Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Proteomics data of extruded germlines from C. elegans upon cey-3 RNAi

ABSTRACT: To shed light on how proteostasis defects in the germline influence somatic tissues, we first assessed the intracellular changes induced by PGL-1 aggregation in germline cells. For this purpose, we examined the proteome of isolated germlines from C. elegans following cey-3 knockdown

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Caenorhabditis Elegans

TISSUE(S): Germ Cell

SUBMITTER: David Vilchez

LAB HEAD: David Vilchez

PROVIDER: PXD025694 | Pride | 2021-04-28

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	EV_120190104_Q1_UC_ColID_747_ProjID_1569_Vilchez_sample_01.raw	Raw
	EV_220190104_Q1_UC_ColID_747_ProjID_1569_Vilchez_sample_02.raw	Raw
	EV_320190104_Q1_UC_ColID_747_ProjID_1569_Vilchez_sample_03.raw	Raw
	cey-3_120190104_Q1_UC_ColID_747_ProjID_1569_Vilchez_sample_07.raw	Raw
	cey-3_220190104_Q1_UC_ColID_747_ProjID_1569_Vilchez_sample_08.raw	Raw

Items per page:

1 - 5 of 9

Similar Datasets

Comparison non-targeting hRNA hESCs versus UBE2K shRNA hESCs

Project description:Histones modulate gene expression by chromatin compaction, regulating numerous processes such as differentiation. However, the mechanisms underlying histone degradation remain elusive. When compared with their differentiated counterparts, immortal human embryonic stem cells (hESCs) have a unique chromatin architecture and low levels of trimethylated histone H3 at lysine 9 (H3K9me3), a heterochromatin-associated modification. Here we assess a link between the intrinsic epigenetic landscape and ubiquitin-proteasome system of hESCs. We find that hESCs exhibit high expression of UBE2K, a ubiquitin-conjugating enzyme. Loss of UBE2K increases the levels of H3K9 trimethyltransferase SETDB1, resulting in H3K9 trimethylation and repression of neurogenic genes during differentiation. Concomitantly, loss of UBE2K impairs the ability of hESCs to differentiate into neural progenitors with neurogenic properties. Besides H3K9 trimethylation, we find that UBE2K binds histone H3 to induce its polyubiquitination and degradation by the proteasome. Notably, ubc-20, the worm orthologue of UBE2K, also regulates both histone H3 levels and H3K9 trimethylation in C. elegans germline. Thus, our results indicate that UBE2K crosses evolutionary boundaries to promote histone H3 degradation and reduce H3K9me3 repressive marks in immortal cells.

2020-06-01 | PXD018625 | Pride

A post-transcriptional program coordinated by CSDE1 prevents intrinsic neural differentiation of human embryonic stem cells

Project description:While the transcriptional network of human embryonic stem cells (hESCs) has been extensively studied, relatively little is known about how post-transcriptional modulations determine hESC function. RNA-binding proteins play central roles in RNA regulation, including translation and turnover. Here we show that the RNA-binding protein CSDE1 is highly expressed in hESCs to maintain their undifferentiated state and prevent default neural fate. Notably, loss of CSDE1 accelerates neural differentiation and potentiates neurogenesis. Conversely, ectopic expression of CSDE1 impairs neural differentiation. We find that CSDE1 post-transcriptionally modulates core components of multiple regulatory nodes of hESC identity, neuroectoderm commitment and neurogenesis. Among these key pro-neural/neuronal factors, CSDE1 binds fatty acid binding protein 7 (FABP7) and vimentin (VIM) mRNAs as well as transcripts involved in neuron projection development regulating their stability and translation. Thus, our results uncover CSDE1 as a central post-transcriptional regulator of hESC identity and neurogenesis.

2018-05-16 | PXD007270 | Pride

Somatic increase of CCT8 mimics proteostasis of human pluripotent stem cells and extends C. elegans lifespan

Project description:Human embryonic stem cells can replicate indefinitely while maintaining their undifferentiated state and, therefore, are immortal in culture. This capacity may demand avoidance of any imbalance in protein homeostasis (proteostasis) that would otherwise compromise stem cell identity. Here we show that human pluripotent stem cells exhibit enhanced assembly of the TRiC/CCT complex, a chaperonin that facilitates the folding of 10% of the proteome. We find that ectopic expression of a single subunit (CCT8) is sufficient to increase TRiC/CCT assembly. Moreover, increased TRiC/CCT complex is required to avoid aggregation of mutant Huntingtin protein. We further show that increased expression of CCT8 in somatic tissues extends Caenorhabditis elegans lifespan in a TRiC/CCT-dependent manner. Ectopic expression of CCT8 also ameliorates the age-associated demise of proteostasis and corrects proteostatic deficiencies in worm models of Huntington’s disease. Our results suggest proteostasis is a common principle that links organismal longevity with hESC immortality.

2017-03-23 | PXD005123 | Pride

Co-immumnoprecipitation experiments to identify protein bindining partners of CSDE1

2018-05-16 | PXD007271 | Pride

HELA cells PARL Immunoprecipitation

Project description:The SPFH (Stomatin, Prohibitin, Flotillin, HflC/K) superfamily is composed of scaffold proteins that form ring-like structures and locally specify the protein-lipid composition in a variety of cellular membranes. Stomatin-like protein 2 (SLP2) is a member of this superfamily that localizes to the mitochondrial inner membrane (IM) where it acts as a membrane organizer. Here, we report that SLP2 anchors a large protease complex composed of the rhomboid protease PARL and the i-AAA protease YME1L, which we term the SPY complex (for SLP2-PARL-YME1L). Association with SLP2 in the SPY complex regulates PARL-mediated processing of PTEN-induced kinase PINK1 and the phosphatase PGAM5 in mitochondria. Moreover, SLP2 inhibits the stress-activated peptidase OMA1, which can bind to SLP2 and cleaves PGAM5 in depolarized mitochondria. SLP2 restricts OMA1-mediated processing of the dynamin-like GTPase OPA1 allowing stress-induced mitochondrial hyperfusion under starvation conditions. Together, our results reveal an important role of SLP2 membrane scaffolds for the spatial organization of IM proteases regulating mitochondrial dynamics, quality control and cell survival.

2016-10-18 | PXD004914 | Pride

YME1L1 KO Hypoxia Proteome - Lipid signalling drives proteolytic rewiring of mitochondria by YME1L

Project description:Mitochondria are central metabolic hubs whose structure and function dynamically adapt to changing metabolic demands and environmental challenges. Metabolic reprogramming of mitochondria occurs during development, cell differentiation and in disease and is coupled to changes in mitochondrial mass and shape. Here, we demonstrate that the i-AAA protease YME1L rewires the proteome of pre-existing mitochondria in response to hypoxia or nutrient starvation. Inhibition of mTORC1 induces a lipid signalling cascade via the phosphatidic acid phosphatase LIPIN1, which decreases phosphatidylethanolamine levels in mitochondrial membranes and promotes proteolysis. YME1L degrades mitochondrial protein translocases, lipid transfer proteins and metabolic enzymes to acutely limit mitochondrial biogenesis and support cell growth. Similar mitochondrial proteome changes in tumor tissues of pancreatic ductal adenocarcinoma patients suggest that YME1L is relevant to the pathophysiology of hypoxic solid tumors. Our results identify the mTORC1-LIPIN1-YME1L axis as a novel post-translational regulator of mitochondrial proteostasis at the interface of metabolism and mitochondrial dynamics.

2019-08-21 | PXD011750 | Pride

The SET-2/SET1 histone H3K4 methyltransferase maintains pluripotency in the caenorhabditis elegans germline.

Project description:Histone H3 Lys 4 methylation (H3K4me) is deposited by the conserved SET1/MLL methyltransferases acting in multiprotein complexes including Ash2 and Wdr5. While individual subunits contribute to complex activity, how they influence gene expression in a specific tissue remains largely unknown. In caenorhabditis elegans, SET-2/SET1, WDR-5.1 and ASH-2 are differentially required for germline H3K4 methylation. Using expression profiling on germlines from animals lacking set-2, ash-2 or wdr-5.1, we show that these subunits play unique and redundant functions to promote expression of germline genes and repress somatic genes. We further show that in set-2 and wdr-5.1 deficient germlines, somatic gene misexpression is associated with conversion of germ cells into somatic cells, and that nuclear RNAi acts in parallel with SET-2 and WDR-5.1 to maintain germline identity. These findings uncover a unique role for SET-2 and WDR-5.1 in preserving germline pluripotency, and underline the complexity of the cellular network regulating this process. Gene misregulation in SET1/set-2, wdr-5.1 and ash-2 defective germlines

2014-09-04 | E-GEOD-61094 | biostudies-arrayexpress

Therapeutic antibodies to ganglioside GD2 evolved from highly selective germline antibodies VI

Project description:Purpose: This study uses a high-throughput glycan microarray to evaluate the immunological evolution of antibodies to the glyco-antigen GD2. The goal is to determine germline and affinity mature antibody specificity and affinities/ Results: Affinity mature anti-GD2 antibodies 3F8 and ch14.18 had high affinity and were highly specific for the target GD2. Germline antibodies were also hihgly specific and had surprisingly high affinity. Conclusion: Antibodies to GD2 evolved from highly specific germlines. Highly specific germlines may be critical in evading autoimmunity issues.

2017-08-25 | GSE100309 | GEO

Therapeutic antibodies to ganglioside GD2 evolved from highly selective germline antibodies II

2017-08-25 | GSE99873 | GEO

Therapeutic antibodies to ganglioside GD2 evolved from highly selective germline antibodies V

2017-08-25 | GSE100308 | GEO