Histone marks in C. elegans IKB mutants
Ontology highlight
ABSTRACT:
ORGANISM(S): Caenorhabditis elegans
PROVIDER: GSE101495 | GEO | 2020/06/27
REPOSITORIES: GEO
Similar Datasets
Project description:Histone marks in C. elegans IKB mutants
| PRJNA394676 | ENA
Project description:NF-κB-mediated signaling is maintained silent by the action of IκB proteins, whose canonical role is to sequester NF-κB in the cytoplasm. An alternative chromatin role for IκB members have been shown to affect stemness and cell differentiation but the involvement of NF-κB in this function has not been excluded. NFKI-1 and IKB-1 are IκB homologs in Caenorhabditis elegans, which lacks NF-κB nuclear effectors. nfki-1 and ikb-1 mutants present developmental defects that phenocopy mutations in Polycomb genes and demethylases as utx-1. suggesting a role for C. elegans IKB proteins in chromatin regulation, which is supported by various lines of evidence:(i) we detected NFKI-1 in the nucleus; (ii) NFKI-1 and IKB-1 bind to histones and Polycomb proteins, (iii) NFKI-1 and IKB-1 bind to chromatin in vivo, and (iv) mutations in nfki-1 and ikb-1 alter chromatin marks . Thus, ancestral IκB inhibitors may exert nuclear functions regulating of gene expression and development.
2020-09-01 | GSE146654 | GEO
Project description:NF-κB-mediated signaling is maintained silent by the action of IκB proteins, whose canonical role is to sequester NF-κB in the cytoplasm. An alternative chromatin role for IκB members have been shown to affect stemness and cell differentiation but the involvement of NF-κB in this function has not been excluded. NFKI-1 and IKB-1 are IκB homologs in Caenorhabditis elegans, which lacks NF-κB nuclear effectors. nfki-1 and ikb-1 mutants present developmental defects that phenocopy mutations in Polycomb genes and demethylases as utx-1. suggesting a role for C. elegans IKB proteins in chromatin regulation, which is supported by various lines of evidence:(i) we detected NFKI-1 in the nucleus; (ii) NFKI-1 and IKB-1 bind to histones and Polycomb proteins, (iii) NFKI-1 and IKB-1 bind to chromatin in vivo, and (iv) mutations in nfki-1 and ikb-1 alter chromatin marks . Thus, ancestral IκB inhibitors may exert nuclear functions regulating of gene expression and development.
2020-09-01 | GSE146652 | GEO
Project description:Gebauer2016 - Genome-scale model of
Caenorhabditis elegans metabolism (without bacteria)
This model is one of the two versions
of ElegCyc presented in the paper. It describes the metabolism of a
worm raised in a medium without bacteria.
This model is described in the article:
A Genome-Scale Database and
Reconstruction of Caenorhabditis elegans Metabolism.
Gebauer J, Gentsch C, Mansfeld J,
Schmeißer K, Waschina S, Brandes S, Klimmasch L, Zamboni N,
Zarse K, Schuster S, Ristow M, Schäuble S, Kaleta C.
Cell Syst 2016 May; 2(5): 312-322
Abstract:
We present a genome-scale model of Caenorhabditis elegans
metabolism along with the public database ElegCyc
(http://elegcyc.bioinf.uni-jena.de:1100), which represents a
reference for metabolic pathways in the worm and allows for the
visualization as well as analysis of omics datasets.
Our model reflects the metabolic peculiarities of
C. elegans that make it distinct from other higher
eukaryotes and mammals, including mice and humans. We
experimentally verify one of these peculiarities by showing
that the lifespan-extending effect of L-tryptophan
supplementation is dose dependent (hormetic). Finally, we show
the utility of our model for analyzing omics datasets through
predicting changes in amino acid concentrations after genetic
perturbations and analyzing metabolic changes during normal
aging as well as during two distinct, reactive oxygen
species (ROS)-related lifespan-extending treatments. Our
analyses reveal a notable similarity in metabolic adaptation
between distinct lifespan-extending interventions and point to
key pathways affecting lifespan in nematodes.
This model is hosted on
BioModels Database
and identified by:
MODEL1704200000.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2017-04-20 | MODEL1704200000 | BioModels
Project description:Gebauer2016 - Genome-scale model of
Caenorhabditis elegans metabolism (with bacteria)
This model is one of the two versions
of ElegCyc presented in the paper. It describes the metabolism of a
worm raised in a medium with bacteria
This model is described in the article:
A Genome-Scale Database and
Reconstruction of Caenorhabditis elegans Metabolism.
Gebauer J, Gentsch C, Mansfeld J,
Schmeißer K, Waschina S, Brandes S, Klimmasch L, Zamboni N,
Zarse K, Schuster S, Ristow M, Schäuble S, Kaleta C.
Cell Syst 2016 May; 2(5): 312-322
Abstract:
We present a genome-scale model of Caenorhabditis elegans
metabolism along with the public database ElegCyc
(http://elegcyc.bioinf.uni-jena.de:1100), which represents a
reference for metabolic pathways in the worm and allows for the
visualization as well as analysis of omics datasets.
Our model reflects the metabolic peculiarities of
C. elegans that make it distinct from other higher
eukaryotes and mammals, including mice and humans. We
experimentally verify one of these peculiarities by showing
that the lifespan-extending effect of L-tryptophan
supplementation is dose dependent (hormetic). Finally, we show
the utility of our model for analyzing omics datasets through
predicting changes in amino acid concentrations after genetic
perturbations and analyzing metabolic changes during normal
aging as well as during two distinct, reactive oxygen
species (ROS)-related lifespan-extending treatments. Our
analyses reveal a notable similarity in metabolic adaptation
between distinct lifespan-extending interventions and point to
key pathways affecting lifespan in nematodes.
This model is hosted on
BioModels Database
and identified by:
MODEL1704200001.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2017-04-20 | MODEL1704200001 | BioModels
Project description:We have developed a single-worm RNA-seq method to effectively profile gene expression in individual C. elegans and applied this method to study C. elegans responses to pathogen infection.
2022-09-21 | GSE197834 | GEO
Project description:Interplay between metabolic state of the cell and its ability to undergo immunological activation has been recently recognized as a treasure chest of novel fundamental regulatory principles. Itaconate, and its membrane permeable derivative dimethyl itaconate (DI) were recently shown to selectively inhibit subset of cytokines during macrophage activation (e.g. Il1b, il6, Il12b but not TNF), yet the precise mechanism of this effect remained unclear. We find that selectivity of DI action stems from the inhibitory effects of electrophilic stress exerted by DI on IkB-zeta protein translation, leading to selective control of the secondary wave of Nfkb-signaling. Mechanistically, DI leads to glutathione depletion and subsequent activation of both Nrf2-dependent and Nrf2-independent stress responses. We find that IkB-zeta regulation is carried out in Nrf2-independent manner, and identify Atf3 as a key mediator of DI effects on IkB-zeta/IL6. This inhibitory effect is conserved across species and cell types, as evident from inhibition of IkB-zeta production in activating human monocytes and IL-17A stimulated keratinocytes of both human and mice. Finally, DI administration in vivo ameliorated IL17/IkB-zeta-driven skin pathology in the mouse model of psoriasis, highlighting therapeutic potential of this regulatory pathway.
2018-04-21 | GSE102190 | GEO
Project description:The nematode Caenorhabditis elegans (C. elegans) is often used as a model organism to study cell and developmental biology. Quantitative mass spectrometry has only recently been performed in C. elegans and, so far, most studies have been done on adult worm samples. Here we use quantitative mass spectrometry to characterise protein level changes across the four larval developmental stages (L1-L4) of C. elegans, in biological triplicate. In total, we identify 4,130 proteins and quantify 1,541 proteins that were identified across all four stages in all three biological repeats with at least 2 unique peptides per protein. Using hierarchical clustering and functional ontological analyses, we identify 21 protein groups containing proteins with similar protein profiles across the four stages, and highlight the most overrepresented biological functions in each of these protein clusters. In addition, we use the dataset to identify putative larval stage specific proteins in each individual developmental stage, as well as in the early and late developmental stages. In summary, this dataset provides a system-wide analysis of protein level changes across the four C. elegans larval developmental stages, which serves as a useful resource for the worm development research community.
2017-12-04 | PXD006676 | Pride
Project description:This study aims on the identification of the NF-kB dependent gene regulatory network during inflammation-associated liver carcinogenesis using the well-established Mdr2 knockout mouse model. We could identify 367 differentially expressed genes comparing expression profiles of tumor samples from Mdr2-KO mice to tumor samples derived from mice with an additional hepatocyte specific expression of an IkB-superrepressor. This IkB-superrepresser is undegradable upon ubiquitinylation initialized by Ikk dependent phosphorylation and therefore impedes NFkB activity. Keywords: NFkB, IkB-superrepressor, inflammation-associated liver carcinogenesis, Mdr2-KO mouse model, hepatocellular carcinoma, gene expression, microarray
2009-05-01 | GSE13599 | GEO
Project description:Genomic response of C. elegans after infection with Microbacterium nematophilum.<br><br>The interaction between the nematode Caenorhabditis elegans and a Gram-positive bacterial pathogen, Microbacterium nematophilum, provides a model for an innate immune response in nematodes. This pathogen adheres to the rectal and post-anal cuticle of the worm, causing slowed growth, constipation, and a defensive swelling response of rectal hypodermal cells. To explore the genomic responses that the worm activates after pathogenic attack we used microarray analysis of transcriptional changes induced after 6 hr infection, comparing virulent with avirulent infection.
2005-01-01 | E-MEXP-696 | biostudies-arrayexpress