ArticleCurrent genetics2006
Increased phosphoglucomutase activity suppresses the galactose growth defect associated with elevated levels of Ras signaling in S. cerevisiae.
Article in Current genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- EngineeredFoods (Basel, Switzerland) · 2025Article
- Enhanced leavening ability of baker's yeast by overexpression of SNR84 with PGM2 deletion.Journal of industrial microbiology & biotechnology · 2015Article
- Recovery of phenotypes obtained by adaptive evolution through inverse metabolic engineering.Applied and environmental microbiology · 2012Article
- PGM2 overexpression improves anaerobic galactose fermentation in Saccharomyces cerevisiae.Microbial cell factories · 2010Article
- Rho5p is involved in mediating the osmotic stress response in Saccharomyces cerevisiae, and its activity is regulated via Msi1p and Npr1p by phosphorylation and ubiquitination.Eukaryotic cell · 2008Article
- Ste50 adaptor protein influences Ras/cAMP-driven stress-response and cell survival in Saccharomyces cerevisiae.Current genetics · 2007Article
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3 authors at 1 institution in 1 country.
Funding
Abstract
The Ras proteins regulate many aspects of cell growth in the budding yeast, Saccharomyces cerevisiae, via the cAMP-dependent protein kinase (PKA). Here, we show that a RAS2(val19) mutant that exhibits elevated levels of Ras/PKA signaling activity is unable to grow on media with galactose as the sole source of carbon. This growth defect was due, at least in part, to a defect in the expression of genes, like GAL1, that encode enzymes needed for the metabolism of galactose. This growth defect was used as the basis for a genetic screen for dosage suppressors of the RAS2(val19) mutant. This screen identified two genes, PGM1 and PCM1, that encode proteins with phosphoglucomutase activity. This activity is responsible for converting the glucose-1-phosphate produced during the metabolism of galactose to glucose-6-phosphate, a precursor that can be metabolized via the glycolytic pathway. The over-expression of PGM1 was not able to suppress any other RAS2(val19) phenotype or the galactose growth defect associated with a gal1Delta mutant. Overall, these data suggest that the elevated levels of phosphoglucomutase activity allow for the more efficient utilization of the limiting levels of glucose-1-phosphate that are present in the RAS2(val19) mutant.
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