Difference between revisions of "YNL098C"

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[[Category:Topic:Alleles, Strains, and Phenotypes:Other Mutation]]
 
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'''Strain Background''': W303-1B<br>
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'''Strain Background''': W303-1B (''see [[CommunityW303.html|detailed notes]] from Rodney Rothstein and Stephan Bartsch for the W303 strain used in the study'')
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<br>
 
'''Together with''': YFH1<br>
 
'''Together with''': YFH1<br>
 
'''Phenotype(s)''': Viable [[Category:Phenotype:Viable]]
 
'''Phenotype(s)''': Viable [[Category:Phenotype:Viable]]
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'''Strain Background''': W303-1B<br>
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'''Strain Background''': W303-1B (''see [[CommunityW303.html|detailed notes]] from Rodney Rothstein and Stephan Bartsch for the W303 strain used in the study'')
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<br>
 
'''Together with''': YFH1<br>
 
'''Together with''': YFH1<br>
 
'''Mutation type(s)''': partial deletion, deletion
 
'''Mutation type(s)''': partial deletion, deletion
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==References==
 
==References==
 
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Revision as of 06:30, 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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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

See Help:References on how to add references

  1. 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
  2. Kataoka T, et al. (1984) Genetic analysis of yeast RAS1 and RAS2 genes. Cell 37(2):437-45 SGD PMID 6327067
  3. 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. 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. 5.0 5.1 submitted by Martin Kucej on 2004-03-26

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