Cited by 130Genomics and Chromatin DynamicsNuclear Structure and FunctionEpigenetics and DNA Methylation

Rtt106p is a histone chaperone involved in heterochromatin-mediated silencing

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Huang, Shengbing, Zhou, Hui, Katzmann, David, Hochstrasser, Mark, Atanasova, Elena, Zhang, Zhiguo·2005·Proceedings of the National Academy of Sciences

Abstract

Epigenetic inheritance of heterochromatin structure is an important cellular process whose mechanism remains elusive. In this article, we describe the identification of nine enhancers of the silencing defect of a Saccharomyces cerevisiae -PCNA mutant by screening a library of ≈4,700 viable yeast deletion mutants. Of the nine mutants identified, six ( hir1 , hir3 , sas2 , sas4 , sas5 , and sir1 ) were previously known to reduce silencing synergistically with a mutation in Cac1p, the large subunit of chromatin assembly factor 1 (CAF-1). The predicted gene products that are affected in three other mutants ( nam7 , msh2 , and rtt106 ) have not been implicated previously in silencing. Characterization of the rtt106 Δ allele revealed that it synergistically reduced heterochromatin silencing when combined with a mutation in Cac1p but not with a mutation in Asf1p (a histone H3 and H4 chaperone). Moreover, Rtt106p interacted with histones H3 and H4 both in vitro and in vivo , and it displayed a nucleosome assembly activity in vitro . Furthermore, Rtt106p interacts with CAF-1 physically through Cac1p. These biochemical and genetic data indicate that Rtt106p is a previously uncharacterized histone chaperone connecting S phase to epigenetic inheritance.

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Crossref · 10.1073/pnas.0506176102

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  • Loss of Rtt106 causes aberrant 'cryptic' transcription initiation within gene bodies and compromised silencing at the mating loci and telomeres, likely due to defective nucleosome assembly.

    “Loss of Rtt106 causes aberrant ‘cryptic’ transcription initiation within gene bodies26 and compromised silencing at the mating loci and telomeres27,28, likely due to defective nucleosome assembly26,27,29.”

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Authors
Huang, S., Zhou, H., Katzmann, D., Hochstrasser, M., Atanasova, E., & Zhang, Z.
Affiliations
Mayo Clinic (US)
Venue
Proceedings of the National Academy of Sciences
Published
2005-09-12
Volume
102
Issue
38
Pages
13410-13415
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W2031481332
Cited by
130
References
64
Citations by year
2026: 3 · 2025: 2 · 2024: 4 · 2023: 3 · 2022: 5 · 2021: 9 · 2020: 4 · 2019: 5 · 2018: 6 · 2017: 8 · 2016: 8 · 2015: 5 · 2014: 6 · 2013: 7 · 2012: 7
FWCI
2.13
Type
journal article
Language
en
Open access
Locations
  • Proceedings of the National Academy of Sciences (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Cancer Research UK
  • University of Toronto
  • National Institutes of Health
  • National Institute of General Medical Sciences (R01GM046904, R37GM046904, GM-46904)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
Keywords
histone chaperone, heterochromatin silencing, epigenetic inheritance, CAF-1, nucleosome assembly, histone H3, histone H4, S phase, Saccharomyces cerevisiae, Sir proteins
MeSH terms
Histones, Ribonucleases, Saccharomyces cerevisiae, Gene Expression Regulation, Fungal, S Phase, Gene Deletion, Proliferating Cell Nuclear Antigen, Molecular Chaperones, Gene Silencing, Saccharomyces cerevisiae Proteins, Chromatin Assembly and Disassembly, Epigenesis, Genetic

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