Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

NRS1, a nitrogen source-regulated microprotein, confers an alternative mechanism of G1/S transcriptional activation in budding yeast

ABSTRACT: Commitment to cell division at the end of G1 phase, termed Start in the budding yeast Saccharomyces cerevisiae, is strongly influenced by nutrient availability. To identify newdominant activators of Start that might operate under different nutrient conditions, we screened a genome-wide ORF overexpression library for genes that bypass a Start arrest caused by absence of the G1 cyclin Cln3 and the transcriptional activator Bck2. We recovered a hypothetical gene YLR053c, renamed NRS1 for Nitrogen-responsive Start Regulator 1, which encodes a poorly characterized 108 amino acid microprotein. Endogenous NRS1 was nuclear-localized, restricted to poor nitrogen conditions, induced upon mTORC1 inhibition, and cell cycle-regulated with a peak at Start. NRS1 interacted genetically with SWI4 and SWI6, which encode the master G1/S transcription factor complex SBF. Correspondingly, NRS1 physically interacted with Swi4 and Swi6 and was localized to G1/S promoter DNA. NRS1 exhibited inherent transactivation activity and fusion of NRS1 to the SBF inhibitor Whi5 was sufficient to suppress other Start defects. NRS1 appears to be a recently evolved microprotein that rewires the G1/S transcriptional machinery under poor nutrient conditions.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Saccharomyces Cerevisiae (baker's Yeast)

TISSUE(S): Cell Culture

SUBMITTER: Eric Bonneil

LAB HEAD: Mike Tyers

PROVIDER: PXD018681 | Pride | 2021-08-25

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	Service_Tyers_110319_1.mgf	Mgf
	Service_Tyers_110319_1.mzid.gz	Mzid
	Service_Tyers_110319_1.pride.mgf.gz	Mgf
	Service_Tyers_110319_1.pride.mztab.gz	Mztab
	Service_Tyers_110319_1.raw	Raw

Items per page:

1 - 5 of 10

Similar Datasets

A nitrogen source-regulated microprotein confers an alternative mechanism of G1/S transcriptional activation in budding yeast

Project description:Commitment to cell division at the end of G1 phase, termed Start in the budding yeast Saccharomyces cerevisiae, is strongly influenced by nutrient availability. To identify new dominant activators of Start that might operate under different nutrient conditions, we screened a genome-wide ORF overexpression library for genes that bypass a Start arrest caused by absence of the G1 cyclin Cln3 and the transcriptional activator Bck2. We recovered a hypothetical gene YLR053c, renamed NRS1 for Nitrogen-Responsive Start regulator 1, which encodes a poorly characterized 108 amino acid microprotein. Endogenous Nrs1 was nuclear-localized, restricted to poor nitrogen conditions, induced upon mTORC1 inhibition, and cell cycle-regulated with a peak at Start. NRS1 interacted genetically with SWI4 and SWI6, which encode subunits of the main G1/S transcription factor complex SBF. Correspondingly, Nrs1 physically interacted with Swi4 and Swi6 and was localized to G1/S promoter DNA. Nrs1 exhibited inherent transactivation activity and fusion of Nrs1 to the SBF inhibitor Whi5 was sufficient to suppress other Start defects. Nrs1 appears to be a recently evolved microprotein that rewires the G1/S transcriptional machinery under poor nutrient conditions.

2021-08-25 | GSE179366 | GEO

Microprotein knockout in rescue cell lines and control conditions

Project description:Microprotein knockout in rescue cell lines and control conditions

| PRJNA971880 | ENA

A nitrogen source-regulated microprotein confers an alternative mechanism of G1/S transcriptional activation in budding yeast

Project description:A nitrogen source-regulated microprotein confers an alternative mechanism of G1/S transcriptional activation in budding yeast

| PRJNA743354 | ENA

MAVI1, an Endoplasmic Reticulum-localized Microprotein, Suppresses Antiviral Innate Immune Response by Targeting MAVS on Mitochondrion

Project description:Pattern recognition receptors (PRRs)-mediated innate immune responses are critical for host defense against microbial pathogens including RNA/DNA viruses. A growing number of coding genes and genes originally defined as non-coding RNAs (ncRNAs) are found to encode short peptides or proteins, named microproteins. However, the landscape of microproteins in responsive to virus infection and the functions of these microproteins remain uncharacterized. Here, we systematically identified microproteins, both from coding and non-coding genes, that are responsive to Vesicular Stomatitis Virus (VSV) infection. Among which, a highly conserved, endoplasmic reticulum (ER) membrane-localized microprotein, , MAVI1 (microprotein in antiviral immunity 1), was found to interact with mitochondrial localized MAVS protein, inhibiting the aggregation of MAVS and the activation of downstream type I interferon (IFN) signaling pathway. The critical role of MAVI1 was highlighted that viral infection was significantly attenuated and survival rate was significantly increased in Mavi1 knockout mice in vivo. A peptide inhibitor targeting the interaction between MAVI1 and MAVS is potent in activating the type I IFN signaling and defending viral infection both in vitro and in vivo. Our findings uncovered that microproteins could play critical roles in regulating antiviral innate immune responses via cross-organelle interaction, and targeting microproteins might represent a potential therapeutic avenue for treating viral infection in clinic.

2024-02-15 | GSE221218 | GEO

The microprotein Minion controls cell fusion and muscle formation

Project description:These findings establish minion as a novel microprotein required for muscle development, and define a two-component program for the induction of mammalian cell fusion.

2017-05-19 | GSE97764 | GEO

Dual regulation of nitrogen metabolism by CodY and GlnR in Streptococcus mutans

Project description:CodY and GlnR are two major transcriptional regulators in nitrogen metabolism in Gram-positive bacteria. CodY regulates genes involved in the adaptive response to poor growth conditions, especially to nutrient limitation. GlnR controls nitrogen utilization according to the availability of nitrogen source. In this study we used microarray to investigate the regulatory roles that CodY and GlnR play in nitrogen metabolism in Streptococcus mutans.

2010-07-01 | GSE13540 | GEO

Microprotein knockout in rescue cell lines and control conditions

Project description:RNA-seq sequencing was carried out to investigate which expression alterations were induced by treatment with sgRNAs targeting the sORFs/microproteins of interest. To test whether any of these changes could be reversed in the microprotein rescue-GFP fusion cells, transcriptional alterations of rescue and parental cells were compared.

2023-10-09 | GSE232375 | GEO

hnRNPA is a novel regulator of a mitochondrial microprotein expression

Project description:Mitochondrial-derived peptides (MDPs) are microproteins that are encoded by short open reading frames within the mitochondrial genome. Several MDPs have been identified in recent years; however, the transcriptional and translational regulation of MDPs remain poorly understood. Here we discovered an RNA binding protein of an MDP called humanin. By conducting RNA pull-down assays from mitochondrial extracts, we confidently pinpointed three humanin RNA binding partners that regulate translation: heterogeneous nuclear ribonucleoproteins A1 (hnRNPA1), hnRNPA2, and hnRNPA3. We also identified a novel post-translational modification in the form of succinylation in hnRNPA1 at lysine residue K-106. Succinylation of hnRNPA1 plays an important role in mitochondrial translocation and binding affinity of hnRNPA1 to humanin mRNA. Furthermore, hnRNPA1 and humanin are highly co-expressed in prostate cancer. We provide the first evidence of mRNA binding proteins modulating the expression of a mitochondrial microprotein. This study articulates important new roles of ribonucleoproteins in modulating microprotein expression in mitochondria.

2024-12-08 | GSE169283 | GEO

Microprotein-Encoding RNA Regulation in Cells Treated with Pro-inflammatory and Pro-Fibrotic Stimuli (RNA-Seq Caco2)

Project description:Recent analysis of the human proteome via proteogenomics and ribosome profiling of the transcriptome revealed the existence of thousands of previously unannotated microprotein-coding small open reading frames (smORFs). Most functional microproteins were chosen for characterization because of their evolutionary conservation. However, one example of a non-conserved immunomodulatory microprotein in mice suggests that strict sequence conservation misses some intriguing microproteins. Here, we examine the ability of gene regulation to identify human microproteins with potential roles in inflammation or fibrosis of the intestine. To do this, we collected ribosome profiling data of intestinal cell lines and peripheral blood mononuclear cells (PBMCs), and then used gene expression of microprotein-encoding transcripts to identify strongly regulated microproteins, including several examples of microproteins that are only conserved with primates. This approach reveals a number of new microproteins worthy of additional functional characterization, and provides a dataset that can be queried in different ways to find additional gut microproteins of interest.

2024-10-23 | GSE269372 | GEO

Microprotein-Encoding RNA Regulation in Cells Treated with Pro-inflammatory and Pro-Fibrotic Stimuli (Ribo-Seq Caco2)

2024-10-23 | GSE269370 | GEO