Replication-Coupled Chromatin Assembly Generates a Neuronal Bilateral Asymmetry in C. elegans
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Nakano-2011-Replication-Coupled.pdf
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Author(s)
Nakano, Shunji
Stillman, Bruce
Horvitz, Howard Robert
Date Issued
December 2011
Journal
Cell
Publisher
Elsevier
Citation
Nakano, Shunji, Bruce Stillman, and H. Robert Horvitz. “Replication-Coupled Chromatin Assembly Generates a Neuronal Bilateral Asymmetry in C. Elegans.” Cell 147, no. 7 (December 2011): 1525–1536. © 2011 Elsevier Inc.
Version
Final published version
Abstract
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.
MIT Department
Massachusetts Institute of Technology. Department of Biology
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Article is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.
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DOI of Published Version
https://doi.org/10.1016/j.cell.2011.11.053
