Difference between revisions of "YNL098C"
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Revision as of 14:05, 19 June 2009
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| Systematic name | YNL098C |
| Gene name | RAS2 |
| Aliases | CTN5, CYR3, GLC5, TSL7 |
| Feature type | ORF, Verified |
| Coordinates | Chr XIV:440572..439604 |
| Primary SGDID | S000005042 |
Description of YNL098C: GTP-binding protein that regulates the nitrogen starvation response, sporulation, and filamentous growth; farnesylation and palmitoylation required for activity and localization to plasma membrane; homolog of mammalian Ras proto-oncogenes[1][2][3]
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Contents
Community Commentary
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Alleles, Strains, and Phenotypes
Other Mutation
Strain Background: W303-1B (see detailed notes from Rodney Rothstein and Stephan Bartsch for the W303 strain used in the study)
Together with: YFH1
Phenotype(s): Viable
Mutation type(s): transposon insertion
A C-terminal truncation of RAS2 increased mRNA levels of CIT2 by a factor of two. [4] [5]
Interactions
Genetic
YNL098C is a suppressor of YFH1
Strain Background: W303-1B (see detailed notes from Rodney Rothstein and Stephan Bartsch for the W303 strain used in the study)
Together with: YFH1
Mutation type(s): partial deletion, deletion
A mutation in RAS2 supressed a growth defect of deltaYFH1 strain on toxic levels of iron in growth media. [4] [5]
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References
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- ↑ Gimeno CJ, et al. (1992) Unipolar cell divisions in the yeast S. cerevisiae lead to filamentous growth: regulation by starvation and RAS. Cell 68(6):1077-90 SGD PMID 1547504
- ↑ Kataoka T, et al. (1984) Genetic analysis of yeast RAS1 and RAS2 genes. Cell 37(2):437-45 SGD PMID 6327067
- ↑ Bhattacharya S, et al. (1995) Ras membrane targeting is essential for glucose signaling but not for viability in yeast. Proc Natl Acad Sci U S A 92(7):2984-8 SGD PMID 7708760
- ↑ 4.0 4.1 Kucej M and Foury F (2003) Iron toxicity protection by truncated Ras2 GTPase in yeast strain lacking frataxin. Biochem Biophys Res Commun 310(3):986-91 SGD PMID 14550302
- ↑ 5.0 5.1 submitted by Martin Kucej on 2004-03-26
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References
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