎模式受形成各种多亚基复合物的Polycomb组（PcG）蛋白调控（Grossniklaus和Paro，2014）。进化保守的Polycomb Repressive Complex 2（PRC2）使赖氨酸27（H3K27me3）上的组蛋白H3三甲基化，并在模型植物拟南芥中具有不同的风味（Forderer等人，2016; Grossniklaus和Paro，2014）。组蛋白甲基转移酶MEDEA（MEA）是种子发育所需的肥料独立种子（FIS）-PRC2的一部分4。尽管源自mea突变卵细胞的胚胎显示出形态异常（Grossniklaus等，1998），胎盘样胚乳发育中的缺陷被认为是种子流产的主要原因（Kinoshita等，1999； Scott等，1998），而FIS-PRC2在胚胎模式中的作用被忽略了（Bouyer等）。 （2011年； Leroy等人，2007年）。在这里，我们证明了缺乏MEA活性的胚乳可以维持正常的胚胎发育，并且即使存在野生型胚乳，源自mea突变卵的胚也会中止，因为MEA是胚胎形成和细胞谱系确定所必需的。我们表明，类似于哺乳动物中的PcG蛋白，MEA通过抑制核心细胞周期成分的转录来调节胚胎的生长。我们的工作表明拟南芥的胚胎发生受母体表达的PcG蛋白的表观遗传控制，