The Rpd3L HDAC complex is essential for the heat stress response in yeast

Ruiz-Roig, Clàudia; Viéitez, Cristina; Posas, Francesc; Nadal, Eulàlia de

doi:10.1111/j.1365-2958.2010.07167.x

Cited by 76 publications

(61 citation statements)

References 75 publications

(99 reference statements)

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“…This core complex also transiently associates with other regulatory proteins including Rb1 and chromatin regulatory enzymes to control gene expression (Kadamb et al, 2013;Silverstein and Ekwall, 2005). In addition to the transcriptional repression activity of the Sin3-Hdac complex, growing evidence suggests that Sin3 might also function to activate transcription of certain target genes in different organisms, including yeast and Drosophila, as well as mammalian systems such as mouse muscle development, mouse embryonic fibroblast and mouse embryonic stem cells (Baltus et al, 2009;Dannenberg et al, 2005;Das et al, 2013;Lin et al, 2005;Ruiz-Roig et al, 2010;van Oevelen et al, 2010;Yoshimoto et al, 1992), which would be consistent with the observation that Sin3 could also serve as a scaffold protein for the histone demethylase dKDM5/LID (Gajan et al, 2016). Thus, these studies suggest that Sin3 modulates transcriptional activity by serving as a scaffold protein able to coordinate multiple histone modification activities, including deacetylation and demethylation in a context-dependent manner.…”

Section: Introductionmentioning

confidence: 99%

Sin3a regulates epithelial progenitor cell fate during lung development

et al. 2017

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Mechanisms that regulate tissue-specific progenitors for maintenance and differentiation during development are poorly understood. Here, we demonstrate that the co-repressor protein Sin3a is crucial for lung endoderm development. Loss of Sin3a in mouse early foregut endoderm led to a specific and profound defect in lung development with lung buds failing to undergo branching morphogenesis and progressive atrophy of the proximal lung endoderm with complete epithelial loss at later stages of development. Consequently, neonatal pups died at birth due to respiratory insufficiency. Further analysis revealed that loss of Sin3a resulted in embryonic lung epithelial progenitor cells adopting a senescence-like state with permanent cell cycle arrest in G1 phase. This was mediated at least partially through upregulation of the cell cycle inhibitors Cdkn1a and Cdkn2c. At the same time, loss of endodermal Sin3a also disrupted cell differentiation of the mesoderm, suggesting aberrant epithelial-mesenchymal signaling. Together, these findings reveal that Sin3a is an essential regulator for early lung endoderm specification and differentiation.

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Section: Introductionmentioning

confidence: 99%

Sin3a regulates epithelial progenitor cell fate during lung development

et al. 2017

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“…Both complexes share a core defined by the Rpd3, Sin3, and Ume1 subunits (Carrozza et al 2005b;Chen et al 2012). Rpd3L is required for stress response and transcriptional silencing (Zhou et al 2009;Ruiz-Roig et al 2010). The Sds3, Dep1, Cti6, Sap30, Rxt2, Rxt3, and Pho23 subunits, in combination with the Rpd3 core, form the Rpd3L complex that is recruited to gene promoters by Ume6 and Ash1 subunits (Carrozza et al 2005a;Zhou et al 2009;Ruiz-Roig et al 2010).…”

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confidence: 99%

“…Rpd3L is required for stress response and transcriptional silencing (Zhou et al 2009;Ruiz-Roig et al 2010). The Sds3, Dep1, Cti6, Sap30, Rxt2, Rxt3, and Pho23 subunits, in combination with the Rpd3 core, form the Rpd3L complex that is recruited to gene promoters by Ume6 and Ash1 subunits (Carrozza et al 2005a;Zhou et al 2009;Ruiz-Roig et al 2010). The Rpd3S complex is formed by the Rpd3 core and the Eaf3 and Rco1 subunits (Carrozza et al 2005b).…”

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confidence: 99%

Bypassing the Requirement for an Essential MYST Acetyltransferase

Torres-Machorro

Pillus

2014

Genetics

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Histone acetylation is a key regulatory feature for chromatin that is established by opposing enzymatic activities of lysine acetyltransferases (KATs/HATs) and deacetylases (KDACs/HDACs). Esa1, like its human homolog Tip60, is an essential MYST family enzyme that acetylates histones H4 and H2A and other nonhistone substrates. Here we report that the essential requirement for ESA1 in Saccharomyces cerevisiae can be bypassed upon loss of Sds3, a noncatalytic subunit of the Rpd3L deacetylase complex. By studying the esa1Δ sds3Δ strain, we conclude that the essential function of Esa1 is in promoting the cellular balance of acetylation. We demonstrate this by fine-tuning acetylation through modulation of HDACs and the histone tails themselves. Functional interactions between Esa1 and HDACs of class I, class II, and the Sirtuin family define specific roles of these opposing activities in cellular viability, fitness, and response to stress. The fact that both increased and decreased expression of the ESA1 homolog TIP60 has cancer associations in humans underscores just how important the balance of its activity is likely to be for human well-being.T HE genetic information of DNA is packed into chromatin, which is predominantly composed of the H3, H4, H2A, and H2B core histone proteins that together with DNA form nucleosomes, the basic subunits of the genome (Kornberg and Lorch 1999). Chromatin structure regulates many cellular processes including gene expression, DNA replication, DNA damage repair, and recombination (Felsenfeld and Groudine 2003). Nucleosomes themselves are tightly regulated by mobilization and positioning that are mediated by ATP-dependent chromatin-remodeling machines (Rando and Winston 2012) and by multiple types of histone posttranslational modifications that include acetylation and many other marks (Campos and Reinberg 2009).Nucleosome acetylation is a highly dynamic modification that is promoted by HATs and removed by HDACs. HATs are classified by sequence into different families (Allis et al. 2007). ESA1/KAT5 belongs to the widely conserved MYST HAT family, named for its founding members (MOZ-YBF2/ SAS3-SAS2-TIP60) (Lafon et al. 2007). Esa1 is an essential HAT in yeast (Smith et al. 1998;Clarke et al. 1999) and the catalytic subunit of two distinct multi-protein complexes: NuA4 and Piccolo (Boudreault et al. 2003). Notably, the human homolog of Esa1 is Tip60, which is also essential in vertebrates and has been linked to multiple human diseases (Squatrito et al. 2006;Avvakumov and Côté 2007;Lafon et al. 2007), thus increasing the relevance of gaining a deeper understanding of essential HAT functions.Esa1 primarily acetylates H4 and H2A in vivo (Clarke et al. 1999;Lin et al. 2008) and regulates the expression of active protein-encoding genes (Reid et al. 2000;Lin et al. 2008). It plays a crucial role in cell cycle progression and ribosomal DNA (rDNA) silencing (Clarke et al. 1999(Clarke et al. , 2006 and is recruited to DNA double-strand breaks (DSBs) to promote damage repair by acetylati...

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“…Dep1 is a component of the Rpd3L histone deacetylase (HDAC) complex, and like mutations in other genes (e.g. RPD3, SIN3, UME1, SPA30 and PHO23) of the Rpd3 complex, mutation of DEP1 displays a thermosensitive growth phenotype (Ruiz-Roig et al, 2010). The Rad3 complex is known to be involved not only in cell adaptation during the heat stress response but also in regulating heterochromatic boundary that restricts the spread of gene silencing (Ehrentraut et al, 2010;Zhou et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

Sphingolipids regulate telomere clustering by affecting transcriptional levels of genes involved in telomere homeostasis

Ikeda

Muneoka

Murakami

et al. 2015

Journal of Cell Science

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In eukaryotic organisms, including mammals, nematodes and yeasts, the ends of chromosomes, telomeres are clustered at the nuclear periphery. Telomere clustering is assumed to be functionally important because proper organization of chromosomes is necessary for proper genome function and stability. However, the mechanisms and physiological roles of telomere clustering remain poorly understood. In this study, we demonstrate a role for sphingolipids in telomere clustering in the budding yeast Saccharomyces cerevisiae. Because abnormal sphingolipid metabolism causes downregulation of expression levels of genes involved in telomere organization, sphingolipids appear to control telomere clustering at the transcriptional level. In addition, the data presented here provide evidence that telomere clustering is required to protect chromosome ends from DNA-damage checkpoint signaling. As sphingolipids are found in all eukaryotes, we speculate that sphingolipid-based regulation of telomere clustering and the protective role of telomere clusters in maintaining genome stability might be conserved in eukaryotes.

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The Rpd3L HDAC complex is essential for the heat stress response in yeast

Cited by 76 publications

References 75 publications

Sin3a regulates epithelial progenitor cell fate during lung development

Sin3a regulates epithelial progenitor cell fate during lung development

Bypassing the Requirement for an Essential MYST Acetyltransferase

Sphingolipids regulate telomere clustering by affecting transcriptional levels of genes involved in telomere homeostasis

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