Difference between revisions of "YNL098C"

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=== Alleles, Strains, and Phenotypes ===
 
[[Category:Topic:Alleles, Strains, and Phenotypes]]
 
==== Other Mutation ====
 
[[Category:Topic:Alleles, Strains, and Phenotypes:Other Mutation]]
 
 
'''Strain Background''': W303-1B<br>
 
'''Together with''': YFH1<br>
 
'''Phenotype(s)''': Viable [[Category:Phenotype:Viable]]
 
'''Mutation type(s)''': transposon insertion
 
 
A C-terminal truncation of RAS2 increased mRNA levels of CIT2 by a factor of two. <ref name='S000075657'>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 {{SGDpaper|S000075657}} PMID 14550302</ref> <ref name = 'CAset3226-2004-03-26'>submitted by [http://db.yeastgenome.org/cgi-bin/colleague/colleagueSearch?id=3226 Martin Kucej] on 2004-03-26</ref>
 
 
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=== Interactions ===
 
[[Category:Topic:Interactions]]
 
==== Genetic ====
 
[[Category:Topic:Interactions:Genetic]]
 
YNL098C is a suppressor of  YFH1 [[Category:Genetic Interaction with YFH1]]
 
 
 
'''Strain Background''': W303-1B<br>
 
'''Together with''': YFH1<br>
 
'''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. <ref name='S000075657'>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 {{SGDpaper|S000075657}} PMID 14550302</ref> <ref name = 'CAset3226-2004-03-26'>submitted by [http://db.yeastgenome.org/cgi-bin/colleague/colleagueSearch?id=3226 Martin Kucej] on 2004-03-26</ref>
 
 
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==Community Commentary==
 
==Community Commentary==

Revision as of 11:51, 24 January 2007

Share your knowledge...Edit this entry!

Systematic name YNL098C
Gene name RAS2
Aliases CTN5, CYR3, GLC5, TSL7
Feature type ORF, Verified
Coordinates Chr XIV:440572..439604
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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]



Community Commentary

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Alleles, Strains, and Phenotypes

Other Mutation

Strain Background: W303-1B
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
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]


References

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  1. 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
  2. Kataoka T, et al. (1984) Genetic analysis of yeast RAS1 and RAS2 genes. Cell 37(2):437-45 SGD PMID 6327067
  3. 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
  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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