Module number 3262




Database revision : gnsdb28.10
Date : Tue Feb 25 17:21:27 2003
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mGAC1:Regulatory subunit for phosphoprotein phosphatase type 1 (PP\n-1), also known as Glc7p, which regulates glycogen synthase-\n2,Glc7p regulatory subunit,Reduced glycogen accumulation\n mSET3:,,\n mYPL208W:Unknown ,, Unknown\n mSNX4:Sorting NeXin,,\n mTKL1:Transketolase 1,transketolase 1,Null mutant is viable; growt\nh on fermentable carbon sources, but not gluconeogenic carbo\nn sources, is reduced; tkl1 tkl2 mutants are auxotrophic for\n aromatic amino acids\n mFET3:FET3 encodes a ferro-O2-oxidoreductase that is part of the h\nigh-affinity iron transport system,multicopper oxidase,The n\null mutant is viable but defective for high affinity Fe(II) \nuptake. The null mutant is inviable when environmental iron \nis limiting.\n mALF1:alpha-tubulin foldin; protein implicated in folding of alpha\n tubulin,tubulin folding cofactor B,Null mutant is viable, b\nenomyl super-sensitive, alf1 tub1 mutants are inviable\n mPRO2:gamma-glutamyl phosphate reductase,gamma-glutamyl phosphate \nreductase,Proline requiring and unable to grow on YPD (yeast\n extract-peptone-glucose); synthetic lethality with ctk1\n mSAP185:SIT4 associated protein, MW of 185 kDa,,Null mutant is viabl\ne; sap185 sap190 double mutants grow slowly; sap155 sap185 s\nap190 triple mutants are inviable in ssd1-d backgrounds\n mCDC3:involved in proper bud growth,,Null mutant is inviable; othe\nr mutants show abnormal cell-wall deposition and bud growth,\n inability to complete cytokinesis, and failure to form the \nring of 10nm filaments in the neck region of budding cells.\n mSCS7:Required for the hydroxylation of the very long chain fatty \nacid (VLCFA), located in the endoplasmic reticulum,desaturas\ne , hydroxylase,Null mutant is viable, suppresses the Ca2+-s\nensitive phenotype of csg2 delta mutants\n mRCY1:Unknown ,, Unknown\n mINO2:Transcription factor required for derepression of inositol-c\nholine-regulated genes involved in phospholipid synthesis,he\nlix-loop-helix protein,The null mutant is viable but auxotro\nphic for inositol and choline. The null mutant can also disp\nlay aberant cell shape and defects in nuclear segregation. H\nomozygous mutant ino2 delta-1 diploids fail to sporulate. Ot\nher mutant alleles show pleiotropic defects in phospholipid \nmetabolism.\n mADO1:adenosine kinase,adenosine kinase,\n mINO4:Transcription factor required for derepression of inositol-c\nholine-regulated genes involved in phospholipid synthesis,ba\nsic helix-loop-helix (bHLH) protein,The null mutant is viabl\ne but auxotrophic for inositol and choline. The null mutant \nexpresses repressed levels of inositol-1-phosphate synthase \n(INO1) mRNA and exhibits reduced phosphatidylcholine biosynt\nhesis.\n mRTF1:Directly or indirectly regulates the DNA-binding properties \nof Spt15p, the TATA box-binding protein, and the relative ac\ntivities of different TATA elements,nuclear protein,Null mut\nant is viable and can suppress TATA box-binding protein muta\nnts (SPT15) in an allele-specific fashion\n mERD1:Protein required for retention of luminal ER proteins,,disru\nption of the retention system for ER proteins; defects in th\ne Golgi-dependent modification of glycoproteins\n mSAC2:May interact with actin as a component or controller of the \nassembly or stability of the actin cytoskeleton,,Null mutant\n is viable, cold-sensitive growth phenotype, suppressor of a\nctin mutation; aberrant organization of intracellular actin \nand deposition of chitin at the cell surface\n mPEP8:Plays a role in delivery of proteins to the vacuole,vacuolar\n protein similar to mouse gene H<beta>58,Null mutant is viab\nle but is defective in processing of soluble vacuole proteas\nes due to inability of soluble vacuolar hydrolase to reach t\nhe vacuole\n mSAC7:Suppressor of actin mutation,GTPase activating protein (GAP)\n for RHO1,null mutant is viable, has growth and actin assemb\nly defects at low temperatures, displays allele-specific sup\npression and double mutant lethality with actin mutations, s\nuprresses tor mutations\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 mYDR269C:Unknown ,, Unknown\n mSCT1:High copy suppresor of choline-transport mutants,,Null mutan\nt is viable\n mVPS17:Peripheral membrane protein required for vacuolar protein so\nrting,,Null mutant is viable, exhibits defect in vacuolar mo\nrphology and protein sorting\n mYDR008C:Unknown ,, Unknown\n mSHM2:serine hydroxymethyltransferase,,Null mutant is viable\n mCSM1:Hypothetical ORF,,missegregates chromosomes in meiosis\n mGCN2:Derepression of GCN4 expression,eukaryotic initiation factor\n 2 alpha (eIF2-alpha) kinase,Null mutant is viable, unable t\no grow on medium containing 3-aminotriazole (3-AT), a compet\nitive inhibitor of histidine biosynthesis, because it cannot\n derepress GCN4 and its target genes in the histidine biosyn\nthetic pathway\n mLYS1:saccharopine dehydrogenase,,Lysine requiring\n mADH3:alcohol dehydrogenase isoenzyme III,alcohol dehydrogenase is\noenzyme III,Null mutant is viable\n mGCN4:transcriptional activator of amino acid biosynthetic genes,t\nranscriptional activator of amino acid biosynthetic genes,Th\ne null mutant is viable but requires arginine on minimal med\nium and issensitive to 3-amino-1,2,4-triazole. General contr\nol of amino acid synthesis non-derepressible in the null mut\nant.\n mYER119C-A:Unknown ,, Unknown\n mCOX12:essential during assembly for full cytochrome c oxidase acti\nvity,cytochrome c oxidase subunit VIb,Null mutant is viable,\n grows poorly at room temperature, fails to grow on glycerol\n/ethanol media at 37 degrees\n mLYS4:homoaconitase,homoaconitase,Lysine requiring\n mLYS5:aminoadipate-semialdehyde dehydrogenase small subunit (alpha\n-aminoadipate reductase),aminoadipate-semialdehyde dehydroge\nnase small subunit (alpha-aminoadipate reductase),Lysine req\nuiring\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 mYGL007W:Unknown ,, Unknown\n mTRP2:anthranilate synthase Component I,anthranilate synthase comp\nonent I,tryptophan requiring\n mADE5,7:glycinamide ribotide synthetase and aminoimidazole ribotide \nsynthetase,aminoimidazole ribotide synthetase , glycinamide \nribotide synthetase,Adenine requiring\n mTRP3:anthranilate synthase Component II and indole-3-phosphate (m\nultifunctional enzyme),anthranilate synthase component II , \nindole-3-phosphate,Null mutant is viable, tryptophan auxotro\nph\n mTRP4:anthranilate phosphoribosyl transferase,anthranilate phospho\nribosyl transferase,tryptophan requiring\n mLYS9:Seventh step in lysine biosynthesis pathway,,lysine auxotrop\nh\n mTRP5:tryptophan synthetase,tryptophan synthetase,Null mutant is v\niable and requires tryptophan\n mSPT8:transcription factor, probable member of histone acetyltrans\nferase SAGA complex,probable member of histone acetyltransfe\nrase SAGA complex , transcription factor,Null mutant is viab\nle, no growth defects, exhibits suppression of Ty insertion \nmutations, defects in Ty transcription\n mYIL103W:Unknown ,, Unknown\n mYDL172C:Unknown ,, Unknown\n mBAS1:Transcription factor regulating basal and induced activity o\nf histidine and adenine biosynthesis genes,transcription fac\ntor,\n mRTG1:Transcription factor (bHLH) involved in interorganelle commu\nnication between mitochondria, peroxisomes, and nucleus,tran\nscription factor,Null mutant is viable but cannot grow on ac\netate as the sole carbon source, is a glutamate and aspartat\ne auxotroph, and shows decreased citrate synthase, acetyl-Co\nA synthetase, NAD isocitrate dehydrogenase, and pyruvate car\nboxylase activities\n mRTG2:Protein involved in interorganelle communication between mit\nochondria, peroxisomes, and nucleus,,Null mutant is viable, \nfails to grow on acetate as a sole carbon source, auxotrophi\nc for glutamate and aspartate; respiratory competent\n mILV1:threonine deaminase,threonine deaminase,Isoleucine-plus-vali\nne requiring\n mPHA2:prephenate dehydratase,prephenate dehydratase,phenylalanine \nrequiring\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mYLR065C:Unknown ,, Unknown\n mAPS3:sigma3-like subunit of the yeast AP-3 complex which function\ns in transport of alkaline phosphatase to the vacuole via th\ne alternate pathway, suppressor of loss of casein kinase 1 f\nunction,,Null mutant is viable, rescues yck1,yck2 double mut\nant\n mCYS4:Cystathionine beta-synthase,cystathionine beta-synthase,Null\n mutant is viable, exhibits vacuolar acidification defects; \ncys2 and cys4 mutations are linked together and co-operative\nly confer cysteine dependence\n mZIP2:Required for 'ZIPpering' up meiotic chromosomes during chrom\nosome synapsis,,Null mutant is viable but is defective in ch\nromosome synapsis, but not chromosome pairing, and causes me\niosis I non-disjunction and reduced homologous recombination\n mYER091C-A:Unknown ,, Unknown\n mSPF1:Sensitivity to a killer toxin (SMK toxin) produced by Pichia\n farinosa,P-type ATPase,The null mutant is viable and resist\nant to the SMK toxin, but grows slowly and has glycosylation\n defects.\n mMET1:Methionine metabolism,,Null mutant is viable, and is a methi\nonine auxotroph\n mLYS12:homo-isocitrate dehydrogenase, an NAD-linked mitochondrial e\nnzyme required for the fourth step in the biosynthesis of ly\nsine, in which homo-isocitrate is oxidatively decarboxylated\n to alpha-ketoadipate.,homo-isocitrate dehydrogenase,Null mu\ntant is viable but shows decreased growth in the absence of \nlysine\n mMET3:ATP sulfurylase,ATP sulfurylase,Null mutant is viable, and i\ns a methionine auxotroph\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 mLYS14:Transcriptional activator of lysine pathway genes with 2-ami\nnoadipate semialdehyde as co-inducer; saccharopine reductase\n synthesis,,Lysine requiring\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 mSTB5:binds Sin3p in two-hybrid assay,,Null mutant is viable\n mYOL138C:Unknown ,, Unknown\n mMET8:Protein involved in the expression of PAPS reductase and sul\nfite reductase,,Null mutant is viable, and is a methionine a\nuxotroph\n mPKH2:Pkb-activating Kinase Homologue,,Null mutant is viable; pkh1\n, pkh2 double mutant is lethal\n mVPS5:vacuolar Protein Sorting Defective; Golgi retention and vacu\nolar protein sorting,simialr to sorting nexin I,Null mutant \nis viable, missort and secrete soluble vacuolar proteins, co\nntain fragmented vacuoles and mislocalize carboxypepsidase a\nnd Vps10p.\n mTIF2:translation initiation factor eIF4A,translation initiation f\nactor eIF4A subunit,viable, tif1tif2 double mutant is lethal\n mAPT1:Adenine phosphoribosyltransferase,adenine phosphoribosyltran\nsferase,\n mCPA1:Carbamoyl phosphate synthetase, arginine specific,arginine s\npecific , carbamoyl phosphate synthetase,Null mutant is viab\nle\n mYJL200C:Unknown ,, Unknown\n mMON1:Product of gene unknown,,null mutant is sensitive to monensi\nn and brefeldin A\n mYDR220C:Unknown ,, Unknown\n mCPA2:carbamyl phosphate synthetase,carbamyl phosphate synthetase,\nNull mutant is viable\n mYIL039W:Unknown ,, Unknown\n mVPS35:Protein involved in vacuolar sorting,retromer complex compon\nent,Null mutant is viable, exhibits defects in sorting of va\ncuolar carboxypeptidase Y, proteinase A, proteinase B, and a\nlkaline phosphatase\n mECM25:ExtraCellular Mutant,,A Tn3 insertion into this gene causes \nhypersensitivity to the cell surface polymer perturbing agen\nt calcofluor white.\n mRPE1:D-ribulose-5-Phosphate 3-epimerase,D-ribulose-5-Phosphate 3-\nepimerase,Null mutants are viable but show no ribulose-5-pho\nsphate epimerase activity, cannot grow on D-xylulose, and ar\ne sensitive to hydrogren peroxide\n mTOS1:Hypothetical ORF,,\n mYDL173W:Unknown ,, Unknown\n mARG1:arginosuccinate synthetase,arginosuccinate synthetase,Argini\nne requiring\n mHOM2:threonine and methionine pathway,aspartic beta semi-aldehyde\n dehydrogenase,Homoserine requiring\n mARG2:First step in ornithine biosynthesis pathway,acetylglutamate\n synthase,\n mHOM3:First step in common pathway for methionine and threonine bi\nosynthesis,aspartate kinase (L-aspartate 4-P-transferase) (E\nC 2.7.2.4),Homoserine requiring; Borrelidin resistance\n mARG3:Sixth step in arginine biosynthesis,ornithine carbamoyltrans\nferase,Arginine requiring\n mYDL072C:Unknown ,, Unknown\n mARG4:argininosuccinate lyase,argininosuccinate lyase,Arginine req\nuiring\n mHOM6:catalyzes third step in common pathway for methionine and th\nreonine biosynthesis,L-homoserine:NADP oxidoreductase , homo\nserine dehydrogenase,Homoserine requiring\n mYDR271C:Unknown ,, Unknown\n mLRS4:Loss of rDNA silencing,,loses rDNA silencing\n mMDM35:Unknown ,, Unknown\n mYKL077W:Unknown ,, Unknown\n mICT1:Increased Copper Tolerance; Similar to Ecm18p,,\n mARG5,6:N-acetyl-gamma-glutamyl-phosphate reductase and acetylglutam\nate kinase,N-acetyl-gamma-glutamyl-phosphate reductase and a\ncetylglutamate kinase,Arginine requiring\n mNEW1:This gene encodes a protein with an Q/N-rich amino terminal \ndomain that acts as a prion, termed [NU]+.,,Null mutant is v\niable\n mERG2:sterol biosynthesis,C-8 sterol isomerase,Null mutant is viab\nle\n mRDR1:Unknown ,, Unknown\n mFTR1:Plasma membrane iron permease,iron permease,Lacks high affin\nity iron uptake\n mARO2:Chorismate synthase,chorismate synthase,aromatic amino acid \nrequiring; lack of premeiotic DNA synthesis; blocked sporula\ntion in homozygous mutant\n mYET1:Yeast BAP31 homolog,yeast endoplasmic reticulum 25 kDa trans\nmembrane protein,Null mutant is viable\n mTRK1:180 kDa high affinity potassium transporter,180 kDa high aff\ninity potassium transporter,Null mutant is viable, requires \nadded potassium; trk1 trk2 double mutants are viable\n mARO7:chorismate mutase,chorismate mutase,Aromatic amino acid requ\niring; Low osmotic pressure sensitive\n mYOR135C:Unknown ,, Unknown\n mYLR089C:Unknown ,, Unknown\n mTHR1:homoserine kinase,homoserine kinase,Null mutant is viable, t\nhreonine auxotroph\n mYPT31:probably involved in intra-Golgi transport or in the formati\non of transport vesicles at the most distal Golgi compartmen\nt,GTPase , YPT32 homolog , ras homolog,YPT1 is required for \nviability in some strain backgrounds but not others; ypt31 y\npt32 double deletion mutants are inviable\n mTHR4:threonine synthase,threonine synthase,threonine requiring\n mAAT2:aspartate aminotransferase, cytosolic,aspartate aminotransfe\nrase,\n mNFU1:Nifu-like protein,,Null mutant is viable on YPD 30 degrees C\n, and is synthetically lethal with SSQ1\n mYOR302W:Unknown ,, Unknown\n mCDC10:cell division cycle blocked at 36 degree C,septin,abnormal c\nell-wall deposition and bud growth, inability to complete cy\ntokinesis, failure to form the ring of 10nm filaments in the\n neck region of budding cells\n mYMR135W-A:Unknown ,, Unknown\n mCCC2:copper-transporting P-type ATPase with similarity to human M\nenkes and Wilsons genes,,Null mutant is viable, exhibits def\nects in respiration and iron uptake\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 mSER1:phosphoserine transaminase,phosphoserine transaminase,Null m\nutant is viable, serine-requiring\n mSER2:phosphoserine phosphatase,phosphoserine phosphatase,serine-r\nequiring\n mMET10:subunit of assimilatory sulfite reductase,assimilatory sulfi\nte reductase subunit,Null mutant is viable, and is a methion\nine auxotroph\n mECM40:ExtraCellular Mutant,acetylornithine acetyltransferase,A Tn3\n insertion into this gene causes hypersensitivity to the cel\nl surface polymer perturbing agent calcofluor white.\n mMET12:Gene encodes mthfr which catalyzes step before methionine sy\nnthesis.,methylenetetrahydrofolate reductase (mthfr) (putati\nve),Null mutant is viable and shows no phenotypes; double di\nsruption of MET12 and MET13 (the two putative mthfr genes) c\nonfers methionine auxotrophy, but has no other known phenoty\npe at this time\n mMET13:putative methylenetetrahydrofolate reductase (mthfr),methyle\nnetetrahydrofolate reductase (mthfr) (putative),Null mutant \nis viable and shows methionine auxotrophy; double disruption\n of MET12 and MET13 (the two putative mthfr genes) also conf\ners methionine auxotrophy, but has no other known phenotype \nat this time.\n mMET14:adenylylsulfate kinase,adenylylsulfate kinase,Null mutant is\n viable, and is a methionine auxotroph\n mPKR1:Pichia farinosa Killer toxin Resistance,,Confers resistance \nto Pichia farinosa killer toxin (SMK toxin) when overexpress\ned\n mMET17:O-Acetylhomoserine-O-Acetylserine Sulfhydralase,O-acetylhomo\nserine (thiol)-lyase,Null mutant is viable, methionine auxot\nroph, becomes darkly pigmented in the presence of Pb2+ ions;\n resistant to methylmercury and exhibits increased levels of\n H2S\n mCCZ1:calcium caffeine zinc sensitivity,,Null mutant is viable, bu\nt is sensitive to caffeine, calcium and zinc; no sporulation\n in homozygous null diploids\n mSRC1:Spliced mRNA and Cell cycle regulated gene,,Null mutant is v\niable and shows normal growth in standard media; expression \nis induced at G2/M transition.\n mCHS5:Involved in chitin synthase III activity, also required for \nhomozygosis in the first stages of mating,,Null mutant is vi\nable, cells exhibit a strong mating defect; sensitive to Cal\ncofluor, reduced amount of chitin in the cell wall\n mADE3:Required for the biosynthesis of purines, thymidylate, methi\nonine, histidine, pantothenic acid and formylmethionyl-tRNA,\nC1-tetrahydrofolate synthase,Null mutant is viable, adenine \nauxotroph, histidine auxotroph\n mADE4:phosphoribosylpyrophosphate amidotransferase,phosphoribosylp\nyrophosphate amidotransferase,Adenine requiring\n mADE6:5'-phosphoribosylformyl glycinamidine synthetase,5'-phosphor\nibosylformyl glycinamidine synthetase,Adenine requiring\n mPDX3:pyridoxine (pyridoxiamine) phosphate oxidase,pyridoxine (pyr\nidoxiamine) phosphate oxidase,\n mADE8:glycinamide ribotide transformylase,glycinamide ribotide tra\nnsformylase,Adenine requiring\n mYJL007C:Unknown ,, Unknown\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 mYDR157W:Unknown ,, Unknown\n mYPL098C:Unknown ,, Unknown\n mYML030W:Unknown ,, Unknown\n mGCS1:Zn-finger-containing protein that functions as ADP-ribosylat\nion factor GTPase-activating protein and is involved in regu\nlating vesicle transport,ADP-ribosylation factor GTPase-acti\nvating protein (ARF GAP),Null mutant is cold-sensitive for r\neentry into mitotic cell cycle from stationary phase and sho\nws inefficient secretion of invertase\n mEMI2:Unknown ,, Unknown\n mSEL1:Unknown ,, Unknown\n mGEF1:Integral membrane protein highly homologous to voltage-gated\n chloride channels from humans, mice and fish,transport prot\nein involved in intracellular iron metabolism (putative),Nul\nl mutant is viable; cells grow slowly on rich media containi\nng carbon sources utilized by respiration; fail to grow on g\nlucose when iron concentrations are low in the media\n mPHM6:Phosphate metabolism; transcription is regulated by PHO syst\nem,,\n mEMP70:identified as a 24 kDa cleavage product in endosome-enriched\n membrane fractions,,\n mORT1:Mitochondrial integral membrane protein, ornithine transport\ner,,Null mutant is viable, arginine bradytroph\n mYNL046W:Unknown ,, Unknown\n mSKY1:SRPK1-like Kinase in Yeast (SRPK1 is a human serine kinase t\nhat specifically phosphoryates arginine-serine rich domains \nfound in the SR family of splicing factors.),,Slow growth; D\necreased in vivo phosphorylation of npl3p\n mCDC10 mCDC3 mTHR4 mHOM2 mAAT2 mCSM1 mLRS4 mCYS4 mINO2 mINO4 mTRP2 mTRP3 mPEP8 mVPS35 mVPS5 mVPS17 mCPA2 mCPA1
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Computational Genomics Lab, Tel-Aviv uniresity