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TORC1 shapes the SUMO proteome to control RNA polymerase III activity

ABSTRACT: Loss of nutrient supply elicits alterations of the SUMO proteome and sumoylation is crucial to various cellular processes including transcription. However, the physiological significance of sumoylation of transcriptional regulators is unclear. To begin clarifying this, we mapped the SUMO proteome under nitrogen-limiting conditions in Saccharomyces cerevisiae. Interestingly, several RNA polymerase III (RNAPIII) components are major SUMO targets under normal growth conditions, including Rpc53, Rpc82, and Ret1, and nutrient starvation results in rapid desumoylation of these proteins. These findings are supported by ChIP-seq experiments that show that SUMO is highly enriched at tDNA genes. Furthermore, RNA-seq experiments revealed that preventing sumoylation results in significantly decreased tRNA transcription. TORC1 inhibition resulted in the same effect, and our data indicate that the SUMO and TORC1 pathways are both required for robust tDNA expression. Importantly, tRNA transcription was strongly reduced in cells expressing a non-sumoylatable Rpc82-4KR mutant, which correlated with a misassembled RNAPIII transcriptional complex. Our data suggest that in addition to TORC1 activity, sumoylation of RNAPIII is key to reaching full translational capacity under optimal growth conditions.

ORGANISM(S): Saccharomyces cerevisiae

PROVIDER: GSE85622 | GEO | 2017/01/01

SECONDARY ACCESSION(S): PRJNA338964

REPOSITORIES: GEO

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Similar Datasets

TORC1 shapes the SUMO proteome to control RNA Polymerase III activity

Project description:Loss of nutrient supply elicits alterations of the SUMO proteome and sumoylation is crucial to various cellular processes including transcription. However, the physiological significance of sumoylation of transcriptional regulators is unclear. To begin clarifying this, we mapped the SUMO proteome under nitrogen-limiting conditions in Saccharomyces cerevisiae. Interestingly, several RNA polymerase III (RNAPIII) components are major SUMO targets under normal growth conditions, including Rpc53, Rpc82, and Ret1, and nutrient starvation results in rapid desumoylation of these proteins. These findings are supported by ChIP-seq experiments that show that SUMO is highly enriched at tDNA genes. Furthermore, RNA-seq experiments revealed that preventing sumoylation results in significantly decreased tRNA transcription. TORC1 inhibition resulted in the same effect, and our data indicate that the SUMO and TORC1 pathways are both required for robust tDNA expression. Importantly, tRNA transcription was strongly reduced in cells expressing a non-sumoylatable Rpc82-4KR mutant, which correlated with a misassembled RNAPIII transcriptional complex. Our data suggest that in addition to TORC1 activity, sumoylation of RNAPIII is key to reaching full translational capacity under optimal growth conditions.

2017-01-21 | PXD005142 | Pride

Genome-wide ChIP-exo profiling of Fpt1 in glucose

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2023-11-21 | GSE228556 | GEO

Cdk1 Gates Cell Cycle-Dependent tRNA Synthesis by Regulating RNA Polymerase III Activity

Project description:tRNA genes are transcribed by RNA polymerase III (RNAPIII). During recent years it has become clear that RNAPIII activity is strictly regulated by the cell in response to environmental cues and the homeostatic status of the cell. However, the molecular mechanisms that control RNAPIII activity to regulate the amplitude of tDNA transcription in normally cycling cells are not well understood. Here, we show that tRNA levels fluctuate during the cell cycle and reveal the underlying molecular mechanism. The cyclin Clb5 recruits the cyclin dependent kinase Cdk1 to tRNA genes to boost tDNA transcription during S phase. At tDNA genes, Cdk1 promotes the recruitment of TFIIIC, stimulates the interaction between TFIIIB and TFIIIC, and increases the dynamics of RNA polymerase III in vivo. Furthermore, we identified Bdp1 as an important Cdk1 substrate in this process. Preventing Bdp1 phosphorylation prevented cell cycle-dependent recruitment of TFIIIC and abolished the cell cycle-induced increase in tDNA transcription. Our findings demonstrate that under optimal growth conditions Cdk1 gates tRNA synthesis in S phase by regulating the RNAPIII machinery, revealing a direct link between the cell cycle and RNAPIII activity.

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Locus-specific proteome decoding reveals Fpt1 as a chromatin-associated negative regulator of RNA Polymerase III assembly

Project description:Transcription of tRNA genes by RNA Polymerase III (RNAPIII) is tuned by signaling cascades. The emerging notion of differential tRNA gene regulation implies the existence of additional regulatory mechanisms. However, tRNA gene-specific regulators have not been described. Decoding the proteome of a native tRNA gene in yeast revealed reprogramming of the RNAPIII transcription machinery upon nutrient perturbation. Among the dynamic proteins, we identified Fpt1, a protein of unknown function that uniquely occupied RNAPIII regulated genes. Fpt1 binding at tRNA genes correlated with the efficiency of RNAPIII eviction upon nutrient perturbation and required the transcription factors TFIIIB and TFIIIC but not RNAPIII. In the absence of Fpt1, eviction of RNAPIII was reduced and the shutdown of ribosome biogenesis genes was impaired upon nutrient perturbation. Our findings provide support for a chromatin-associated mechanism required for RNAPIII eviction from tRNA genes and for tuning the physiological response to changing metabolic demands.

2023-11-28 | PXD045463 | Pride

Global analysis of transcriptionally engaged yeast RNA polymerase III reveals extended tRNA transcripts

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SUMOylation restrains the degradation of ACE2 through TOLLIP-mediated selective autophagy to facilitate the host susceptibility to SARS-CoV-2 infection

Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of the ongoing coronavirus disease 2019 (COVID-19) pandemic. Alongside investigations into the virology of SARS-CoV-2, understanding the host–virus dependencies are vital for the identification and rational design of effective antiviral therapy. Here, we report the dominant SARS-CoV-2 entry receptor, ACE2, conjugates with small ubiquitin-like modifier 3 (SUMO3) through a proteome-wide protein interaction analysis. We further demonstrate that E3 SUMO ligase PIAS4 prompts the SUMOylation and stabilization of ACE2, whereas deSUMOylation enzyme SENP3 reverses this process. Conjugation of SUMO3 with ACE2 at lysine (K) 187 hampers the K48-linked ubiquitination of ACE2, thus suppressing its subsequent cargo receptor TOLLIP-dependent autophagic degradation. Pharmacological intervention of ACE2 SUMOylation blocks the entry of SARS-CoV-2 and viral infection-triggered immune responses. Collectively, our findings suggest selective autophagic degradation of ACE2 orchestrated by SUMOylation and ubiquitination can be targeted to future antiviral therapy of SARS-CoV-2.

2022-07-18 | GSE171130 | GEO

Global analysis of transcriptionally engaged yeast RNA polymerase III reveals extended tRNA transcripts

Project description:RNA polymerase III (RNAPIII) synthesizes a range of highly abundant small stable RNAs, principally pre-tRNAs. Here we report the genome-wide analysis of nascent transcripts attached to RNAPIII under permissive and restrictive growth conditions. This revealed strikingly uneven polymerase distributions across transcription units, generally with a predominant 5´ peak. This peak was higher for more heavily transcribed genes, suggesting that initiation site clearance is rate limiting during RNAPIII transcription. Down-regulation of RNAPIII transcription under stress conditions was found to be uneven; a subset of tRNA genes showed low response to nutrient shift or loss of the major transcription regulator Maf1, suggesting potential “housekeeping” roles. Many tRNA genes were found to generate long, 3´-extended forms due to read-through of the canonical poly(U) terminators. The degree of read-through was anti-correlated with the density of T-residues in the coding strand, and multiple, functional terminators can be located far downstream. The steady-state levels of 3´-extended pre-tRNA transcripts are low, apparently due to targeting by the nuclear surveillance machinery; especially the RNA-binding protein Nab2, cofactors for the nuclear exosome and the 5´-exonuclease Rat1.

2016-05-18 | GSE77863 | GEO

SUMOylation on plant chromatin controls transcription switches between development and heat response [ChIP-Seq]

Project description:SUMOylation, a post-translational protein modification, is dramatically upregulated and critically involved in heat stress response conservatively among species. Previous studies in Arabidopsis indicated that numerous chromatin associated proteins are SUMOylation substrates and most of heat-enhancing SUMOylation reactions occur in nucleus. However, the global functional connection between gene expression regulation and SUMOylation on chromatin is completely unknown in plant cells. Here we show a genome-wide relationship of chromatin-associated SUMOylation and transcription switches under room temperature, heat stress, and recovering conditions in Arabidopsis. The SUMO-associated chromatin sites, characterized via whole-genome ChIP-seq assays, are generally correlated with active chromatin markers. In response to heat stress, we found chromatin-associated SUMO signals increased at promoter-transcriptional start site regions and decreased in the gene bodies. Further RNA-seq analysis supported the role of chromatin-associated SUMOylation in activation of transcription during rapid responses to high temperature. Changing of SUMO signals on chromatin is correlated with upregulation of heat-responsive genes and downregulation of growth-related genes. Disruption of the SUMO ligase gene SIZ1 abolishes SUMO signals on chromatin and attenuates the rapid transcriptional responses to heat stress. Interestingly, the SUMO signal peaks are enriched in DNA elements recognized by distinguished groups of transcription factors under different temperature conditions. Collectively, our data provide evidence that SUMOylation on chromatin regulates transcription switches during development and heat stress response, improving our understanding on the precise roles of SUMOylation in plant cells.

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SUMOylation on plant chromatin controls transcription switches between development and heat response [RNA-Seq]

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Project description:Reduced oxygen availability (hypoxia) triggers adaptive cellular responses via hypoxia-inducible factor (HIF)-dependent transcriptional activation. Adaptation to hypoxia also involves transcription-independent processes like post-translational modifications, however these mechanisms are poorly characterized. Investigating the involvement of protein SUMOylation in response to hypoxia, we discovered that hypoxia strongly decreases the SUMOylation of Exosome subunit 10 (EXOSC10), the catalytic subunit of the RNA exosome, in a HIF-independent manner. EXOSC10 is a multifunctional exoribonuclease enriched in the nucleolus that mediates the processing and degradation of various RNA species. We demonstrate that the Ubiquitin-specific protease 36 (USP36) SUMOylates EXOSC10 and we reveal SUMO1/sentrin-specific peptidase 3 (SENP3) as the enzyme mediating deSUMOylation of EXOSC10. Under hypoxia, EXOSC10 dissociates from USP36 and translocates from the nucleolus to the nucleoplasm concomitant with its deSUMOylation. Loss of EXOSC10 SUMOylation does not detectably affect rRNA maturation but affects the mRNA transcriptome by modulating the expression levels of hypoxia-related genes. Our data suggest that dynamic modulation of EXOSC10 SUMOylation and localization under hypoxia regulates the RNA degradation machinery to facilitate cellular adaptation to low oxygen conditions.

2024-01-30 | GSE229894 | GEO

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