Module number 3080




Database revision : gnsdb28.10
Date : Tue Feb 25 17:14:29 2003
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Cond955:TPK3_MT1val\n mYCK1:membrane-bound casein kinase I homolog,casein kinase I homol\nog,Null mutant is viable; yck1 yck2 double deletion mutants \nare inviable; yck1 point mutants suppress defective Snf1p ki\nnase activity in snf4 strains\n mOCA1:Unknown ,, Unknown\n mTRP1:Note that the sequence of TRP1 from strain S228C, which is t\nhe sequence stored in SGD, contains an ochre mutation at cod\non 67.,N-(5'-phosphoribosyl)-anthranilate isomerase,tryptoph\nan requiring\n mBAP2:contains 12 predicted transmembrane domains,amino acid perme\nase for leucine, valine, and isoleucine (putative),reduced u\nptake of leucine, isoleucine, and valine\n mLEU4:leucine biosynthesis,alpha-isopropylmalate synthase (2-isopr\nopylmalate synthase),Null mutant is viable, Leu+\n Cond952:TPK1_MT2val\n COMP.KO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n Cond950:TPK1_MT1val\n Cond954:TPK2_MT2val\n Cell Cycle.alpha:Comprehensive identification of cell cycle-regulated genes o\nf the yeast Saccharomyces cerevisiae by microarray hybridiza\ntion. Mol Biol Cell. 1998 Dec;9(12):3273-97.\n Cond956:TPK3_MT2val\n mMUP1:high affinity methionine permease,high affinity methionine p\nermease,Null mutant is viable but cannot perform high-affini\nty methionine update.\n TPK.TPK:The yeast A kinases differentially regulate iron uptake and \nrespiratory function. Proc Natl Acad Sci U S A. 2000 May 23\n;97(11):5984-8.\n Cond949:WT1val\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mTAT1:Amino acid transport protein for valine, leucine, isoleucine\n, and tyrosine,amino acid transport protein for valine, leuc\nine, isoleucine, and tyrosine,\n Cond99:med2(haploid)\n mMIG2:Involved in repression, along with Mig1p, of SUC2 (invertase\n) expression by high levels of glucose; binds to Mig1p-bindi\nng sites in SUC2 promoter,contains zinc fingers very similar\n to zinc fingers in Mig1p,Null mutant is viable; a strain th\nat contains a double disruption of MIG1 and MIG2 is defectiv\ne in glucose repression of SUC2 expression\n mIES6:Ino Eighty Subunit 6,,Null: non essential.\n mHTA2:Histone H2A (HTA1 and HTA2 code for nearly identical protein\ns),histone H2A (HTA1 and HTA2 code for nearly identical prot\neins),Null mutant is viable. Deletion of the HTA2-HTB2 (TRT2\n) locus has no reported observable phenotypes, presumably be\ncause HTA1-HTB1 (TRT1) expression is upregulated and can com\npensate in the absence of TRT2. Overexpression of TRT2 can s\nuppress Ty insertion mutations\n Cond953:TPK2_MT1val\n Cond554:alpha21\n Cond951:WT2val\n
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Computational Genomics Lab, Tel-Aviv uniresity