Ontology highlight
ABSTRACT:
PROVIDER: PRJNA531242 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8862072.fastq.gz | Fastqsanger.gz | |||
| SRR8862073.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 2 of 2 |
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Project description:Polyketide synthase (PKS) and nonribosomal peptide synthetase (NRPS) hybrid systems typically use complex protein-protein interactions to facilitate direct transfer of intermediates between these multimodular megaenzymes. In the canal-associated neurons (CANs) of Caenorhabditis elegans, PKS-1 and NRPS-1 produce the nemamides, the only known hybrid polyketide-nonribosomal peptides biosynthesized by animals, through a poorly understood mechanism. Here, we use genome editing and mass spectrometry to map the roles of individual PKS-1 and NRPS-1 enzymatic domains in nemamide biosynthesis. Furthermore, we show that nemamide biosynthesis requires at least five additional enzymes expressed in the CANs that are encoded by genes distributed across the worm genome. We identify the roles of these enzymes and discover a mechanism for trafficking intermediates between a PKS and an NRPS. Specifically, the enzyme PKAL-1 activates an advanced polyketide intermediate as an adenylate and directly loads it onto a carrier protein in NRPS-1. This trafficking mechanism provides a means by which a PKS-NRPS system can expand its biosynthetic potential and is likely important for the regulation of nemamide biosynthesis.
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Project description:We observed that deletion of polyketide synthase (pks) from E. coli NC101 reduces its ability to induce tumors in interleukin-10 knockout (Il10-/-) mice injected with azoxymethane (AOM), without altering histologic inflammation. The goal of this experiment is to assess inflammatory cytokine levels in colonic tissue of these mice.
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Project description:Using genetic engineering tools available for the model organism Aspergillus nidulans, we constructed two recombinant strains; one expressing the model polyketide Penicillium griseofulvum 6-methylsalicylic acid (6-MSA) polyketide synthase gene, and one expressing the 6-MSA gene and overexpressing the native phosphoketolase (phk) for increasing the pool of polyketide precursor levels. The physiology of the recombinant strains and a reference wild type were characterized on glucose, xylose, glycerol and ethanol medium in controlled bioreactors. Glucose was found to be the preferable carbon source for 6-MSA production and 6-MSA titers up to 455 mg/L were achieved. Our findings indicate that overexpression of phk does not directly improve 6-MSA production on glucose but if the lower glycolysis is lowered, it is possible to obtain quite high conversion yields of sugar to 6-MSA. Systems biology tools were employed for in-depth analysis of the metabolic processes. Transcriptome analysis of 6-MSA producing strains on glucose and xylose in the presence and absence of phk overexpression combined with flux and physiology data enabled us to propose a model of phk/6msas interaction describing two different responses influencing 6-MSA production. Four strains on two carbon sources
2009-02-27 | E-GEOD-12859 | biostudies-arrayexpress
Project description:Knockout mutants of polyketide synthase genes were generated (pks1, pks2, pks3, pks14, pks18, pks37) and compared to wild-type AX2 strain of Dictyostelium discoideum using Agilent custom microarrays. The Dictyostelium cells were harvested at eight developmental stages (Amoeboid, Intiation of starvation, loose aggregate, Streaming, Mound, Slug, early culminant, Fruiting body) and subjected to microarray based expression profiling.
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Project description:We observed that deletion of polyketide synthase (pks) from E. coli NC101 reduces its ability to induce tumors in interleukin-10 knockout (Il10-/-) mice injected with azoxymethane (AOM), without altering histologic inflammation. The goal of this experiment is to assess inflammatory cytokine levels in colonic tissue of these mice. 2 germ-free Il10-/- mice were assayed and used as controls. 3 E. coli NC101 and 3 E. coli NC101-delta-pks monoassociated mice were experimental samples.
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Project description:Using genome-wide transcriptional profiling and whole-mount expression analyses of zebrafish larvae, we have identified hyaluronan synthase 3 (has3) as an upregulated gene during caudal fin regeneration. has3 expression is induced in the wound epithelium within hours after tail amputation, and its onset and maintenance requires fibroblast growth factor, phosphoinositide 3-kinase, and transforming growth factor-β signaling. Inhibition of hyaluronic acid (HA) synthesis by the small molecule 4-methylumbelliferone (4-MU) impaired tail regeneration in zebrafish larvae by preventing injury-induced cell proliferation. In addition, 4-MU reduced the expression of genes associated with wound epithelium and blastema function. Treatment with the glycogen synthase 3-kinase inhibitors rescued 4-MU-induced defects in cell proliferation and tail regeneration, even though only a subset of wound epithelium and blastema markers was restored. Our findings uncover a role for HA biosynthesis in zebrafish tail regeneration and its epistatic relationships with other regenerative processes.
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Project description:Using genetic engineering tools available for the model organism Aspergillus nidulans, we constructed two recombinant strains; one expressing the model polyketide Penicillium griseofulvum 6-methylsalicylic acid (6-MSA) polyketide synthase gene, and one expressing the 6-MSA gene and overexpressing the native phosphoketolase (phk) for increasing the pool of polyketide precursor levels. The physiology of the recombinant strains and a reference wild type were characterized on glucose, xylose, glycerol and ethanol medium in controlled bioreactors. Glucose was found to be the preferable carbon source for 6-MSA production and 6-MSA titers up to 455 mg/L were achieved. Our findings indicate that overexpression of phk does not directly improve 6-MSA production on glucose but if the lower glycolysis is lowered, it is possible to obtain quite high conversion yields of sugar to 6-MSA. Systems biology tools were employed for in-depth analysis of the metabolic processes. Transcriptome analysis of 6-MSA producing strains on glucose and xylose in the presence and absence of phk overexpression combined with flux and physiology data enabled us to propose a model of phk/6msas interaction describing two different responses influencing 6-MSA production.
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Project description:ATF6 is a key regulator of the unfolded protein response. Through use of zebrafish and cultured cells we demonstrate that ATF6 drives fatty liver disease by interaction with fatty acid synthase (FASN).
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