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Replication-coupled chromatin assembly generates a neuronal bilateral asymmetry in C. elegans.

Although replication-coupled chromatin assembly is known to be important for the maintenance of patterns of gene expression through sequential cell divisions, the role of replication-coupled chromatin assembly in controlling cell differentiation during animal development remains largely unexplored. Here we report that the CAF-1 protein complex, an evolutionarily conserved histone chaperone that deposits histone H3-H4 proteins onto replicating DNA, is required to generate a bilateral asymmetry in the C. elegans nervous system. A mutation in 1 of 24 C. elegans histone H3 genes specifically eliminates this aspect of neuronal asymmetry by causing a defect in the formation of a histone H3-H4 tetramer and the consequent inhibition of CAF-1-mediated nucleosome formation. Our results reveal that replication-coupled nucleosome assembly is necessary to generate a bilateral asymmetry in C. elegans neuroanatomy and suggest that left-right asymmetric epigenetic regulation can establish bilateral asymmetry in the nervous system.

Pubmed ID: 22177093


  • Nakano S
  • Stillman B
  • Horvitz HR



Publication Data

December 23, 2011

Associated Grants

  • Agency: NCI NIH HHS, Id: CA13106
  • Agency: NCI NIH HHS, Id: P01 CA013106
  • Agency: Howard Hughes Medical Institute, Id:
  • Agency: Howard Hughes Medical Institute, Id:

Mesh Terms

  • Amino Acid Sequence
  • Animals
  • Body Patterning
  • Caenorhabditis elegans
  • Caenorhabditis elegans Proteins
  • Chromatin Assembly and Disassembly
  • DNA Replication
  • Epigenomics
  • Histones
  • Molecular Sequence Data
  • Nervous System
  • Neurons
  • Nucleosomes
  • Sequence Alignment