scholarly journals The Polycomb group protein MEDEA controls cell proliferation and embryonic patterning in Arabidopsis

2021 ◽  
Author(s):  
Sara Simonini ◽  
Marian Bemer ◽  
Stefano Bencivenga ◽  
Valeria Gagliardini ◽  
Nuno D. Pires ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Polycomb Group ◽  
Embryonic Patterning ◽  
Polycomb Group Protein ◽  
Group Protein

scholarly journals The Polycomb group protein MEDEA controls cell proliferation and embryonic patterning in Arabidopsis

2020 ◽  
Author(s):  
Sara Simonini ◽  
Marian Bemer ◽  
Stefano Bencivenga ◽  
Valeria Gagliardini ◽  
Nuno D. Pires ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Lineage ◽  
Embryonic Cell ◽  
The Body ◽  
Polycomb Group ◽  
Normal Embryo ◽  
Embryonic Patterning ◽  
Polycomb Group Protein ◽  
Group Protein

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 (Förderer 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.

scholarly journals Mel-18, a Polycomb Group Protein, Regulates Cell Proliferation and Senescence via Transcriptional Repression of Bmi-1 and c-Myc Oncoproteins

2007 ◽  
Vol 18 (2) ◽  
pp. 536-546 ◽  
Author(s):  
Wei-Jian Guo ◽  
Sonal Datta ◽  
Vimla Band ◽  
Goberdhan P. Dimri
Keyword(s):  
Cell Proliferation ◽  
Transcriptional Repression ◽  
Target Genes ◽  
Human Fibroblasts ◽  
Ring Finger ◽  
Polycomb Group ◽  
Polycomb Group Protein ◽  
Down Regulation ◽  
Group Protein ◽  
Bona Fide

Polycomb group (PcG) protein Bmi-1 is an important regulator of cell proliferation. It regulates cellular senescence and proliferation of cells via the transcriptional repression of INK4a/ARF locus and other target genes. Here, we report that Mel-18, a PcG ring finger protein (PCGF) transcriptionally down-regulates Bmi-1. Furthermore, the expression of Bmi-1 and Mel-18 inversely correlates in proliferating and senescent human fibroblasts. Bmi-1 down-regulation by Mel-18 results in accelerated senescence and shortening of the replicative life span in normal human cells. Importantly, using promoter-reporter, chromatin immunoprecipitation, and quantitative real-time primary transcript RT-PCR assays, and an RNA interference approach, we demonstrate that Bmi-1 is a bona fide target of c-Myc oncoprotein. Finally, our data suggest that Mel-18 regulates Bmi-1 expression during senescence via down-regulation of c-Myc. These studies link c-Myc and polycomb function in cell proliferation and senescence.

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