Module number 1006




Database revision : gnsdb28.10
Date : Tue Feb 25 17:29:39 2003
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mHIS4:histidinol dehydrogenase,histidinol dehydrogenase,Null mutan\nt is viable and requires histidine\n Cond663:mec1_plus_gamma_10_min\n mSET2:Contains a 'SET' or 'TROMO' domain at the N-terminus of the \nprotein,contains SET domain , transcription factor,null is v\niable; a point mutant suppresses deletion of the UAS in the \nGAL4 promoter\n mHIS5:responsive to control of general amino acid biosynthesis,his\ntidinol-phosphate aminotransferase,Null mutant is viable and\n requires histidine\n mSIP3:Interacts with SNF1 protein kinase,transcriptional activator\n (putative),Null mutant is viable; does not confer snf1 phen\notypes\n mPDR16:involved in pleiotropic drug resistance by controlling lipid\ns in various cellular compartments; positively regulated by \nPDR1,Pdr17p homolog , Sec14p homolog,Null mutant is viable, \nexhibits hypersensitivity to azole inhibitors of ergosterol \nbiosynthesis, alterations in sterol composition of the plasm\na membrane; pdr16 pdr17 double deletion mutants exhibit addi\ntive exacerbated phenotypes\n mURA1:dihydroorotate dehydrogenase,dihydroorotate dehydrogenase,ur\nacil requiring\n mURA2:First and second steps of pyrimidine biosynthesis,aspartate \ntranscarbamylase , carbamoyl phosphate synthetase , glutamin\ne amidotransferase,uracil requiring\n mHYR1:Hydroperoxide resistance conferring gene,glutathione-peroxid\nase (putative),Null mutant is hypersensitive to oxidative st\nress\n mURA4:Third step in pyrimidine biosynthesis pathway,dihydrooratase\n,Null mutant is viable and requires uracil\n mYJR097W:Unknown ,, Unknown\n mBEM3:Gtpase-activating protein activity toward the essential bud-\nsite assembly GTPase Cdc42,rho GTPase activating protein (GA\nP),Null mutant is viable.\n mYDR179W-A:Unknown ,, Unknown\n mFRE4:similar to FRE2,,\n mYNL127W:Unknown ,, Unknown\n mTPM2:Tropomyosin isoform 2,tropomyosin isoform II,Null mutant is \nviable, exhibits no detectable phenotype; tpm1 tpm2 double d\neletion mutants are inviable; TPM2 overexpression does not s\nuppress tpm1 mutant phenotypes\n mDLD2:D-lactate dehydrogenase, located in mitochondrial matrix,,Nu\nll mutant is viable\n mFUS1:cell-surface protein required for cell fusion,,Null mutant i\ns viable; in fus1 x fus1 matings there is an interruption of\n the mating process just before cytoplasmic fusion\n mCYB5:cytochrome b5,cytochrome b5,Null mutant is viable, cyb5 muta\ntions suppress ketoconazole hypersensitivity of a P450 reduc\ntase deficient strain\n mYPL150W:Unknown ,, Unknown\n mHIT1:Protein required for growth at high temperature,,no growth a\nt high temperature; confers pet phenotype\n mOAC1:oxaloacetate carrier,oxaloacetate transport protein,\n mNOP13:Nucleolar Protein 13,,\n mNMD2:Protein involved in decay of mRNA containing nonsense codons\n,,Null mutant is viable, exhibits stabilization of nonsense-\ncontaining mRNAs\n mYPL136W:Unknown ,, Unknown\n COMP.:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mBAR1:extracellular protease synthesized in a-cells that cleaves a\nnd inactivates alpha factor,protease , synthesized in a-cell\ns; cleaves and inactivates alpha factor,MATa bar1 cells are \nsupersensitive to the G1 arrest induced by alpha factor\n mDAN1:Delayed Anaerobic,cell wall mannoprotein , induced during an\naerobic growth,Null mutant is viable\n mYKL206C:Unknown ,, Unknown\n mYLR108C:Unknown ,, Unknown\n mSPL2:Suppressor of plc1-delta. Isolated as a dosage suppressor of\n the temperature-sensitive phenotype of a plc1 null mutant. \nAlso suppresses the hyperosmotic-sensitive phenotype of the \nplc1 null mutant.,,Null mutant is viable and shows no obviou\ns phenotype; spl2-delta plc1-delta double mutant fails to gr\now on SCD complete media, but grows on YPD at 25 degrees C\n mYHR162W:Unknown ,, Unknown\n mHMX1:Unknown ,, Unknown\n mHOR7:hyperosmolarity-responsive gene,,\n mDDR48:DNA damage inducible; implicated in the production or recove\nry of mutations,contains >35 repeats of the amino acid seque\nnce NNNDSYGS , flocculent specific protein,Null mutant is vi\nable, displays reduced spontaneous mutation rate\n mYNL179C:Unknown ,, Unknown\n mYGL152C:Unknown ,, Unknown\n mRMD6:Unknown ,, Unknown\n mGIS2:GIG3 suppressor,,\n mSHM2:serine hydroxymethyltransferase,,Null mutant is viable\n mADH6:Unknown ,, Unknown\n mLHP1:Protein homologous to human La (SS-B) autoantigen,,Null muta\nnt is viable\n mSIR1:repressor of silent mating loci,silent mating loci repressor\n,\n mANB1:hypusine containg protein; ANB1 is expressed under anaerobic\n conditions and repressed under aerobic conditions whereas i\nts homolog HYP2 is inversely regulated,translation initiatio\nn factor eIF-5A, anaerobically expressed form,null mutant is\n viable; a double mutant containing disruptions of both ANB1\n and and the highly homologous HYP2 is inviable\n mRUD3:Relieves uso1-1 transport defect; golgin-160 related protein\n,,Null mutant shows severe growth defect or inviability in c\nombination with many ER-to-Golgi transport mutants, such as \nuso1-1, sec34, sec35-1, sec22-3, and bos1-1. Overproduction \nsuppresses mutations in many of the same genes.\n mSCM4:Protein that suppresses ts allele of CDC4 when overexpressed\n,,viable, suppressor of cdc4ts allele\n mVIP1:Homologous to S. pombe asp1+,,\n mSEO1:Suppressor of Sulfoxyde Ethionine resistance,permease (putat\nive),\n mSKT5:protoplast regeneration and killer toxin resistance gene, ma\ny be a post-translational regulator of chitin synthase III a\nctivity, interacts with Chs3p,,Null mutant is viable, resist\nant to Calcofluor white, exhibits a reduction in cell wall c\nhitin and chitin synthase III activity\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mGIT1:permease involved in the uptake of glycerophosphoinositol (G\nroPIns),permease involved in the uptake of glycerophosphoino\nsitol (GroPIns),Null mutant is viable, exhibits decreased Gr\noPIns transport\n mYMR073C:Unknown ,, Unknown\n mGRX3:Member of a glutaredoxin subfamily in Sc together with GRX4 \n& GRX5. Sign. sequence diff. with the other glutaredoxin sub\nfamily, formed by the previously described GRX1 & GRX2 gluta\nredoxins (Luikenhuis MBC 9:1081, 1998),glutaredoxin,Null mut\nant is viable and shows moderate sensitivity to oxidative st\nress and increased oxidation levels of cell proteins\n mCHA1:catabolism of hydroxy amino acids,catabolic serine (threonin\ne) dehydratase,Null mutant is viable and cannot grow on medi\na with L-serine or L-threonine as sole nitrogen source\n mYOL093W:Unknown ,, Unknown\n mYJL207C:Unknown ,, Unknown\n mDRS2:P-type ATPase, potential aminophospholipid translocase,P-typ\ne ATPase, potential aminophospholipid translocase , cation t\nransport (E1-E2) ATPase family member , P-type ATPase, poten\ntial aminophospholipid translocase , cation transport (E1-E2\n) ATPase family member,Null mutant is viable but cold sensit\nive with perturbed late Golgi function; drs2 arf1 double mut\nants are inviable.\n mIDP1:Mitochondrial form of NADP-specific isocitrate dehydrogenase\n,NADP-dependent isocitrate dehydrogenase,Null mutant is viab\nle\n mMET6:vitamin B12-(cobalamin)-independent isozyme of methionine sy\nnthase (also called N5-methyltetrahydrofolate homocysteine m\nethyltransferase or 5-methyltetrahydropteroyl triglutamate h\nomocysteine methyltransferase),vitamin B12-(cobalamin)-indep\nendent isozyme of methionine synthase (also called N5-methyl\ntetrahydrofolate homocysteine methyltransferase or 5-methylt\netrahydropteroyl triglutamate homocysteine methyltransferase\n),Null mutant is viable, and is a methionine auxotroph\n mMDH2:cytosolic malate dehydrogenase,malate dehydrogenase,Null mut\nant is viable; fails to grow on minimal medium with acetate \nor ethanol as carbon source\n mYHL045W:Unknown ,, Unknown\n mYJL192C:Unknown ,, Unknown\n mERV25:COPII coat component of certain ER-derived vesicles,vesicle \ncoat component,Null mutant is viable, displays a selective d\nefect in transport of secretory proteins from the ER to Golg\ni complex.\n mYDL050C:Unknown ,, Unknown\n Cond664:mec1_plus_gamma_20_min\n mTEC1:transcription factor of the TEA/ATTS DNA-binding domain fami\nly, regulator of Ty1 expression,TEA/ATTS DNA-binding domain \nfamily, regulator of Ty1 expression , transcription factor,N\null mutant is viable\n mYOL124C:Unknown ,, Unknown\n mARG4:argininosuccinate lyase,argininosuccinate lyase,Arginine req\nuiring\n mSAM2:methionine biosynthesis regulation,,Null mutant is viable\n mSSU1:sensitive to sulfite,major facilitator superfamily,Null muta\nnt is viable; sulfite sensitive\n mUIP3:Unknown ,, Unknown\n mSSF2:high copy suppressor of G beta subunit temperature sensitive\n mutation,,Null mutant is viable; displays double mutant let\nhality with ssf1 null mutations. Ssfp depletion is associate\nd with arrest of cell division and decreased mating\n mAAD6:high degree of similarity with the AAD of P. chrysosporium,a\nryl-alcohol dehydrogenase (putative),Responds to oxidative s\ntress induced by diamide and di-ethyl maleic acid ester in Y\nAP1 dependant manner\n mMHT1:S-Methylmethionine:Homocysteine methylTransferase,,Does not \nuse S-methylmethionine as a sulfur source\n mURE2:Nitrogen catabolite repression regulator that acts by inhibi\ntion of GLN3 in good nitrogen source. Altered form of Ure2p\n creates [URE3] prion.,glutathione transferase (putative) , \nprion , transcriptional regulator,Null mutant is viable but \nexhibits defects in nitrogen catabolite repression (NCR), an\nd null mutant diploids are defective in pseudohyphal growth \nand display an increased incidence of random bud patterns.\n mYOR192C:Unknown ,, Unknown\n mECM1:putative transmembrane domain protein involved in cell wall \nbiogenesis,,A Tn3 insertion into ECM1 causes hypersensitivit\ny to the cell surface polymer perturbing agent calcofluor wh\nite.\n mERG5:cytochrome P450 involved in C-22 denaturation of the ergoste\nrol side-chain,cytochrome P450 , involved in C-22 denaturati\non of the ergosterol side-chain,Null mutant is viable\n mYHR151C:Unknown ,, Unknown\n mYPL176C:Unknown ,, Unknown\n mSDT1:suppressor of deletion of TFIIS,,null mutant is viable, but \nis sensitive to 6-azauracil\n mYML079W:Unknown ,, Unknown\n mTSA1:antioxidant enzyme that provides protection against oxidatio\nn systems capable of generating reactive oxygen and sulfur s\npecies,thioredoxin-peroxidase (TPx); reduces H2O2 and alkyl \nhydroperoxides with the use of hydrogens provided by thiored\noxin, thioredoxin reductase, and NADPH,Null mutant is viable\n, grows slower than wild-type under aerobic conditions\n mMGA2:Product of gene unknown,,Null mutant is viable, shows subtle\n effects on growth, UV sensitivity, and galactose utilizatio\nn; mga2 spt23 double deletion mutants are inviable\n mJNM1:coiled-coil domain protein required for proper nuclear migra\ntion during mitosis (but not during conjugation),,Null mutan\nt is viable but is cold-sensitive\n mPPR1:Positive regulator of URA1 and URA3,zinc finger transcriptio\nn factor of the Zn(2)-Cys(6) binuclear cluster domain type,N\null mutant is viable, deficient in pyrimidine biosynthetic p\nathway\n mYSY6:Protein that participates in secretory pathway,,\n mPAI3:Cytoplasmic inhibitor of proteinase Pep4p,inhibitor of prote\ninase Pep4p,Null mutant is viable but shows increased rate o\nf protein degradation\n mSPP1:YPL138C,,\n mCBF1:centromere binding factor; binds in vivo to CDE I sites in c\nentromeres (and some promoters), and induces DNA bending, re\nquired for mitotic segregation and normal growth rate,basic \nhelix-loop-helix protein,Null mutant is viable, but grows sl\nowly and causes partial loss of centromere function (increas\ned chromosome loss), benomyl and thiabendazole sensitivity, \nmethionine auxotrophy, and changes in chromatin structure at\n CENs and some promoters. Null mutation causes precocious si\nster segregation at MI, and reduced spore viability.\n mYHR029C:Unknown ,, Unknown\n mSER1:phosphoserine transaminase,phosphoserine transaminase,Null m\nutant is viable, serine-requiring\n mRHO4:ras homolog--GTP binding protein,GTP-binding protein , ras h\nomolog,Null mutant is viable; rho3 rho4 cells are inviable a\nt 30 degrees C\n mATR1:aminotriazole resistance,very hydrophobic, has many membrane\n-spanning regions, several potential glycosylation sites, po\ntential ATP-binding site,Null mutant is viable, but is sensi\ntive to very low (5 mM) levels of aminotriazole and to 4-nit\nroquinoline-N-oxide (4-NQO); multiple copies of ATR1 confer \nhyper-resistance to 4-NQO; multiple copies of ATR1 in gcn4 b\nackground confer resistance to high (80mM) levels of aminotr\niazole\n mYNR040W:Unknown ,, Unknown\n mERP3:Emp24p/Erv25p related protein 2,p24 protein involved in memb\nrane trafficking,viable\n mYPR151C:Unknown ,, Unknown\n mYBR235W:Unknown ,, Unknown\n mIDS2:IME2-Dependent Signalling,,Null mutations reduce or abolish \nthe ability of IME2p to activate expression of early, middle\n, and late meiotic genes. Recessive and null ids2 mutants pr\nevent toxicity of Ime2p expression in rad52 haploids, but do\n not affect Ime2p polypeptide accumulation.\n Cond666:mec1_plus_gamma_45_min\n mYNL089C:Unknown ,, Unknown\n mCNB1:Type 2B protein phosphatase; regulatory B subunit of calcine\nurin,calcineurin regulatory B subunit , type 2B protein phos\nphatase , calcineurin regulatory B subunit , type 2B protein\n phosphatase,Null mutant is viable, Li+ and Na+ sensitive, c\nnb1 fks1 and cnb1 vma3 double mutants are inviable\n mPHO81:Positive regulatory protein of phosphate pathway,,phosphatas\ne deficient\n mVTC3:Phosphate metabolism; transcription is regulated by PHO syst\nem,polyphosphate synthetase (putative),Null nutant is viable\n; no polyphosphate accumulation in a vtc2(phm1)/vtc3(phm2) d\nouble disruptant\n mRAD14:Involved in nucleotide excision repair,human xeroderma pigme\nntosum group A DNA repair gene homolog,Null mutant is viable\n and radiation sensitive\n mGLO2:Cytoplasmic glyoxylase-II,glyoxylase-II,Null mutant is viabl\ne but shows increased sensitivity to methylglyoxal\n mYPR021C:Unknown ,, Unknown\n mPHO84:inorganic phosphate transporter, transmembrane protein,inorg\nanic phosphate transporter,Null mutant is viable\n mTMT1:Trans-aconitate Methyltransferase 1,,\n mYPL004C:Unknown ,, Unknown\n Cond667:mec1_plus_gamma_60_min\n mMET22:Putative phosphatase gene involved in salt tolerance and met\nhionine biogenesis; halotolerance,3'(2')5'-bisphosphate nucl\neotidase,Methionine requiring; lacks 3'-phosphoadenylylsulfa\nte (PAPS) reductase activity; unable to grow on sulfate as s\nole sulfur source\n mYJL064W:Unknown ,, Unknown\n mYJL123C:Unknown ,, Unknown\n mPCL5:PHO85 cyclin,,Null mutant is viable.\n mYPL170W:Unknown ,, Unknown\n mEAF6:Unknown ,, Unknown\n mPUT1:proline oxidase,proline oxidase,inability to use proline as \na nitrogen source\n mYFR043C:Unknown ,, Unknown\n mBNA1:biosynthesis of nicotinic acid,3-hydroxyanthranilic acid dio\nxygenase,Null mutant is viable, nicotinic acid auxotroph\n mHMG1:3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase is\nozyme,3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reduct\nase isozyme,Null mutant is viable, sensitive to compactin, a\n competitive inhibitor of HMG-CoA reductase; hmg1 hmg2 doubl\ne deletion mutants are inviable\n mYBR062C:Unknown ,, Unknown\n mADE17:AICAR transformylase/IMP cyclohydrolase,5-aminoimidazole-4-c\narboxamide ribonucleotide (AICAR) transformylase/IMP cyclohy\ndrolase,Null mutant is viable; ade16 ade17 double mutants re\nquire adenine\n mYLR454W:Unknown ,, Unknown\n mRER1:Protein involved in retention of membrane proteins, includin\ng Sec12p, in the ER; localized to Golgi, where it may functi\non in returning membrane proteins to the ER,,Null mutant is \nviable and shows mislocalization of transmembrane proteins t\nhat are normally retained in the early secretory compartment\ns\n mMMP1:S-MethylMethionine Permease,high affinity S-methylmethionine\n permease,Null mutant is viable but is unable to use S-methy\nlmethionine as a sulfur source\n mPTP1:phosphotyrosine-specific protein phosphatase,phosphotyrosine\n-specific protein phosphatase,viable\n mFAA1:cellular lipid metabolism and protein N-myristolation,long c\nhain fatty acyl:CoA synthetase,Null mutant is viable as long\n as fatty acid synthase (fas) complex is active\n mYMR153C-A:Unknown ,, Unknown\n Cond665:mec1_plus_gamma_30_min\n mARR4:Unknown ,, Unknown\n mURA1 mRHO4 mYNL127W mYPL004C mYPL150W
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Computational Genomics Lab, Tel-Aviv uniresity