PUBLICATION

The X-linked mental retardation gene SMCX/JARID1C defines a family of histone H3 lysine 4 demethylases

Authors
Iwase, S., Lan, F., Bayliss, P., de la Torre-Ubieta, L., Huarte, M., Qi, H.H., Whetstine, J.R., Bonni, A., Roberts, T.M., and Shi, Y.
ID
ZDB-PUB-100427-27
Date
2007
Source
Cell   128(6): 1077-1088 (Journal)
Registered Authors
Bayliss, Peter, Roberts, Thomas M.
Keywords
none
MeSH Terms
  • Animals
  • Cell Line, Tumor
  • Cell Survival
  • DNA, Complementary
  • DNA-Binding Proteins/genetics
  • DNA-Binding Proteins/metabolism
  • Gene Library
  • Histone Demethylases
  • Histone-Lysine N-Methyltransferase/genetics
  • Histone-Lysine N-Methyltransferase/metabolism
  • Histones/chemistry
  • Histones/metabolism*
  • Humans
  • Intracellular Signaling Peptides and Proteins/genetics
  • Intracellular Signaling Peptides and Proteins/metabolism
  • Jumonji Domain-Containing Histone Demethylases
  • Lysine/metabolism
  • Methylation
  • Mice
  • Neoplasm Proteins/genetics
  • Neoplasm Proteins/metabolism
  • Neurons/cytology
  • Neurons/metabolism
  • Oxidoreductases, N-Demethylating/genetics*
  • Oxidoreductases, N-Demethylating/metabolism
  • Proteins/genetics*
  • Proteins/metabolism
  • Retinoblastoma-Binding Protein 2
  • Tumor Suppressor Proteins/genetics
  • Tumor Suppressor Proteins/metabolism
  • X-Linked Intellectual Disability/genetics*
PubMed
17320160 Full text @ Cell
Abstract
Histone methylation regulates chromatin structure and transcription. The recently identified histone demethylase lysine-specific demethylase 1 (LSD1) is chemically restricted to demethylation of only mono- and di- but not trimethylated histone H3 lysine 4 (H3K4me3). We show that the X-linked mental retardation (XLMR) gene SMCX (JARID1C), which encodes a JmjC-domain protein, reversed H3K4me3 to di- and mono- but not unmethylated products. Other SMCX family members, including SMCY, RBP2, and PLU-1, also demethylated H3K4me3. SMCX bound H3K9me3 via its N-terminal PHD (plant homeodomain) finger, which may help coordinate H3K4 demethylation and H3K9 methylation in transcriptional repression. Significantly, several XLMR-patient point mutations reduced SMCX demethylase activity and binding to H3K9me3 peptides, respectively. Importantly, studies in zebrafish and primary mammalian neurons demonstrated a role for SMCX in neuronal survival and dendritic development and a link to the demethylase activity. Our findings thus identify a family of H3K4me3 demethylases and uncover a critical link between histone modifications and XLMR.
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