Maintenance of Nucleosomal Balance in cis by Conserved AAA-ATPase Yta7
Open accessAbstract
The extent of chromatin compaction is a fundamental driver of nuclear metabolism . Yta7 is a chromatin-associated AAA-ATPase, the human ortholog of which, ANCCA/ATAD2 transcriptionally activates pathways of malignancy in a broad range of cancers. Yta7 directly binds histone H3, and bulk chromatin exhibits increased nucleosomal density in yta7Δ mutants. The suppression of yta7Δ mutant growth and transcriptional phenotypes in budding yeast by decreased dosage of histones H3 and H4 indicates the acute sensitivity of cells to deviations in nucleosome spacing. This study investigated the global changes in chromatin structure upon Yta7 loss or overexpression and determined which of these effects reflected direct Yta7 activity. Metagene analysis of Yta7’s genome-wide localization indicated peak binding of Yta7 just downstream of the transcription start site. Cells lacking Yta7 exhibited increased nucleosome density within genes downstream of the +1 nucleosome, as defined by decreased internucleosomal distance, resulting in progressively 5′-shifted nucleosomes within the gene. In contrast, cells overexpressing Yta7 displayed profound 3′-shifts in nucleosome position and reduced nucleosome density within genes. Importantly, Yta7-bound regions were enriched for nucleosomal shifts, indicating that Yta7 acted locally to modulate nucleosome spacing. The phenotype of cells lacking both Yta7 and Rtt106, the histone H3/H4 chaperone, indicated that Yta7 functions in both Rtt106-dependent and Rtt106-independent ways to modulate nucleosome spacing within genes. This study suggested that Yta7 affected nucleosome density throughout the gene by both blocking Rtt106 from entering the gene, as shown previously at HTA1, and facilitating the loss of nucleosomes from the 5′-end.
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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.”
From SWI/SNF and the histone chaperone Rtt106 drive expression of the Pleiotropic Drug Resistance network genes (2022) · cites this paper as [29]
The increased mRNA in rtt106Δ may reflect increased transcription initiation caused by defective histone deposition or increased nucleosome spacing.
“This may reflect increased transcription initiation that could be caused by defective histone deposition or increased nucleosome spacing in rtt106Δ26,27,29.”
From SWI/SNF and the histone chaperone Rtt106 drive expression of the Pleiotropic Drug Resistance network genes (2022) · cites this paper as [29]
The yta7Δ mutation does not cause Rtt106 binding to spread from PDRE-containing promoters, unlike at the histone promoters where Rtt106 spreads into regions normally occupied by Yta7.
“However, the yta7Δ mutation did not cause Rtt106 binding to spread from PDRE-containing promoters, unlike at the histone promoters where Rtt106 was observed to spread into regions normally occupied by Yta7 (Fig. 2a, b, compare our Rtt106 ChIP data with the published Yta7 ChIP data shown at bottom29).”
From SWI/SNF and the histone chaperone Rtt106 drive expression of the Pleiotropic Drug Resistance network genes (2022) · cites this paper as [29]
The effect of Rtt106 on PDR5 transcription is not directly mediated through the SWI/SNF effect on nucleosome position.
“However, while the +1 nucleosome at the PDR5 promoter was shifted in the snf2 mutant, in the absence of Rtt106 nucleosome positioning was not obviously changed29 (Supplementary Fig. 7c), suggesting that the effect of Rtt106 on PDR5 transcription is not directly mediated through the SWI/SNF effect on nucleosome position.”
From SWI/SNF and the histone chaperone Rtt106 drive expression of the Pleiotropic Drug Resistance network genes (2022) · cites this paper as [29]
In the absence of Rtt106, nucleosome positioning at the PDR5 promoter was not obviously changed.
“However, while the +1 nucleosome at the PDR5 promoter was shifted in the snf2 mutant, in the absence of Rtt106 nucleosome positioning was not obviously changed29 (Supplementary Fig. 7c), suggesting that the effect of Rtt106 on PDR5 transcription is not directly mediated through the SWI/SNF effect on nucleosome position.”
From SWI/SNF and the histone chaperone Rtt106 drive expression of the Pleiotropic Drug Resistance network genes (2022) · cites this paper as [29]
Loss of Rtt106 does not change the steady-state level of nucleosomes at the PDR5 promoter.
“In contrast, loss of Rtt106 does not change the steady-state level of nucleosomes at the PDR5 promoter (Supplementary Fig. 7c)29, leaving the possibility that at the PDR5 promoter Rtt106 may regulate nucleosome turnover, an effect not observable by MNase-seq nucleosome mapping.”
From SWI/SNF and the histone chaperone Rtt106 drive expression of the Pleiotropic Drug Resistance network genes (2022) · cites this paper as [29]
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References 50 · Cited by 16
- Authors
- Lombardi, L. M., Davis, M. D., & Rine, J.
- Affiliations
- QB3 (US)
- The University of Texas at Austin (US)
- Corresponding author
- Rine, Jasper
- Venue
- Genetics
- Publisher
- Oxford University Press (OUP)
- Published
- 2014-11-17
- Volume
- 199
- Issue
- 1
- Pages
- 105-116
- ISSN
- 0016-6731 (ISSN-L)
- 1943-2631
- PMC
- PMC4286676
- OpenAlex
- W2061413037
- Cited by
- 16
- References
- 50
- Citations by year
- 2025: 1 · 2022: 5 · 2021: 3 · 2020: 1 · 2019: 1 · 2018: 1 · 2016: 1 · 2015: 3
- FWCI
- 0.55
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model (vor)
- Locations
- Genetics (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of General Medical Sciences (GM31105, R01GM031105, R37GM031105, T32GM007232)
- 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 › Chromatin Remodeling and Cancer
- Keywords
- AAA+ ATPase, nucleosome spacing, chromatin condensation, histone H3, histone H4, histone chaperone, nucleosome density, nucleosome positioning, transcription start sites, Saccharomyces cerevisiae, chromatin structure
- MeSH terms
- Chromosomal Proteins, Non-Histone, Nucleosomes, Saccharomyces cerevisiae, Conserved Sequence, Molecular Chaperones, Saccharomyces cerevisiae Proteins
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