PRC2: Difference between revisions
GiovCodPis (talk | contribs) m since there is no page in Wikipedia on PRC1 I removed the link. |
GiovCodPis (talk | contribs) mNo edit summary |
||
| Line 1: | Line 1: | ||
[[File:Molecular-architecture-of-human-polycomb-repressive-complex-2-elife00005m002.ogv|thumb|3D reconstruction of the human PRC2-[[AEBP2]] complex.]] |
[[File:Molecular-architecture-of-human-polycomb-repressive-complex-2-elife00005m002.ogv|thumb|3D reconstruction of the human PRC2-[[AEBP2]] complex.]] |
||
'''PRC2''' (Polycomb Repressive Complex 2) is one of the two classes of [[polycomb-group proteins]] or (PcG). The other component of this group of proteins is PRC1 (Polycomb |
'''PRC2''' (Polycomb Repressive Complex 2) is one of the two classes of [[polycomb-group proteins]] or (PcG). The other component of this group of proteins is PRC1 (Polycomb Repressive Complex 1). |
||
This complex has [[histone]] [[methyltransferase]] activity and primarily trimethylates [[histone H3]] on [[lysine]] 27 (i.e. H3K27me3),<ref name="pmid22211105">{{cite journal | author = Yoo KH, Hennighausen L | title = EZH2 methyltransferase and H3K27 methylation in breast cancer | journal = International Journal of Biological Sciences | volume = 8 | issue = 1 | pages = 59–65 |date=November 2012 | pmid = 22211105 | pmc = 3226033 | doi=10.7150/ijbs.8.59}}</ref><ref name="pmid21367748">{{cite journal | author = Chase A, Cross NC | title = Aberrations of EZH2 in cancer | journal = Clinical Cancer Research | volume = 17 | issue = 9 | pages = 2613–2618 |date=May 2011 | pmid = 21367748 | url = http://clincancerres.aacrjournals.org/content/17/9/2613.long | doi=10.1158/1078-0432.CCR-10-2156}}</ref> a mark of transcriptionally silent [[chromatin]]. PRC2 is required for initial targeting of genomic region (PRC Response Elements or PRE) to be silenced, while PRC1 is required for stabilizing this [[Gene silencing|silencing]] and underlies [[Epigenetics|cellular memory]] of silenced region after [[cellular differentiation]]. PRC1 also mono-ubiquitinates histone H2A on lysine 119 (H2AK119Ub1). These [[protein]]s are required for long term epigenetic silencing of chromatin and have an important role in [[stem cell]] differentiation and early [[embryo]]nic development. PRC2 are present in all [[multicellular organism]]s. |
This complex has [[histone]] [[methyltransferase]] activity and primarily trimethylates [[histone H3]] on [[lysine]] 27 (i.e. H3K27me3),<ref name="pmid22211105">{{cite journal | author = Yoo KH, Hennighausen L | title = EZH2 methyltransferase and H3K27 methylation in breast cancer | journal = International Journal of Biological Sciences | volume = 8 | issue = 1 | pages = 59–65 |date=November 2012 | pmid = 22211105 | pmc = 3226033 | doi=10.7150/ijbs.8.59}}</ref><ref name="pmid21367748">{{cite journal | author = Chase A, Cross NC | title = Aberrations of EZH2 in cancer | journal = Clinical Cancer Research | volume = 17 | issue = 9 | pages = 2613–2618 |date=May 2011 | pmid = 21367748 | url = http://clincancerres.aacrjournals.org/content/17/9/2613.long | doi=10.1158/1078-0432.CCR-10-2156}}</ref> a mark of transcriptionally silent [[chromatin]]. PRC2 is required for initial targeting of genomic region (PRC Response Elements or PRE) to be silenced, while PRC1 is required for stabilizing this [[Gene silencing|silencing]] and underlies [[Epigenetics|cellular memory]] of silenced region after [[cellular differentiation]]. PRC1 also mono-ubiquitinates histone H2A on lysine 119 (H2AK119Ub1). These [[protein]]s are required for long term epigenetic silencing of chromatin and have an important role in [[stem cell]] differentiation and early [[embryo]]nic development. PRC2 are present in all [[multicellular organism]]s. |
||
Revision as of 07:25, 25 March 2017
PRC2 (Polycomb Repressive Complex 2) is one of the two classes of polycomb-group proteins or (PcG). The other component of this group of proteins is PRC1 (Polycomb Repressive Complex 1).
This complex has histone methyltransferase activity and primarily trimethylates histone H3 on lysine 27 (i.e. H3K27me3),[1][2] a mark of transcriptionally silent chromatin. PRC2 is required for initial targeting of genomic region (PRC Response Elements or PRE) to be silenced, while PRC1 is required for stabilizing this silencing and underlies cellular memory of silenced region after cellular differentiation. PRC1 also mono-ubiquitinates histone H2A on lysine 119 (H2AK119Ub1). These proteins are required for long term epigenetic silencing of chromatin and have an important role in stem cell differentiation and early embryonic development. PRC2 are present in all multicellular organisms.
The mouse PRC2 has four subunits: Suz12 (zinc finger), Eed, Ezh1 or Ezh2 (SET domain with histone methyltransferase activity[1][2]) and RbAp48 (histone binding domain)
PRC2 has a role in X chromosome inactivation, in maintenance of stem cell fate, and in imprinting. Aberrant expression of PRC2 has been observed in cancer.[1][2]
The PRC2 is evolutionary conserved, and has been found in mammals, insects, and plants.
In plants
In Arabidopsis thaliana, a plant model organism, several variants of the core subunits have been identified. Homologs of the Suz12 subunit are: EMBRYONIC FLOWER 2 (EMF2), REDUCED VERNALIZATION RESPONSE 2 (VRN2), FERTILIZATION INDEPENDENT SEED 2 (FIS2).[3] There is one Eed homolog, FERTILIZATION INDEPENDENT ENDOSPERM (FIE).[3] three Ezh1/Ezh2 homologs, CURLY LEAF (CLF), SWINGER (SWN), MEDEA (MEA),[3] and one RbAp48 homolog, MULTICOPY SUPPRESSOR OF IRA1 (MSI1).[3]
See also
References
- ^ a b c Yoo KH, Hennighausen L (November 2012). "EZH2 methyltransferase and H3K27 methylation in breast cancer". International Journal of Biological Sciences. 8 (1): 59–65. doi:10.7150/ijbs.8.59. PMC 3226033. PMID 22211105.
- ^ a b c Chase A, Cross NC (May 2011). "Aberrations of EZH2 in cancer". Clinical Cancer Research. 17 (9): 2613–2618. doi:10.1158/1078-0432.CCR-10-2156. PMID 21367748.
- ^ a b c d Koehler, Claudia; Hennig, Lars (2010). "Regulation of cell identity by plant Polycomb and trithorax group proteins". Current Opinion in Genetics & Development. 20 (5): 541–547. doi:10.1016/j.gde.2010.04.015.