ArticlePLoS genetics2012
Functional antagonism between Sas3 and Gcn5 acetyltransferases and ISWI chromatin remodelers.
Article in PLoS genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Histone acetyltransferase Sas3 in Phomopsis liquidambaris promotes spermidine biosynthesis against Fusarium graminearum in wheat.TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2025Article
- H3K14: A histone site closely related to diseases.Journal of Cancer · 2025Review
- The yeast ISW1b ATP-dependent chromatin remodeler is critical for nucleosome spacing and dinucleosome resolution.Scientific reports · 2021Article
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- TheFrontiers in microbiology · 2018Article
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- The chromatin remodelers RSC and ISW1 display functional and chromatin-based promoter antagonism.eLife · 2015Article
- The histone acetyltransferase MOF activates hypothalamic polysialylation to prevent diet-induced obesity in mice.Molecular metabolism · 2014Article
- Article
- Comprehensive analysis of interacting proteins and genome-wide location studies of the Sas3-dependent NuA3 histone acetyltransferase complex.FEBS open bio · 2014Article
- SAHA enhances Proteostasis of epilepsy-associated α1(A322D)β2γ2 GABA(A) receptors.Chemistry & biology · 2013Article
- Balancing chromatin remodeling and histone modifications in transcription.Trends in genetics : TIG · 2013Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Chromatin-modifying enzymes and ATP-dependent remodeling complexes have been intensely studied individually, yet how these activities are coordinated to ensure essential cell functions such as transcription, replication, and repair of damage is not well understood. In this study, we show that the critical loss of Sas3 and Gcn5 acetyltransferases in yeast can be functionally rescued by inactivation of ISWI remodelers. This genetic interaction depends on the ATPase activities of Isw1 and Isw2, suggesting that it involves chromatin remodeling activities driven by the enzymes. Genetic dissection of the Isw1 complexes reveals that the antagonistic effects are mediated specifically by the Isw1a complex. Loss of Sas3 and Gcn5 correlates with defective RNA polymerase II (RNAPII) occupancy at actively transcribed genes, as well as a significant loss of H3K14 acetylation. Inactivation of the Isw1a complex in the acetyltransferase mutants restores RNAPII recruitment at active genes, indicating that transcriptional regulation may be the mechanism underlying suppression. Dosage studies and further genetic dissection reveal that the Isw1b complex may act in suppression through down-regulation of Isw1a. These studies highlight the importance of balanced chromatin modifying and remodeling activities for optimal transcription and cell growth.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.