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Defining changes in the levels of Ub-modified peptides upon rpn-6 knockdown

ABSTRACT: Here we defined changes in the levels of Ub-modified peptides upon rpn-6 knockdownthat in young C. elegans adults (day 5)

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Caenorhabditis Elegans

TISSUE(S): Whole Body

SUBMITTER: David Vilchez

LAB HEAD: David Vilchez

PROVIDER: PXD024094 | Pride | 2021-05-26

REPOSITORIES: Pride

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			Action	DRS
	2018127_Q1_AWH_ColID_747_ProjID_1562_Vilchez_sample_1_Vector_RNAi_1.raw	Raw
	2018127_Q1_AWH_ColID_747_ProjID_1562_Vilchez_sample_2_Vector_RNAi_2.raw	Raw
	2018127_Q1_AWH_ColID_747_ProjID_1562_Vilchez_sample_3_Vector_RNAi_3.raw	Raw
	2018127_Q1_AWH_ColID_747_ProjID_1562_Vilchez_sample_4_RPN-6_RNAi_1.raw	Raw
	2018127_Q1_AWH_ColID_747_ProjID_1562_Vilchez_sample_5__RPN-6_RNAi_2.raw	Raw

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Publications

Rewiring of the ubiquitinated proteome determines ageing in C. elegans.

Koyuncu Seda S Loureiro Rute R Lee Hyun Ju HJ Wagle Prerana P Krueger Marcus M Vilchez David D

Nature 20210728 7871

Ageing is driven by a loss of cellular integrity<sup>1</sup>. Given the major role of ubiquitin modifications in cell function<sup>2</sup>, here we assess the link between ubiquitination and ageing by quantifying whole-proteome ubiquitin signatures in Caenorhabditis elegans. We find a remodelling of the ubiquitinated proteome during ageing, which is ameliorated by longevity paradigms such as dietary restriction and reduced insulin signalling. Notably, ageing causes a global loss of ubiquitinatio ...[more]

PMID: 34321666

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Defining changes in the steady-state levels of ubiquitinated peptides in aging and longevity

Project description:We performed diGLY enrichment followed by label-free proteomics in C. elegans to define and quantify changes in the ubiquitinated (Ub)-proteome during the aging process. More specifically, we compared wild-type worms at the first day of adulthood with young (day 5), mid-age (day 10) and aged adults (day 15). Moreover, we assessed the Ub-modified proteome of age-matched long-lived genetic models of dietary restriction (eat-2(ad1116)) and reduced reduced insulin/IGF-1 signaling (daf-2(e1370)).

2021-05-27 | PXD024338 | Pride

Defining changes in the total levels of proteins upon RPN-6 RNAi

Project description:Here we defined changes in the total levels of individual proteins upon RPN-6 RNAi in young C. elegans adults (day 5)

2021-05-26 | PXD024095 | Pride

Defining changes in the total levels of proteins during aging of C. elegans

Project description:We performed label-free proteomics in C. elegans to define and quantify changes in the ubiquitinated (Ub)-proteome during the aging process. More specifically, we compared wild-type worms at the first day of adulthood with young (day 5), mid-age (day 10) and aged adults (day 15). Moreover, we assessed protein levels of age-matched long-lived genetic models of dietary restriction (eat-2(ad1116)) and reduced insulin/IGF-1 signaling (daf-2(e1370)).

2021-05-26 | PXD025128 | Pride

Ubiquitinome of Plasmodium yoelii lines NSS and NSR

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HELA cells Sphingolipid pulldown (Cers6 and Cers5)

Project description:Ectopic lipid deposition and altered mitochondrial dynamics contribute to the development of obesity and insulin resistance. However, the mechanistic link between both processes remains unclear. Here we demonstrate that abrogation of ceramide synthase (CerS)6, which generates C16:0-sphingolipids, but not of the alternative C16:0-sphingolipid synthetizing CerS5 protects from obesity and insulin resistance, and both enzymes regulate C16:0-sphingolipid synthesis in distinct intracellular compartments. Moreover, we identify proteins, which specifically interact with C16:0-sphingolipids derived from CerS5 or CerS6. Here, only CerS6-derived C16:0-sphingolipids bind the mitochondrial fission factor (Mff). CerS6- and Mff-deficiency protects from fatty acid-induced mitochondrial fragmentation in vitro, and both proteins genetically interact in vivo in obesity-induced mitochondrial fragmentation and development of insulin resistance. Our experiments reveal an unprecedented specificity of sphingolipid-signaling depending on specific synthetizing enzymes, provide a mechanistic link between lipid deposition and mitochondrial dynamics in obesity, and define the CerS6/sphingolid/Mff interaction as a therapeutic target for obesity and diabetes.

2019-05-20 | PXD007158 | Pride

HEK NICD AP-MS - Notch signaling is a core patterning module for vascular morphogenesis, which co-determines the sprouting behaviour of endothelial cells (ECs)

Project description:Notch signaling is a core patterning module for vascular morphogenesis, which co-determines the sprouting behaviour of endothelial cells (ECs). Tight quantitative and temporal control of Notch activity is essential for vascular development, yet the details of Notch regulation in ECs are incompletely understood. We found that ubiquitin-specific peptidase 10 (USP10) interacted with the NOTCH1 intracellular domain (NICD1) to slow the ubiquitin-dependent turnover of this short-lived form of the activated NOTCH1 receptor. Accordingly, inactivation of USP10 reduced NICD1 abundance and stability, and diminished Notch-induced target gene expression in ECs. In mice, loss of endothelial Usp10 increased vessel sprouting and partially restored the patterning defects caused by ectopic expression of NICD1. Thus, USP10 functions as an NICD1 deubiquitinase, which fine-tunes endothelial Notch responses during angiogenic sprouting.

2019-04-11 | PXD013192 | Pride

Promoters Active in Interphase are Bookmarked during Mitosis by Ubiquitination

Project description:We analyzed genome-wide modification of chromatin by ubiquitination in human cells and whether this mark changes through the cell cycle using modified ChIP-seq technique (ChAP-seq). Chromatin affinity purification was based on a standard ChIP method with modification of a two-step affinity purification.

2013-04-04 | E-GEOD-45771 | biostudies-arrayexpress

The Insulin/IGF Signaling Cascade Modulates SUMOylation to Regulate Aging and Proteostasis in C. elegans.

Project description:In this project we asked how reducing the activity of the insulin/IGF signaling (IIS) cascade by knocking down the expression of daf-2, affects global protein SUMOylation of C. elegans. We found that among other proteins, IIS reduction lowers the SUMOylation of CAR-1, a protein that negatively regulates the activity of the worm’s notch receptor, GLP-1. Thus, the knockdown of car-1 hyper-activates GLP-1, shortens lifespan and exposes the worm to toxic protein aggregation (proteotoxicity). In contrast, the expression of a SUMOylation resistant CAR-1 (K185R) promotes longevity and protects model nematodes from proteotoxicity.

2018-06-06 | PXD010011 | Pride

Proteome dysregulation induced by 5-fluoro-2′-deoxyuridine (FUdR) in C. elegans

Project description:The effect of 5-fluoro-2′-deoxyuridine (FUdR) on the proteome of C. elegans (wild type and glp-1/skn-1 mutants) was studied. Total protein extracts were obtained from the wild type and mutant worms subjected to the FUdR or control treatment and relative protein levels assessed by shotgun proteomics (TMT).

2024-07-18 | PXD045805 | Pride

K48- and K63-linked ubiquitin chain interactome reveals branch- and length-specific ubiquitin interactors

Project description:Ubiquitin-interactor co-pulldown coupled with mass spectrometry used to elucidate K48- and K63-linked interactomes including those of Ub chains of varying length (Ub-Ub3) and heterotypic branched Ub chains. Ubiquitin-interactors were enriched from human HeLa and yeast s. cerevisiae cell lysate with either chloroacetamide (CAA) or N-ethylmaleimide (NEM) as DUB inhibitors.

2024-05-15 | PXD051890 | Pride

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