Cited by 114Genomics and Chromatin DynamicsFungal and yeast genetics researchChromatin Remodeling and Cancer

Regulation of Histone Gene Expression in Budding Yeast

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Eriksson, Peter R, Ganguli, Dwaipayan, Nagarajavel, V, Clark, David J·2012·Genetics

Abstract

We discuss the regulation of the histone genes of the budding yeast Saccharomyces cerevisiae. These include genes encoding the major core histones (H3, H4, H2A, and H2B), histone H1 (HHO1), H2AZ (HTZ1), and centromeric H3 (CSE4). Histone production is regulated during the cell cycle because the cell must replicate both its DNA during S phase and its chromatin. Consequently, the histone genes are activated in late G1 to provide sufficient core histones to assemble the replicated genome into chromatin. The major core histone genes are subject to both positive and negative regulation. The primary control system is positive, mediated by the histone gene-specific transcription activator, Spt10, through the histone upstream activating sequences (UAS) elements, with help from the major G1/S-phase activators, SBF (Swi4 cell cycle box binding factor) and perhaps MBF (MluI cell cycle box binding factor). Spt10 binds specifically to the histone UAS elements and contains a putative histone acetyltransferase domain. The negative system involves negative regulatory elements in the histone promoters, the RSC chromatin-remodeling complex, various histone chaperones [the histone regulatory (HIR) complex, Asf1, and Rtt106], and putative sequence-specific factors. The SWI/SNF chromatin-remodeling complex links the positive and negative systems. We propose that the negative system is a damping system that modulates the amount of transcription activated by Spt10 and SBF. We hypothesize that the negative system mediates negative feedback on the histone genes by histone proteins through the level of saturation of histone chaperones with histone. Thus, the negative system could communicate the degree of nucleosome assembly during DNA replication and the need to shut down the activating system under replication-stress conditions. We also discuss post-transcriptional regulation and dosage compensation of the histone genes.

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Authors
Eriksson, P. R., Ganguli, D., Nagarajavel, V, & Clark, D. J.
Affiliations
National Institutes of Health (US)
Corresponding author
Clark, David J
Venue
Genetics
Published
2012-05-01
Volume
191
Issue
1
Pages
7-20
ISSN
  • 0016-6731 (ISSN-L)
  • 1943-2631
OpenAlex
W2158298861
Cited by
114
References
117
Citations by year
2026: 4 · 2025: 4 · 2024: 6 · 2023: 5 · 2022: 7 · 2021: 6 · 2020: 26 · 2019: 5 · 2018: 9 · 2017: 10 · 2016: 9 · 2015: 7 · 2014: 6 · 2013: 6 · 2012: 4
FWCI
0.67
Type
journal article
Language
en
Open access
Locations
  • Genetics (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Institute of Child Health and Human Development
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
Keywords
histone gene expression, Saccharomyces cerevisiae, core histones, histone H1, histone H2A variant, CENH3, upstream activating sequence, simulated body fluid, MBF, RSC complex, SWI/SNF complex, histone chaperone, Asf1, histone acetyltransferase, chromatin remodeling, nucleosome assembly, replication stress, post-transcriptional regulation, dosage compensation, cell cycle regulation
MeSH terms
Base Sequence, Cell Cycle, Histones, Saccharomyces cerevisiae, Transcription, Genetic, Transcriptional Activation, Gene Expression Regulation, Fungal

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