PMID- 24671995
OWN - NLM
STAT- MEDLINE
DCOM- 20140519
LR  - 20211021
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 34
IP  - 13
DP  - 2014 Mar 26
TI  - Coordinated regulation of dendrite arborization by epigenetic factors CDYL and 
      EZH2.
PG  - 4494-508
LID - 10.1523/JNEUROSCI.3647-13.2014 [doi]
AB  - Dendritic arborization is one of the key determinants of precise circuits for 
      information processing in neurons. Unraveling the molecular mechanisms underlying 
      dendrite morphogenesis is critical to understanding the establishment of neuronal 
      connections. Here, using gain- and loss-of-function approaches, we defined the 
      chromodomain protein and transcription corepressor chromodomain Y-like (CDYL) 
      protein as a negative regulator of dendrite morphogenesis in rat/mouse 
      hippocampal neurons both in vitro and in vivo. Overexpressing CDYL decreased, 
      whereas knocking it down increased, the dendritic complexity of the primary 
      cultured rat neurons. High-throughput DNA microarray screening identified a 
      number of CDYL downstream target genes, including the brain-derived neurotrophic 
      factor (BDNF). Knock-down of CDYL in neuronal cells led to increased expression 
      of BDNF, which is primarily responsible for CDYL's effects on dendrite patterns. 
      Mechanistically, CDYL interacts with EZH2, the catalytic subunit of Polycomb 
      Repressive Complex 2 (PRC2), directly and recruits the H3K27 methyltransferase 
      activity to the promoter region of the BDNF gene. In doing so, CDYL and EZH2 
      coordinately restrict dendrite morphogenesis in an interdependent manner. 
      Finally, we found that neural activity increased dendritic complexity through 
      degradation of CDYL protein to unleash its inhibition on BDNF. These results 
      link, for the first time, the epigenetic regulators CDYL and EZH2 to dendrite 
      morphogenesis and might shed new light on our understanding of the regulation of 
      the neurodevelopment.
FAU - Qi, Cai
AU  - Qi C
AD  - Neuroscience Research Institute, Department of Neurobiology, School of Basic 
      Medical Sciences, Key Laboratory for Neuroscience, Ministry of Education/National 
      Health and Family Planning Commission and Key Laboratory of Carcinogenesis and 
      Translational Research (Ministry of Education), Department of Biochemistry and 
      Molecular Biology, Peking University Health Science Center, Beijing 100191, 
      China, Tianjin Key Laboratory of Medical Epigenetics, Tianjin Medical University, 
      Tianjin 300070, China, and PKU-IDG/McGovern Institute for Brain Research, Peking 
      University, Beijing 100871, China.
FAU - Liu, Shumeng
AU  - Liu S
FAU - Qin, Rui
AU  - Qin R
FAU - Zhang, Yu
AU  - Zhang Y
FAU - Wang, Guoqiang
AU  - Wang G
FAU - Shang, Yongfeng
AU  - Shang Y
FAU - Wang, Yun
AU  - Wang Y
FAU - Liang, Jing
AU  - Liang J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Co-Repressor Proteins)
RN  - 0 (Proteins)
RN  - 0 (RNA, Small Interfering)
RN  - EC 2.1.1.43 (EZH2 protein, human)
RN  - EC 2.1.1.43 (Enhancer of Zeste Homolog 2 Protein)
RN  - EC 2.1.1.43 (Polycomb Repressive Complex 2)
RN  - EC 4.2.1.- (CDYL protein, human)
RN  - EC 4.2.1.- (Hydro-Lyases)
SB  - IM
EIN - J Neurosci. 2015 Feb 4;35(5):2321
MH  - Animals
MH  - Cells, Cultured
MH  - Co-Repressor Proteins
MH  - Dendrites/*physiology
MH  - Embryo, Mammalian
MH  - Enhancer of Zeste Homolog 2 Protein
MH  - Female
MH  - Gene Expression Regulation, Developmental/genetics/*physiology
MH  - Hippocampus/cytology
MH  - Humans
MH  - Hydro-Lyases
MH  - Male
MH  - Mice
MH  - Mice, Inbred ICR
MH  - Mice, Transgenic
MH  - Mutation/genetics
MH  - Neurons/*cytology
MH  - Polycomb Repressive Complex 2/genetics/*metabolism
MH  - Proteins/genetics/*metabolism
MH  - RNA, Small Interfering/genetics/metabolism
MH  - Rats
MH  - Time Factors
PMC - PMC6608133
EDAT- 2014/03/29 06:00
MHDA- 2014/05/20 06:00
PMCR- 2014/09/26
CRDT- 2014/03/28 06:00
PHST- 2014/03/28 06:00 [entrez]
PHST- 2014/03/29 06:00 [pubmed]
PHST- 2014/05/20 06:00 [medline]
PHST- 2014/09/26 00:00 [pmc-release]
AID - 34/13/4494 [pii]
AID - 3647-13 [pii]
AID - 10.1523/JNEUROSCI.3647-13.2014 [doi]
PST - ppublish
SO  - J Neurosci. 2014 Mar 26;34(13):4494-508. doi: 10.1523/JNEUROSCI.3647-13.2014.