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Cell Rep. 2016 Oct 18;17(4):987-996. doi: 10.1016/j.celrep.2016.09.074.

Replication-Independent Histone Variant H3.3 Controls Animal Lifespan through the Regulation of Pro-longevity Transcriptional Programs.

Author information

1
German Center for Neurodegenerative Diseases (DZNE), Ludwig-Erhard-Allee 2, 53175 Bonn, Germany.
2
Samantha Dickson Brain Cancer Unit, University College London Cancer Institute (UCL), 72 Huntley Street, London WC1E 6DD, UK.
3
German Center for Neurodegenerative Diseases (DZNE), Ludwig-Erhard-Allee 2, 53175 Bonn, Germany. Electronic address: daniele.bano@dzne.de.

Abstract

Chromatin structure orchestrates the accessibility to the genetic material. Replication-independent histone variants control transcriptional plasticity in postmitotic cells. The life-long accumulation of these histones has been described, yet the implications on organismal aging remain elusive. Here, we study the importance of the histone variant H3.3 in Caenorhabditis elegans longevity pathways. We show that H3.3-deficient nematodes have negligible lifespan differences compared to wild-type animals. However, H3.3 is essential for the lifespan extension of C. elegans mutants in which pronounced transcriptional changes control longevity programs. Notably, H3.3 loss critically affects the expression of a very large number of genes in long-lived nematodes, resulting in transcriptional profiles similar to wild-type animals. We conclude that H3.3 positively contributes to diverse lifespan-extending signaling pathways, with potential implications on age-related processes in multicellular organisms.

KEYWORDS:

Caenorhabditis elegans; aging; histone variant H3.3; insulin/IGF-1 signaling pathway

PMID:
27760329
PMCID:
PMC5081402
DOI:
10.1016/j.celrep.2016.09.074
[Indexed for MEDLINE]
Free PMC Article

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