Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

8 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Stabilized biological production by product addiction

ABSTRACT: Populations of engineered metabolite-producing microorganisms are prone to evolutionary production declines during industrial-scale cultivations. In this study, we develop a synthetic product addiction system in E coli that addicts mevalonic acid production cells to mevalonic acid. Through experimentally simuluated long-term fermentation, we investigate how product-addicted organisms remain stable and avoid formation of genetic subpopulations of fit, non-producing cells.

INSTRUMENT(S): Illumina MiSeq

ORGANISM(S): Escherichia coli K-12

SUBMITTER: Peter Rugbjerg

PROVIDER: E-MTAB-6182 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Time-lapse Deep-seq of E. coli Metabolite Production Pathway

Project description:Understand the mechanisms of evolution in large-scale bio-production by tracking population dynamics leading to production decline in mevalonic acid-producing Escherichia coli. Industrial bioproduction entails growth of the production host to large bioreactors (e.g. 1-300 m3). This may put the organism at risk for generating non-producing subpopulations of genetic heterogeneity, which is not phenotypically detected at lab-scale (e.g. 2 L). To study these dynamics, we experimentally simulated these growth durations by passing mevalonic acid-producing E. coli to maintain the populations in exponential growth for 45 generations.

2018-01-19 | E-MTAB-5862 | biostudies-arrayexpress

Strain-dependent Genetic Heterogeneity Shapes Long-term Stability of Bioproduction in E. coli

Project description:Deep-sequencing of the engineered production genes in five E coli production chassis strains (BL21(DE3), MG1655, TOP10, W and W3110) producing two case metabolic products, 2,3-butanediol and mevalonic acid

2020-11-17 | E-MTAB-9800 | biostudies-arrayexpress

Lymphomas that recur after MYC suppression continue to exhibit oncogene addiction

Project description:The suppression of oncogenic levels of MYC is sufficient to induce sustained tumor regression associated with proliferative arrest, differentiation, cellular senescence and/or apoptosis, a phenomenon known as oncogene addiction. However, after prolonged inactivation of MYC in a conditional transgenic mouse model of Em-tTA/tetO-MYC T-acute lymphomablastic lymphoma (T-ALL), some of the tumors recur, recapitulating what is frequently observed in human tumors in response to targeted therapies. Here we report that these recurring lymphomas express high levels of either transgenic or endogenous Myc suggesting that tumors continue to be addicted to oncogenic levels of MYC. Many of the recurring lymphomas (76%) harbored mutations in the tetracycline transactivator (tTA) resulting in expression of the MYC transgene even in the presence of doxycycline. Many of the remaining recurring tumors expressed high levels of endogenous Myc which was in some cases associated with a genomic rearrangement of the endogenous Myc locus or overexpression of Notch1. Gene expression profiling confirmed that the primary and recurring tumors have highly similar transcriptomes. Importantly, shRNA-mediated suppression of the high levels of MYC in recurring tumors elicited both suppression of proliferation and increased apoptosis confirming that these tumors remain oncogene addicted. These results suggest that tumors caused by MYC overexpression remain addicted to high levels of expression of this oncogene. 13 samples, no replicates included

2011-09-23 | E-GEOD-32341 | biostudies-arrayexpress

A specific prelimbic-nucleus accumbens pathway controls resilience versus vulnerability to develop food addiction.

Project description:The aim of this study was to analyse the whole transcriptome profile of medial prefrontal cortex of food addicted and non-addicted Glu-CB1-WT and Glu-CB1-KO mice using total RNA-seq.

2020-02-18 | GSE139482 | GEO

Lymphomas that recur after MYC suppression continue to exhibit oncogene addiction

2011-09-24 | GSE32341 | GEO

miR-125b: A Rheostat of Growth versus Stress-Induced MAPKs That Governs Stemness and OncomiR Addiction in Skin

Project description:We analyze the globel gene expression changes in the tumor initiating cells of regressing miR-125b addicted tumors after oncomiR withdrawal

2014-02-12 | GSE54704 | GEO

Stabilized biological production by product addiction

Project description:Stabilized biological production by product addiction

| PRJEB24416 | ENA

Proteomic and phosphoproteomics profiling depict drug addiction mechanisms in BRAFi-resistant melanoma

Project description:Acquired resistance to MAPK inhibitors limits the clinical efficacy in melanoma treatment. We and others have recently shown that BRAF inhibitors (BRAFi)-resistant melanoma cells can develop a dependency on the therapeutic drugs to which they have acquired resistance, creating a vulnerability for these cells that can potentially be exploited in cancer treatment. In drug addicted melanoma cells, it was shown that this induction of cell death was preceded by a specific ERK2-dependent phenotype switch, however, the underlying molecular mechanisms are largely lacking. To increase the molecular understanding of this drug dependency, we applied a mass spectrometry-based proteomic approach on BRAFi-resistant BRAFMUT 451Lu cells, in which ERK1, ERK2 and JUNB were silenced separately using CRISPR–Cas9. Inactivation of ERK2 and, to a lesser extent, JUNB prevents drug addiction in these melanoma cell while, conversely, knock out of ERK1 fails to reverse this phenotype, showing a response similar to control cells. Our analysis reveals that ERK2 and JUNB share comparable proteome responses dominated by reactivation of cell division. Importantly, we find that EMT activation in drug addicted melanoma cells upon drug withdrawal is affected by silencing ERK2 but not ERK1. Moreover, transcription factor (regulator) enrichment shows that PIR acts as an effector of ERK2 and phosphoproteome analysis reveals that silencing of ERK2 but not ERK1 leads to amplification of GSK3 kinase activity. Our results depict possible mechanisms of drug addiction in melanoma, which may provide a guide for strategies in drug-resistant melanoma.

2022-02-17 | PXD026557 | Pride

ADDICTION OF MERKEL CELL CARCINOMA TO MUC1-C IDENTIFIES A POTENTIAL NEW TARGET FOR TREATMENT OF THIS RECALCITRANT MALIGNANCY

Project description:MCCP and MCCN cells are addicted to the oncogenic MUC1-C protein. MUC1-C is a druggable target that may provide new opportunities for advancing MCC treatment.

2021-07-29 | GSE180876 | GEO

ADDICTION OF MERKEL CELL CARCINOMA TO MUC1-C IDENTIFIES A POTENTIAL NEW TARGET FOR TREATMENT OF THIS RECALCITRANT MALIGNANCY [MCC26]

Project description:MCCP and MCCN cells are addicted to the oncogenic MUC1-C protein. MUC1-C is a druggable target that may provide new opportunities for advancing MCC treatment.

2021-07-30 | GSE180891 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data