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UFM1 E3 ligase promotes recycling of 60S ribosomal subunits from the ER

ABSTRACT: Supporting MS data for paper (doi: 10.1038/s41586-024-07073-0) by DaRosa P.A., Penchev I. et al., titled "UFM1 E3 ligase promotes recycling of 60S ribosomal subunits from the ER". Index of MS supporting files uploaded: - Related to Fig. 1a and Extended Data Fig. 1a (AO3435-AO3440: TMT proteomics (Unimod: 35; 737; 4)). - Related to Fig. 1b, c (see MSV000093721).

INSTRUMENT(S): Orbitrap Fusion Lumos, Orbitrap Exploris 480

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Alban Ordureau Joao A. Paulo

PROVIDER: MSV000093510 | MassIVE | Mon Nov 27 07:56:00 GMT 2023

REPOSITORIES: MassIVE

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UFM1 E3 ligase promotes recycling of 60S ribosomal subunits from the ER.

DaRosa Paul A PA Penchev Ivan I Gumbin Samantha C SC Scavone Francesco F Wąchalska Magda M Paulo Joao A JA Ordureau Alban A Peter Joshua J JJ Kulathu Yogesh Y Harper J Wade JW Becker Thomas T Beckmann Roland R Kopito Ron R RR

Nature 20240221 8003

Reversible modification of target proteins by ubiquitin and ubiquitin-like proteins (UBLs) is widely used by eukaryotic cells to control protein fate and cell behaviour<sup>1</sup>. UFM1 is a UBL that predominantly modifies a single lysine residue on a single ribosomal protein, uL24 (also called RPL26), on ribosomes at the cytoplasmic surface of the endoplasmic reticulum (ER)<sup>2,3</sup>. UFM1 conjugation (UFMylation) facilitates the rescue of 60S ribosomal subunits (60S) that are released aft ...[more]

PMID: 38383785

Similar Datasets

UFM1 E3 ligase promotes recycling of 60S ribosomal subunits from the ER

Project description:Supporting MS data for paper (doi: 10.1038/s41586-024-07073-0) by DaRosa P.A., Penchev I. et al., titled "UFM1 E3 ligase promotes recycling of 60S ribosomal subunits from the ER". Index of MS supporting files uploaded: Related to Related to Fig. 1b, c (xb01004(UFM1), xb01005(SBP-UFM1): LFQ IP-MS (Unimod: 35; 4)). See also MSV000093510

2023-12-22 | MSV000093721 | MassIVE

Hcr1/eIF3j is a 60S ribosomal subunit recycling accessory factor in vivo

Project description:Hcr1/eIF3j is a sub-stoichiometric subunit of eukaryotic initiation factor 3 (eIF3) that can dissociate the post-termination 40S ribosomal subunit from mRNA in vitro. We examined this ribosome recycling role in vivo by ribosome profiling and reporter assays and found that loss of Hcr1 led to reinitiation of translation in 3’UTRs, consistent with a defect in recycling. However, the defect appeared to be in recycling of the 60S subunit, rather than the 40S subunit, because reinitiation did not require an AUG codon and was suppressed by overexpression of the 60S dissociation factor Rli1/ABCE1. Consistent with a 60S recycling role, overexpression of Hcr1 could not compensate for loss of 40S recycling factors Tma64/eIF2D and Tma20/MCT-1. Intriguingly, loss of Hcr1 triggered higher expression of RLI1 via an apparent feedback loop. These findings suggest Hcr1/eIF3j is recruited to ribosomes at stop codons and may coordinate the transition to a new round of translation.

2019-05-23 | GSE124204 | GEO

Recycling of autophagosomal components from autolysosomes by the recycler complex

Project description:The autophagic SNARE protein STX17 is recruited to autophagosomes and translocated to autolysosome after fusion of autophagosomes with lysosomes 30-32. We observed that the number of autophagic vacuoles with STX17 significantly increased after 2 hours of starvation. However, the number of STX17 puncta significantly decreased during prolonged starvation of 5 hours (Fig. 1a). Interestingly, no obvious degradation of STX17 was observed after prolonged starvation (Fig. 1b)

2022-01-24 | PXD031183 | iProX

40S ribosome profiling reveals distinct roles for Tma20/Tma22 (MCT-1/DENR) and Tma64 (eIF2D) in 40S subunit recycling

Project description:The recycling of ribosomes at stop codons for use in further rounds of translation is critical for efficient protein synthesis. Removal of the 60S subunit is catalyzed by the ATPase Rli1 (ABCE1) while removal of the 40S is thought to require Tma64 (eIF2D), Tma20 (MCT-1), and Tma22 (DENR). However, it remains unclear how these Tma proteins cause 40S removal and control reinitiation of downstream translation. Here we developed an enhanced 40S ribosome footprinting strategy to directly observe intermediate steps of ribosome recycling in cells. Deletion of the genes encoding these Tma proteins resulted in broad accumulation of unrecycled 40S subunits at stop codons, directly establishing their role in 40S recycling. Furthermore, the Tma20/Tma22 heterodimer was responsible for a majority of 40S recycling events while Tma64 played a minor role. Introduction of an autism-associated mutation into TMA22 resulted in a loss of 40S recycling activity, linking ribosome recycling and neurological disease.

2021-03-01 | GSE145904 | GEO

Tma64 (eIF2D), Tma20 (MCT-1), and Tma22 (DENR) recycle post-termination 40S subunits in vivo

Project description:The recycling of ribosomal subunits after translation termination is critical for efficient gene expression. Tma64 (eIF2D), Tma20 (MCT-1), and Tma22 (DENR) function as 40S recycling factors in vitro, but it is unknown whether they perform this function in vivo or serve as alternative initiation factors. Ribosome profiling of strains missing these factors revealed 80S ribosomes queued behind the stop codon, consistent with a block in 40S recycling. We found that unrecycled ribosomes could reinitiate translation at AUG codons in the 3’UTR, as evidenced by peaks in the footprint data and 3’UTR reporter analysis. In vitro translation experiments using reporter mRNAs containing upstream ORFs (uORFs) further established that reinitiation increased in the absence of these proteins. In some cases, 40S ribosomes appeared to rejoin with 60S subunits and undergo an alternative 80S reinitiation process in 3’UTRs. These results support a crucial role for Tma64, Tma20, and Tma22 in the recycling of 40S ribosomal subunits at stop codons and translation reinitiation.

2018-08-30 | GSE108942 | GEO

Hcr1/eIF3j is a 60S ribosomal subunit recycling accessory factor in vivo

Project description:Hcr1/eIF3j is a 60S ribosomal subunit recycling accessory factor in vivo

| PRJNA510985 | ENA

In Vitro Transcription Recycling Assay Identifies PAF1 as a Driver of RNA Pol II Recycling

Project description:RNA Polymerase II transcriptional recycling is an underappreciated mechanism for which the required factors and contributions to overall gene expression levels are poorly understood. We describe an in vitro methodology facilitating unbiased identification of novel RNA Pol II transcriptional recycling factors and quantitative measurement of transcriptional output from recycled transcriptional components. Proof-of-principle experiments identified PAF1 complex components among recycling factors and detected defective transcriptional output from RNA Pol II recycling following PAF1 depletion. Dynamic ChIP-seq confirmed in vivo PAF1 complex cycling through gene bodies with RNA Pol II and recycling back to the transcription start sites, while PAF1 silencing triggered defective RNA Pol II recycling. Prostate tumors exhibited enhanced transcriptional recycling, which was attenuated by antibody-based PAF1 depletion. These findings identify RNA Pol II recycling as a potential target in cancer and demonstrate the assay’s applicability to characterize RNA Pol II recycling in cells and tissues from other disease states.

2021-10-07 | GSE133655 | GEO

The Alzheimer’s gene SORL1 is a key regulator of endosomal recycling in human neurons

Project description:Loss of the Sortilin-related receptor 1 (SORL1) gene seems to act as a causal event for Alzheimer’s disease (AD). Recent studies have established that loss of SORL1, as well as mutations in autosomal dominant AD genes APP and PSEN1/2, pathogenically converge by swelling early endosomes, AD’s cytopathological hallmark. Acting together with the retromer trafficking complex, SORL1 has been shown to regulate the recycling of the amyloid precursor protein (APP) out of the endosome, contributing to endosomal swelling and to APP misprocessing. We hypothesized that SORL1 plays a broader role in neuronal endosomal recycling and used human induced pluripotent stem cell derived neurons (hiPSC-Ns) to test this hypothesis. In SORL1 deficient (SORL1KO) cell lines, we map the trafficking of the glutamate receptor and the BDNF neurotrophic receptor, two kinds of transmembrane proteins that depend on endosomal recycling and that are linked to AD pathophysiology. We find that as with APP, SORL1 is required for efficient endosomal recycling of the glutamate receptor AMPA1 (GLUA1) and the BDNF receptor Tropomyosin-related kinase B (TRKB). Next, we used cell lines engineered to overexpress SORL1 and find that increased SORL1 expression enhances recycling for APP and GLUA1. Finally, we performed an unbiased transcriptomic screen of SORL1KO neurons and the data further support SORL1’s role in endosomal recycling. We observed altered expression networks that regulate cell surface trafficking and neurotrophic signaling. Collectively, and together with other recent observations, these findings suggest that SORL1 is a key and broad regulator of retromer-dependent endosomal recycling in neurons, a conclusion that has both pathogenic and therapeutic implications.

2022-03-01 | GSE180793 | GEO

Phosphorylated MED1 Links Transcription Recycling and Cancer Growth

Project description:Mammalian RNA polymerase II (Pol II) initiation, elongation, termination and reinitiation are well studied, but how Pol II dynamically recycles after the transcription cycle remains unclear. By establishing in vitro and in vivo transcription recycling systems, we find that human Mediator 1 (MED1), when phosphorylated at the mammal-specific threonine 1032 by cyclin-dependent kinase 9, dynamically travels with Pol II throughout the transcribed genes to drive Pol II recycling. Mechanistically, MED1 phosphorylation leads to an increase of recycled Pol II via the molecular bridge of MED31, enhancing mRNA output during the transcription recycling process. Importantly, MED1 phosphorylation increases during prostate cancer progression to the lethal phase, and pharmacological inhibition of CDK9 decreases prostate tumor growth through decreasing MED1 phosphorylation and Pol II recycling. Our findings reveal essential mechanisms underlying Pol II recycling and suggest a neglected, yet fundamental Pol II transcription process for therapeutic intervention.

2022-04-20 | GSE127894 | GEO

Human cerebrospinal fluid autoantibody lipid microarray profiling

Project description:This SuperSeries is composed of the following subset Series: GSE37664: Human cerebrospinal fluid autoantibody lipid microarray profiling (Fig. 1A) GSE37670: Human cerebrospinal fluid autoantibody lipid microarray profiling (Fig. 2A) GSE37826: Human cerebrospinal fluid autoantibody lipid microarray profiling (Fig. 2C) Refer to individual Series

2012-05-08 | E-GEOD-37830 | biostudies-arrayexpress

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