Tryptophan as a miR team organizer prevents colon cancer liver metastasis [colon]
Ontology highlight
ABSTRACT:
ORGANISM(S): synthetic construct Mus musculus
PROVIDER: GSE212633 | GEO | 2023/09/03
REPOSITORIES: GEO
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Project description:Tryptophan treatment play a significant role in miR expression. We have characterized the miR expression network through miR-on-chip profiling of the mouse treated with or without tryptophan. In this dataset, we include the expression data from mouse small intestine and colon tissue treated with or without tryptophan.
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Project description:Tryptophan as a miR team organizer prevents colon cancer liver metastasis [colon]
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Project description:Tryptophan as a miR team organizer prevents colon cancer liver metastasis [small intestine]
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Project description:DNA microarray analysis of gene expression in response to physiological and genetic changes that affect tryptophan metabolism in Escherichia coli. We investigated the global changes in mRNA abundance in Escherichia coli elicited by various perturbations of tryptophan metabolism. To do so we printed DNA microarrays containing 95% of all annotated E. coli ORFs. We determined the expression profile that is predominantly dictated by the activity of the tryptophan repressor. Only three operons, trp, mtr, and aroH, exhibited appreciable expression changes consistent with this profile. The quantitative changes we observed in mRNA levels for the five genes of the trp operon were consistent within a factor of 2, with expectations based on established Trp protein levels. Several operons known to be regulated by the TyrR protein, aroF-tyrA, aroL, aroP, and aroG, were down-regulated on addition of tryptophan. TyrR can be activated by any one of the three aromatic amino acids. Only one operon, tnaAB, was significantly activated by the presence of tryptophan in the medium. We uncovered a plethora of likely indirect effects of changes in tryptophan metabolism on intracellular mRNA pools, most prominent of which was the sensitivity of arginine biosynthetic operons to tryptophan starvation. This study is detailed in Khodursky AB et al.(2000) Proc Natl Acad Sci U S A 97:12170-5 Keywords: other
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Project description:Activated T cells secrete interferon-gamma (IFN) that triggers an intra-cellular tryptophan shortage through the activation of the Indoleamine 2,3-Dioxygenase 1 (IDO1) enzyme. Surprisingly, we here show that despite tryptophan depletion, in-frame protein synthesis bypassing tryptophan codons continues. Using mass spectrometry, we identified tryptophan to phenylalanine (W>F) substitution as the major event that facilitates in-frame protein synthesis in IFN-treated and tryptophan-depleted cells. We validated their expression using in vitro reporter assays, and pinpoint tryptophanyl-tRNA synthetase (WARS1) as the candidate gene that accounts for this event. We named these mRNA-translation-driven aberrations ‘substitutants’ to distinguish them from somatic genetic variants. To uncover their biological relevance, we interrogated cancer proteomes and phosphoproteomes of breast, lung and kidney cancers. Interestingly, we specifically identified a high level of tryptic peptides containing W>F substitutants with strong association to IDO1 expression, T cell activity, p53 mutations, and oncogenic MAPK signaling, indicating a role of infiltrating T cells in their production and highlighting cancer relevance. We further show that substitutants can impair protein function and be processed and presented at the cell surface to elicit immune cell recognition. Indeed, immunopeptidomics data from of colorectal-cancer organoids and glioblastoma cell lines revealed a large number of W>F substitutant-peptides being presented on HLA class I molecules following IFN treatment. Thus, W>F substitutants are a novel form of non-genetic mutations induced by tumor-infiltrating T cells with potential impact on gene function and on the repertoire of neopeptides presented by cancer cells.
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Project description:Isobutanol is considered a potential biofuel and can be produced by genetically modified microorganisms. Saccharomyces cerevisiae inherently produces isobutanol through valine intermediate(s), so it serves as a good host. However, isobutanol's toxicity remains a key obstacle for bioproduction. In our study, we first used image recognition to screen the colony growth of a yeast gene deletion library and inferred that genes involved in tryptophan biosynthesis, ubiquitination, and the pentose phosphate pathway (PPP) contribute to isobutanol tolerance. The importance of tryptophan in yeast's tolerance to isobutanol was confirmed by the recovery of isobutanol tolerance in a tryptophan biosynthesis defective strain by adding exogenous tryptophan. Transcriptomic analysis revealed that amino acid biosynthesis- and transportation-related genes in a tryptophan biosynthesis defective host were up regulated under conditions such as nitrogen starvation. This may explain why ubiquitination for protein degradation was involved for the protein turnover. PPP metabolites and vitamin B1/B6 may serve as precursors and cofactors in tryptophan biosynthesis to enhance isobutanol tolerance. Furthermore, the tolerance mechanism may also be linked to tryptophan metabolism, including the kynurenine pathway and nicotinamide adenine dinucleotide biosynthesis. Both pathways are responsible for cellular redox balance and antioxidative ability and figured out that tryptophan may play a crucial role on isobutanol tolerance. Our study highlights the central role of tryptophan in yeast's isobutanol tolerance and offers new clues for engineering a yeast host with strong isobutanol tolerance.
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