| http://purl.uniprot.org/citations/20066047 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/20066047 | http://www.w3.org/2000/01/rdf-schema#comment | "BackgroundA point mutation in the Drosophila gene technical knockout (tko), encoding mitoribosomal protein S12, was previously shown to cause a phenotype of respiratory chain deficiency, developmental delay, and neurological abnormalities similar to those presented in many human mitochondrial disorders, as well as defective courtship behavior.Methodology/principal findingsHere, we describe a transcriptome-wide analysis of gene expression in tko(25t) mutant flies that revealed systematic and compensatory changes in the expression of genes connected with metabolism, including up-regulation of lactate dehydrogenase and of many genes involved in the catabolism of fats and proteins, and various anaplerotic pathways. Gut-specific enzymes involved in the primary mobilization of dietary fats and proteins, as well as a number of transport functions, were also strongly up-regulated, consistent with the idea that oxidative phosphorylation OXPHOS dysfunction is perceived physiologically as a starvation for particular biomolecules. In addition, many stress-response genes were induced. Other changes may reflect a signature of developmental delay, notably a down-regulation of genes connected with reproduction, including gametogenesis, as well as courtship behavior in males; logically this represents a programmed response to a mitochondrially generated starvation signal. The underlying signalling pathway, if conserved, could influence many physiological processes in response to nutritional stress, although any such pathway involved remains unidentified.Conclusions/significanceThese studies indicate that general and organ-specific metabolism is transformed in response to mitochondrial dysfunction, including digestive and absorptive functions, and give important clues as to how novel therapeutic strategies for mitochondrial disorders might be developed."xsd:string |
| http://purl.uniprot.org/citations/20066047 | http://purl.org/dc/terms/identifier | "doi:10.1371/journal.pone.0008549"xsd:string |
| http://purl.uniprot.org/citations/20066047 | http://purl.uniprot.org/core/author | "Chen S."xsd:string |
| http://purl.uniprot.org/citations/20066047 | http://purl.uniprot.org/core/author | "Jacobs H.T."xsd:string |
| http://purl.uniprot.org/citations/20066047 | http://purl.uniprot.org/core/author | "Fernandez-Ayala D.J."xsd:string |
| http://purl.uniprot.org/citations/20066047 | http://purl.uniprot.org/core/author | "Kemppainen E."xsd:string |
| http://purl.uniprot.org/citations/20066047 | http://purl.uniprot.org/core/author | "O'Dell K.M."xsd:string |
| http://purl.uniprot.org/citations/20066047 | http://purl.uniprot.org/core/date | "2010"xsd:gYear |
| http://purl.uniprot.org/citations/20066047 | http://purl.uniprot.org/core/name | "PLoS One"xsd:string |
| http://purl.uniprot.org/citations/20066047 | http://purl.uniprot.org/core/pages | "e8549"xsd:string |
| http://purl.uniprot.org/citations/20066047 | http://purl.uniprot.org/core/title | "Gene expression in a Drosophila model of mitochondrial disease."xsd:string |
| http://purl.uniprot.org/citations/20066047 | http://purl.uniprot.org/core/volume | "5"xsd:string |
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