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Survival in quiescence requires the euchromatic deployment of Clr4/SUV39H by Argonaute-associated small RNAs [sRNA-Seq]

ABSTRACT: Cellular quiescence (G0) is a ubiquitous stress response through which cells enter a state of reversible dormancy, acquiring distinct properties including reduced metabolism, resistance to stress and long life. G0 entry involves dramatic changes to the chromatin landscape and transcriptional program of cells, but the mechanisms coordinating these processes remain poorly understood. Using the fission yeast, here we track the G0-associated chromatin and transcriptional changes temporally. We show that as cells enter G0, their survival and global gene expression programs become increasingly dependent on Clr4/SUV39H, the sole histone H3 lysine 9 (H3K9) methyltransferase, and RNA interference (RNAi) proteins. Notably, G0 entry results in RNAi-dependent H3K9 methylation of several euchromatic regions, prior to which Argonaute 1-associated small RNAs from these regions emerge. Overall our data reveal a new function for constitutive heterochromatin proteins in establishing the global G0 transcriptional program and suggest that stress-induced alterations in Argonaute-associated sRNAs can specify the deployment of transcriptional regulatory proteins to unique sites in eukaryotic genomes.

ORGANISM(S): Schizosaccharomyces pombe

PROVIDER: GSE89149 | GEO | 2016/12/05

SECONDARY ACCESSION(S): PRJNA350403

REPOSITORIES: GEO

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Survival in quiescence requires the euchromatic deployment of Clr4/SUV39H by Argonaute-associated small RNAs [siRNA-Seq]

Project description:Cellular quiescence (G0) is a ubiquitous stress response through which cells enter a state of reversible dormancy, acquiring distinct properties including reduced metabolism, resistance to stress and long life. G0 entry involves dramatic changes to the chromatin landscape and transcriptional program of cells, but the mechanisms coordinating these processes remain poorly understood. Using the fission yeast, here we track the G0-associated chromatin and transcriptional changes temporally. We show that as cells enter G0, their survival and global gene expression programs become increasingly dependent on Clr4/SUV39H, the sole histone H3 lysine 9 (H3K9) methyltransferase, and RNA interference (RNAi) proteins. Notably, G0 entry results in RNAi-dependent H3K9 methylation of several euchromatic regions, prior to which Argonaute 1-associated small RNAs from these regions emerge. Overall our data reveal a new function for constitutive heterochromatin proteins in establishing the global G0 transcriptional program and suggest that stress-induced alterations in Argonaute-associated sRNAs can specify the deployment of transcriptional regulatory proteins to unique sites in eukaryotic genomes.

2016-12-05 | GSE89150 | GEO

Survival in quiescence requires the euchromatic deployment of Clr4/SUV39H by Argonaute-associated small RNAs [ChIP-Seq]

2016-12-05 | GSE89142 | GEO

Survival in quiescence requires the euchromatic deployment of Clr4/SUV39H by Argonaute-associated small RNAs [RNA-Seq]

2016-12-05 | GSE89145 | GEO

A screen for histone mutations that affect quiescence in S. cerevisiae.

Project description:Quiescence is a distinct cell cycle phase, termed G0, in which growth, transcription, translation, and replication are suppressed. Yeast cells enter G0 following glucose exhaustion but remain viable for an extended period and can re-enter the cell cycle when returned to glucose-rich medium. Quiescence is a feature of all organisms and is essential for the maintenance of stem cells and tissue renewal. Quiescence is also related to chronological lifespan (CLS) - or the capacity of post-mitotic quiescent cells to survive over time - and thus contributes to longevity. However, important questions remain to be answered regarding the mechanisms that control entry into quiescence, the maintenance of quiescence, and the re-entry of quiescent cells into the cell cycle. Histone acetylation is lost during the formation of quiescent yeast cells, and chromatin becomes highly condensed. This unique chromatin landscape plays a key role in supporting quiescence-specific transcriptional repression and has been linked to the formation and maintenance of quiescent cells. To ask if other chromatin features regulate quiescence, we conducted a comprehensive screen of histone H3 and H4 mutants. We identified several mutants that show altered quiescence entry and have characterized their chromatin phenotypes. None of these mutants retain histone acetylation, while several have altered chromatin condensation. Additionally, a screen for H3 and H4 mutants with altered chronological lifespan showed that CLS is highly correlated with quiescence entry.

2023-03-01 | GSE210305 | GEO

Chromatin structure restricts origin utilization when quiescent cells re-enter the cell cycle

Project description:Quiescent cells reside in G0 phase, which is characterized by the absence of cell growth and proliferation. These cells remain viable and re-enter the cell cycle when prompted by appropriate signals. Using a budding yeast model of cellular quiescence, we investigated the program that initiated DNA replication when these G0 cells resumed growth. We performed BrdU IP-Seq to examine the DNA replication profile genome-wide. These data revealed that the initiation of replication was delayed and fewer origins were active when G0 cells entered the cell cycle compared to the entry of G1 cells into S phase. We found that both the transcript and protein levels of these replication factors were significantly diminished during the development of proliferating cells into quiescence. The levels of these factors, including MCM2-7 helicase, increased as G0 cells re-entered the cell cycle, suggesting that the replication program is re-established de novo. Consistent with these results, Mcm4 ChIP-seq analysis showed fewer and reduced binding at a number of origins during the re-entry of G0 cells into the cell cycle. In support of this evidence, the chromatin context surrounding inactive origins of G0 cells exhibits greater increased nucleosome occupancy and reduced periodicity of nucleosome positioning. Altogether, these observations provide insights into the important role of chromatin context that determines the ability of replication origin to accrue limiting replication factors during the the re-entry of quiescent cells into the cell cycle.

2020-08-07 | GSE155831 | GEO

Tailing and degradation of Argonaute-bound small RNAs protect the genome from uncontrolled RNAi

Project description:RNAi is a conserved mechanism in which small RNAs induce silencing of complementary targets. How Argonaute-bound small RNAs are targeted for degradation is not well understood. We show here that the adenyl-transferase Cid14, a member of the TRAMP complex, and the uridyl-transferase Cid16 add non-templated nucleotides to Argonaute-bound small RNAs in fission yeast. The tailing of Argonaute-bound small RNAs in vitro recruits the 3’-5’ exonuclease Rrp6 to degrade small RNAs. Failure in degradation of Argonaute-bound small RNAs results in accumulation of “noise” small RNAs on Argonaute and targeting of diverse euchromatic genes by RNAi. To protect themselves from uncontrolled RNAi, cid14Δ cells exploit the RNAi machinery and silence genes essential for RNAi itself, which is required for their viability. Our data indicate that surveillance of Argonaute-bound small RNAs by Cid14/Cid16 and the exosome protects the genome from uncontrolled RNAi and reveal a rapid RNAi-based adaptation to stress conditions.

2017-05-09 | GSE95821 | GEO

Distinct Functions of Argonaute Slicer in siRNA Maturation and Heterochromatin Formation

Project description:Small-RNA (sRNA)-guided transcriptional gene silencing by Argonaute (Ago)-containing complexes is fundamental to genome integrity and epigenetic inheritance. The RNA cleavage (“Slicer”) activity of Argonaute has been implicated in both sRNA maturation and target RNA cleavage. Typically, Argonaute slices and releases the passenger strand of duplex sRNA to generate active silencing complexes, but it remains unclear whether slicing of target nascent RNAs, or other RNAi components, also contributes to downstream transcriptional silencing. Here, we develop a strategy for loading the fission yeast Ago1 with a single-stranded sRNA guide, which bypasses the requirement for slicer activity in generation of active silencing complexes. We show that slicer-defective Ago1 can mediate secondary sRNA generation, H3K9 methylation, and silencing similar to or better than wild-type and associates with chromatin more efficiently. The results define an ancient and minimal sRNA-mediated chromatin silencing mechanism, which resembles the germline-specific sRNA-dependent transcriptional silencing pathways in Drosophila and mammals. This SuperSeries is composed of the SubSeries listed below.

2016-12-19 | GSE81734 | GEO

CDK4/6 inhibitor-mediated cell overgrowth triggers an osmotic stress response

Project description:Cell size and the cell cycle are intrinsically coupled and abnormal increases in cell size are associated with senescence and permanent cell cycle arrest. The mechanism by which overgrowth primes cells to withdraw from the cell cycle remains unknown. We investigate this here using CDK4/6 inhibitors that arrest cell cycle progression during G0/G1 and are used in the clinic to treat ER+/HER2- metastatic breast cancer. We demonstrate that CDK4/6 inhibition promotes cellular overgrowth during G0/G1, causing p38MAPK-p53-p21-dependent cell cycle withdrawal. We find that cell cycle withdrawal is triggered by two waves of p21 induction. First, overgrowth during a long-term G0/G1 arrest induces an osmotic stress response. This stress response produces the first wave of p21 induction. Second, when CDK4/6 inhibitors are removed, a fraction of cells escape long term G0/G1 arrest and enter S-phase where overgrowth-driven replication stress results in a second wave of p21 induction that causes cell cycle withdrawal from G2, or the subsequent G1. We propose a model whereby both waves of p21 induction contribute to promote permanent cell cycle arrest. This model could explain why cellular hypertrophy is associated with senescence and why CDK4/6 inhibitors have long-lasting effects in patients.

2023-11-27 | PXD036519 | Pride

The Conserved RNA Binding Cyclophilin, Rct1, Regulates Small RNA Biogenesis and Splicing Independent of Heterochromatin Assembly [small RNA]

Project description:RNAi factors and their catalytic activities are essential for heterochromatin assembly in S. pombe. This has led to the idea that siRNAs can promote H3K9 methylation by recruiting the Cryptic Loci Regulator Complex (CLRC), also known as Recombination In K Complex (RIKC), to the nucleation site. The conserved RNA-binding protein Rct1 (AtCyp59/SIG-7) interacts with splicing factors and with RNA polymerase II. Here we show that Rct1 promotes processing of pericentromeric transcripts into siRNAs, via the RNA recognition motif. Surprisingly, loss of siRNA in rct1 mutant cells has no effect on H3K9 di- or tri-methylation, resembling other splicing mutants, and suggesting post-transcriptional gene silencing per se is not required to maintain heterochromatin. Splicing of the Argonaute gene is also defective in rct1 mutants, and contributes to loss of silencing but not to loss of siRNA. Our results suggest that Rct1 guides transcripts to the RNAi machinery by promoting splicing of elongating non-coding transcripts.

2017-06-20 | GSE97748 | GEO

The Conserved RNA Binding Cyclophilin, Rct1, Regulates Small RNA Biogenesis and Splicing Independent of Heterochromatin Assembly [RNA-seq]

2017-06-20 | GSE97747 | GEO

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