scholarly journals Polycomb Group Complexes Mediate Developmental Transitions in Plants

2011 ◽  
Vol 158 (1) ◽  
pp. 35-43 ◽  
Author(s):  
Sarah Holec ◽  
Frédéric Berger
2014 ◽  
Vol 15 (5) ◽  
pp. 412-428 ◽  
Author(s):  
Rong-gang Ma ◽  
Yang Zhang ◽  
Ting-ting Sun ◽  
Bo Cheng

2000 ◽  
Vol 20 (9) ◽  
pp. 3069-3078 ◽  
Author(s):  
Joyce Ng ◽  
Craig M. Hart ◽  
Kelly Morgan ◽  
Jeffrey A. Simon

ABSTRACT The extra sex combs (ESC) and Enhancer of zeste [E(Z)] proteins, members of the Polycomb group (PcG) of transcriptional repressors, interact directly and are coassociated in fly embryos. We report that these two proteins are components of a 600-kDa complex in embryos. Using gel filtration and affinity chromatography, we show that this complex is biochemically distinct from previously described complexes containing the PcG proteins Polyhomeotic, Polycomb, and Sex comb on midleg. In addition, we present evidence that ESC is phosphorylated in vivo and that this modified ESC is preferentially associated in the complex with E(Z). Modified ESC accumulates between 2 and 6 h of embryogenesis, which is the developmental time whenesc function is first required. We find that mutations inE(z) reduce the ratio of modified to unmodified ESC in vivo. We have also generated germ line transformants that express ESC proteins bearing site-directed mutations that disrupt ESC-E(Z) binding in vitro. These mutant ESC proteins fail to provideesc function, show reduced levels of modification in vivo, and are still assembled into complexes. Taken together, these results suggest that ESC phosphorylation normally occurs after assembly into ESC-E(Z) complexes and that it contributes to the function or regulation of these complexes. We discuss how biochemically separable ESC-E(Z) and PC-PH complexes might work together to provide PcG repression.


2000 ◽  
Vol 20 (9) ◽  
pp. 3187-3197 ◽  
Author(s):  
Béatrice Horard ◽  
Christophe Tatout ◽  
Sylvain Poux ◽  
Vincenzo Pirrotta

ABSTRACT Polycomb response elements (PREs) are regulatory sites that mediate the silencing of homeotic and other genes. The bxd PRE region from the Drosophila Ultrabithorax gene can be subdivided into subfragments of 100 to 200 bp that retain different degrees of PRE activity in vivo. In vitro, embryonic nuclear extracts form complexes containing Polycomb group (PcG) proteins with these fragments. PcG binding to some fragments is dependent on consensus sequences for the GAGA factor. Other fragments lack GAGA binding sites but can still bind PcG complexes in vitro. We show that the GAGA factor is a component of at least some types of PcG complexes and may participate in the assembly of PcG complexes at PREs.


2014 ◽  
Author(s):  
Qi Cao ◽  
Xiaoju Wang ◽  
Meng Zhao ◽  
Rendong Yang ◽  
Rohit Malik ◽  
...  

2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Qi Cao ◽  
Xiaoju Wang ◽  
Meng Zhao ◽  
Rendong Yang ◽  
Rohit Malik ◽  
...  

EMBO Reports ◽  
2006 ◽  
Vol 7 (9) ◽  
pp. 947-952 ◽  
Author(s):  
Grigory Makarevich ◽  
Olivier Leroy ◽  
Umut Akinci ◽  
Daniel Schubert ◽  
Oliver Clarenz ◽  
...  

2018 ◽  
Author(s):  
Iris Wever ◽  
Cindy M.R.J. Wagemans ◽  
Marten P. Smidt

AbstractThe polycomb group proteins (PcGs) are a group of epigenetic factors associated with gene silencing. They are found in several families of multiprotein complexes, including Polycomb Repressive Complex (PRC) 2. EZH2, EED and SUZ12 form the core components of the PRC2 complex, which is responsible for the mono, di- and trimethylation of lysine 27 of histone 3 (H3K27Me3), the chromatin mark associated with gene silencing. Loss-of-function studies of Ezh2, the catalytic subunit of PRC2, have shown that PRC2 plays a role in regulating developmental transitions of neuronal progenitor cells; from self-renewal to differentiation and the neurogenic-to-gliogenic fate switch.To further address the function of EZH2 and H3K27me3 during neuronal development we generated a conditional mutant in which Ezh2 was removed in the mammalian isthmic (mid-hindbrain) region from E10.5 onward. Loss of Ezh2 changed the molecular coding of the anterior ventral hindbrain leading to a fate switch and the appearance of ectopic dopaminergic neurons. The correct specification of the isthmic region is dependent on the signaling factors produced by the Isthmic organizer (IsO), located at the border of the mid- and hindbrain. We propose that the change of cellular fate is a result of the presence of Otx2 in the hindbrain of Ezh2 conditional knock-outs and a dysfunctional IsO, as represented by the loss of Fgf8 and Wnt1. Our work implies that next to controlling developmental transitions, EZH2 mediated gene silencing is important for specification of the isthmic region by influencing IsO functioning and repressing Otx2 in the hindbrain.


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