<scp>C</scp>‐terminus of the <scp>S</scp>gf73 subunit of <scp>SAGA</scp> and <scp>SLIK</scp> is important for retention in the larger complex and for heterochromatin boundary function

Kamata, Kazuma; Hatanaka, Akira; Goswami, Gunajit; Shinmyozu, Kaori; Nakayama, Jun‐ichi; Urano, Takeshi; Hatashita, Masanori; Uchida, Hiroyuki; Oki, Masaya

doi:10.1111/gtc.12075

Cited by 17 publications

(20 citation statements)

References 54 publications

(147 reference statements)

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“…Future studies of telomeres with different genomic composition and structural features will clarify whether these effects are linked to aging. In addition, given that SAGA and Sgf73 have roles in heterochromatin-euchromatin barrier formation (Oki et al, 2004), with the C-terminus of the Sgf73 subunit of SAGA and SLIK important for retention of the larger complex and for heterochromatin boundary function (Kamata et al, 2013), it will be important to better understand the role of the DUBm in the context of the greater complex.…”

Section: Discussionmentioning

confidence: 99%

The SAGA Histone Deubiquitinase Module Controls Yeast Replicative Lifespan via Sir2 Interaction

et al. 2014

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SUMMARY We have analyzed the yeast replicative lifespan of a large number of ORF deletions. Here we report that strains lacking genes SGF73, SGF11, and UBP8, encoding SAGA/SLIK complex histone deubiquitinase module (DUBm) components, are exceptionally long-lived. Strains lacking other SAGA/SALSA components, including the acetyltransferase encoded by GCN5, are not long-lived; however, these genes are required for the lifespan extension observed in DUBm deletions. Moreover, the SIR2-encoded histone deacetylase is required, and we document both a genetic and physical interaction between DUBm and Sir2. A series of studies, assessing Sir2-dependent functions, lead us to propose that DUBm strains are exceptionally long-lived because they promote multiple pro-longevity events, including reduced rDNA recombination and altered silencing of telomere-proximal genes. As ataxin-7, the human Sgf73 ortholog, causes the neurodegenerative disease spinocerebellar ataxia type 7, our findings indicate that the genetic and epigenetic interactions between DUBm and SIR2 will be relevant to neurodegeneration and aging.

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Section: Discussionmentioning

confidence: 99%

The SAGA Histone Deubiquitinase Module Controls Yeast Replicative Lifespan via Sir2 Interaction

et al. 2014

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“…Based on studies of the yeast SAGA complex, Sgf73 is believed to be a component of DUB and link the HAT and TAF modules within the complex (24)(25)(26)(27). To determine whether C. parasitica SGF73 works as a component of SAGA to induce dcl2 in response to virus infection, other SAGA component genes representing HAT and DUB were tested.…”

Section: Saga Mediates Virus-responsive Induction Of Rnai Key Genesmentioning

confidence: 99%

“…However, we cannot exclude the possibility that complexes other than SAGA, such as the SAGA-like complex (27,38), components of which are shared with SAGA, mediate transcriptional regulation of dcl2. Roles of the SAGA complex in abiotic stress responses have been extensively studied in other organisms, particularly in yeast (34,39,40), but rarely in biotic stress conditions, including virus infection.…”

Section: Saga Mediates Virus-responsive Induction Of Rnai Key Genesmentioning

confidence: 99%

SAGA complex mediates the transcriptional up-regulation of antiviral RNA silencing

Andika

Jamal

Kondō

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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Pathogen recognition and transcriptional activation of defenserelated genes are crucial steps in cellular defense responses. RNA silencing (RNAi) functions as an antiviral defense in eukaryotic organisms. Several RNAi-related genes are known to be transcriptionally up-regulated upon virus infection in some host organisms, but little is known about their induction mechanism. A phytopathogenic ascomycete, Cryphonectria parasitica (chestnut blight fungus), provides a particularly advantageous system to study RNAi activation, because its infection by certain RNA viruses induces the transcription of dicer-like 2 (dcl2) and argonaute-like 2 (agl2), two major RNAi players. To identify cellular factors governing activation of antiviral RNAi in C. parasitica, we developed a screening protocol entailing multiple transformations of the fungus with cDNA of a hypovirus mutant lacking the RNAi suppressor (CHV1-Δp69), a reporter construct with a GFP gene driven by the dcl2 promoter, and a random mutagenic construct. Screening for GFP-negative colonies allowed the identification of sgf73, a component of the SAGA (Spt-Ada-Gcn5 acetyltransferase) complex, a well-known transcriptional coactivator. Knockout of other SAGA components showed that the histone acetyltransferase module regulates transcriptional induction of dcl2 and agl2, whereas histone deubiquitinase mediates regulation of agl2 but not dcl2. Interestingly, full-scale induction of agl2 and dcl2 by CHV1-Δp69 required both DCL2 and AGL2, whereas that by another RNA virus, mycoreovirus 1, required only DCL2, uncovering additional roles for DCL2 and AGL2 in viral recognition and/or RNAi activation. Overall, these results provide insight into the mechanism of RNAi activation.Cryphonectria parasitica | hypovirus | RNAi | mycovirus | antiviral defense

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“…Next, we investigated why Gic1 has two domains that are important for its boundary function and whether the same proteins can bind to both domains. We performed mass spectrometry to identify binding proteins of the boundary domains (228-241 aa and 283-302 aa) by constructing strains expressing the minimum domains tagged with G196 (a gift from Dr. T. Urano) (Kamata et al, 2013). However, we could not identify a protein that specifically binds to these domains (data not shown).…”

Section: Gic1 Has Two Small Boundary Domainsmentioning

confidence: 99%

“…For example, Sas2, the best-known boundary protein, prevents the deacetylase activity of Sir2 (Kimura et al, 2002;Suka et al, 2002). Sgf29 and Sgf73 are components of the SAGA, SAGA-like, ADA and HAT-2 complexes (Kamata et al, 2013(Kamata et al, , 2014. GIC1 does not belong to the Histone modifications, Transcription factors or Cell cycle groups.…”

Section: Gic1 Has a Novel Boundary Function In Vivomentioning

confidence: 99%

Gic1 is a novel heterochromatin boundary protein in vivo

Mitsumori

Shinmyozu²,

Nakayama

et al. 2016

Genes Genet. Syst.

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In Saccharomyces cerevisiae, HMR/HML, telomeres and ribosomal DNA are heterochromatin-like regions in which gene transcription is prevented by the silent information regulator (Sir) complex. The Sir complex (Sir2, Sir3 and Sir4) can spread through chromatin from the silencer. Boundaries prevent Sir complex spreading, and we previously identified 55 boundary genes among all ~6,000 yeast genes. These boundary proteins can be distinguished into two types: those that activate transcription to prevent spreading of silencing, and those that prevent gene silencing by forming a boundary. We selected 44 transcription-independent boundary proteins from the 55 boundary genes by performing a one-hybrid assay and focused on GIC1 (GTPase interaction component 1). Gic1 is an effector of Cdc42, which belongs to the Rho family of small GTPases, and has not been reported to function in heterochromatin boundaries in vivo. We detected a novel boundary-forming activity of Gic1 at HMR-left and telomeric regions by conducting a chromatin immunoprecipitation assay with an anti-Sir3 antibody. We also found that Gic1 bound weakly to histones in two-hybrid analysis. Moreover, we performed domain analysis to identify domain(s) of Gic1 that are important for its boundary activity, and identified two minimum domains, which are located outside its Cdc42-binding domain.

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C‐terminus of the Sgf73 subunit of SAGA and SLIK is important for retention in the larger complex and for heterochromatin boundary function

Cited by 17 publications

References 54 publications

The SAGA Histone Deubiquitinase Module Controls Yeast Replicative Lifespan via Sir2 Interaction

The SAGA Histone Deubiquitinase Module Controls Yeast Replicative Lifespan via Sir2 Interaction

SAGA complex mediates the transcriptional up-regulation of antiviral RNA silencing

Gic1 is a novel heterochromatin boundary protein in vivo

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