Module number 3269




Database revision : gnsdb28.10
Date : Tue Feb 25 17:22:40 2003
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mYER130C:Unknown ,, Unknown\n mYJL211C:Unknown ,, Unknown\n mCPT1:Phospholipid biosynthesis,sn-1,2-diacylglycerol cholinephosp\nhotransferase,Null mutant is viable, cpt1 ept1 double deleti\non mutants are viable\n mSAP30:Hypothetical ORF,,\n mYIL029C:Unknown ,, Unknown\n mYKL037W:Unknown ,, Unknown\n mYKR047W:Unknown ,, Unknown\n mYDR326C:Unknown ,, Unknown\n mPUF4:member of the PUF protein family,,\n mFYV2:Function required for Yeast Viability on toxin exposure,,K1 \nkiller toxin hypersensitivity\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 mSTV1:Stv1p and Vph1p may be equivalent subunits for vacuolar-type\n H(+)-ATPases located on different organelles,110 kDa subuni\nt; not in vacuole membrane , vacuolar H-ATPase,Null mutant i\ns viable, displays additive phenotypes in combination with v\nph1 null mutations\n mCLB3:Involved in mitotic induction and perhaps in DNA replication\n and spindle assembly,B-type cyclin,Null mutant is viable\n mYBR027C:Unknown ,, Unknown\n mMDM1:Intermediate filament protein involved in organelle inherita\nnce,intermediate filament protein,Null mutant is inviable; t\nemperature sensitive mutants display defective transfer of n\nuclei and mitochondria into developing buds at the non-permi\nssive temperature\n mDAL81:Positive regulator of multiple nitrogen catabolic genes,tran\nscriptional activator for allantoin and GABA catabolic genes\n, contains a Zn[2]-Cys[6] fungal-type binuclear cluster doma\nin in the N-terminal region,Null mutant is viable, unable to\n degrade allantoin\n mNAP1:nucleosome assembly protein I,nucleosome assembly protein I,\nNull mutant is viable but exhibits defects in Clb2 function.\n mYNL127W:Unknown ,, Unknown\n mMNN2:Probable type II membrane protein involved in mannan synthes\nis,golgi alpha-1,2-mannosyltransferase (putative),Null mutan\nt is viable. Mannan lacks the main alpha-1,2-linked branches\n mDAL82:Positive regulator of allophanate inducible genes,positive t\nranscriptional regulator,loss of induction for allantoin deg\nradation pathways\n mKAR9:cortical protein required for cytoplasmic microtubule orient\nation; localizes to the tip of shmoo projections and to the \ntip of budding cells in a cell-cycle dependent manner,,Null \nmutant is viable; cytoplasmic microtubule orientation defect\ns, nuclear migration defects, benomyl sensitive\n mYHR126C:Unknown ,, Unknown\n mYFL013W-A:Unknown ,, Unknown\n mPEX14:Peroxisomal peripheral membrane protein (peroxin) involved i\nn import of peroxisomal matrix proteins,,Null mutant is viab\nle but is unable to grow on oleate and lacks peroxisomes\n mBUL2:a homologue of BUL1,,Null mutant is viable; the bul1 bul2 do\nuble disruptant is sensitive to various stresses\n mYPL150W:Unknown ,, Unknown\n mZRC1:Zinc- and cadmium-resistance protein,,Null mutant is viable \nand sensitive to zinc\n mDCW1:Unknown ,, Unknown\n mGPM2:Similar to GPM1 (phosphoglycerate mutase); converts 3-phosph\noglycerate to 2-phosphoglycerate in glycolysis,,Null mutant \nis viable, gpm2 gpm3 double deletion mutants exhibit no synt\nhetic phenotypes\n mNPR1:protein kinase homolog,protein kinase homolog,inactive ammon\nia-sensitive amino acid permeases\n mSMM1:Suppressor of Mitochondrial Mutation in the tRNAasp gene; Di\nhydrouridine synthase 2,tRNA dihydrouridine synthase,Overexp\nression weakly suppresses a mutation affecting the maturatio\nn of mitochondrial tRNA-Asp.\n mNPR2:Putative post-transcriptional regulator of nitrogen permease\ns,,Changes in urea and proline transport capacities\n mDAN1:Delayed Anaerobic,cell wall mannoprotein , induced during an\naerobic growth,Null mutant is viable\n mJEM1:DnaJ-like protein of the endoplasmic reticulum membrane,,Nul\nl mutant is viable but has karyogamy defect; jem1 scj1 doubl\ne mutant is temperature sensitive\n mYDR203W:Unknown ,, Unknown\n mSTE24:zinc metallo-protease that catalyzes the first step of N-ter\nminal processing of the yeast a-factor precursor,zinc metall\no-protease,Null mutant is viable, exhibits a mating efficien\ncy of ~5% that of a wild-type strain and an a-factor process\ning defect\n mMAK10:Glucose-repressible protein,,Null mutant is viable, grows po\norly on nonfermentable carbons sources\n mGAL1:Haploid specific protein localized in the Golgi and plasma m\nembrane,galactokinase,Null mutant is viable and cannot utili\nze galactose.\n mIES1:Hypothetical ORF,,Null mutant is viable\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 mVPS13:vacuolar Protein Sorting,,Null mutant is viable but exhibits\n defects in vacuolar protein sorting.\n mSSK1:Two-component signal transducer that with Sln1p regulates os\nmosensing MAP kinase cascade(suppressor of sensor kinase),tw\no-component signal transducer that with Sln1p regulates osmo\nsensing MAP kinase cascade(suppressor of sensor kinase),Null\n mutant is viable; suppresses the lethality of sln1 or ypd1 \ndisruption mutants\n mYJR142W:Unknown ,, Unknown\n mWSC2:cell wall integrity and stress response component 2,contains\n novel cysteine motif , integral membrane protein (putative)\n , similar to SLG1 (WSC1), WSC3 and WSC4,Null mutant is viab\nle and shows no phenotypes; slg1 (wsc1)-null wsc2-null doubl\ne mutant shows a lysis defect on YPD at room temperature and\n heat shock sensitivity; overexpression of WSC genes suppres\nses heat shock sensitivity of hyperactivated ras mutant; hea\nt shock sensitivity of wsc mutant strain is suppressed by de\nletion of ras2\n mYKR100C:Unknown ,, Unknown\n mGIS2:GIG3 suppressor,,\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 mYBL083C:Unknown ,, Unknown\n mPEX6:Required for peroxisome assembly,AAA ATPase,lack of peroxiso\nme biogenesis\n mBSD2:metal homeostasis protein; putative membrane protein,,Null m\nutant is viable; suppressor of oxygen toxicity in sod1 mutan\nts, increased sensitivity to copper and cadmium toxicity, el\nevation in copper ion accumulation\n mYGR206W:Unknown ,, Unknown\n mYBR108W:Unknown ,, Unknown\n mYMR102C:Unknown ,, Unknown\n mYLR137W:Unknown ,, Unknown\n mMRS2:mitochondrial magnesium ion transporter similar to bacterial\n CorA, essential for splicing of group II introns,magnesium \nion transporter,Null mutant is viable; has a pet- phenotype,\n associated with a block in mitochondrial RNA splicing of al\nl mitochondrial group II introns\n mYKL033W-A:Unknown ,, Unknown\n mPTK1:Putative serine/threonine protein kinase,,Mutant shows decre\nase in total polyamine accumulation and resistance to polyam\nine analogs; ptk1 ptk2 double mutant shows virtually abolish\ned high-affinity spermidine transport\n mYHL044W:Unknown ,, Unknown\n mFZF1:involved in sulfite resistance,contains five zinc fingers , \ntranscription factor (putative) , contains five zinc fingers\n , transcription factor (putative),Null mutant is viable, su\nlfite sensitive. FZF1 is a high copy suppressor of grr1 muta\nnts\n mDIG1:Down-regulator of Invasive Growth, Regulator of Sterile Twel\nve, binds Fus3 and Ste12,MAP kinase-associated protein,Null \nmutant is viable, shows abnormal bud morphology; dig1 dig2 d\nouble mutants show constitutive mating defect and invasive g\nrowth; overexpression causes pheromone resistance\n mYBR246W:Unknown ,, Unknown\n mIMP2':Protein involved in nucleo-mitochondrial control of maltose,\n galactose and raffinose utilization,transcription factor,Nu\nll mutant is viable, Inability to grow on maltose, galactose\n and raffinose in respiratory-deficient conditions or in the\n presence of ethidium bromide and erythromycin; leaky phenot\nype on oxidizable carbon sources: sensitivity to heat shock \nand sporulation deficiency\n mYNL136W:Unknown ,, Unknown\n mKRE11:Involved in biosynthetic pathway for cell wall beta-glucans,\n,Null mutant is viable; killer toxin resistant; reduced leve\nls of 1,6-beta-glucan in cell wall\n mOST3:Catalyzes the transfer of oligosaccharide from dolichol-olig\nosaccharide donor to consensus glycosylation acceptor sites \n(asparagines) in newly synth. proteins - ER lumen; may enhan\nce oligosacch. transfer to subset of acceptor substrates,oli\ngosaccharyl transferase glycoprotein complex 34 kDa gamma su\nbunit,Null mutant is viable but shows underglycosylation of \nsoluble and membrane-bound glycoproteins and contains less o\nligosaccharyltransferase activity in vitro\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 mYOS9:Unknown ,, Unknown\n mPPH3:protein phosphatase type 2A,protein phosphatase type 2A,Null\n mutant is viable, pph3 pph21 pph22 mutants are inviable\n mOST6:Putative new 37kDa subunit of N-oligosaccharyltransferase co\nmplex,N-oligosaccharyltransferase complex 37kDa subunit (put\native),\n mVPS29:vacuolar protein sorting,,Defective for sorting of soluble h\nydrolases to the vacuole. Mislocalisation of the vacuolar hy\ndrolase sorting receptor Vps10p.\n mYBR174C:Unknown ,, Unknown\n mYKL061W:Unknown ,, Unknown\n mYKL207W:Unknown ,, Unknown\n mFCY21:identical to FCY2,purine-cytosine permease,\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 mMAI1:Unknown ,, Unknown\n mSBE22:functionally redundant and similar in structure to SBE2,,syn\nthetic lethal with sbe2 mutation\n mYJL207C:Unknown ,, Unknown\n mYPR170C:Unknown ,, Unknown\n mVPS4:Defective in vacuolar protein sorting; homologous to mouse S\nKD1 and to human hVPS4,AAA ATPase,Null mutant is viable, exh\nibits protein sorting and morphological defects\n mYDR466W:Unknown ,, Unknown\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 mYJL192C:Unknown ,, Unknown\n mRCE1:Protease involved in ras and a-factor terminal proteolysis,p\nrotease,Null mutant is viable, has defects in Ras localizati\non and signaling, and suppresses the activated phenotype of \nthe RAS2val19 allele\n mSAT4:Protein with similarity to Npr1p protein kinase,,\n mYER140W:Unknown ,, Unknown\n mPIN4:[PSI+] induction,,Other phenotypes: overexpression of PIN4 a\nllows for the induction of the [PSI+] prion by Sup35p overpr\noduction in the strains cured of [PIN+].\n mNBP2:interacts with Nap1, which is involved in histone assembly,,\n mGTS1:Protein homologous to Drosophila clock protein,glycine-threo\nnine-serine repeat protein,Null mutant is viable; shows redu\nced lag phase\n mYJL178C:Unknown ,, Unknown\n mYDL203C:Unknown ,, Unknown\n mKRE20:Killer toxin REsistant,,Null mutant is viable but exhibits K\n1 killer toxin resistance.\n mYDL050C:Unknown ,, Unknown\n mMYO5:contains proline-rich tail homology 2 (TH2) and SH3 domains,\nmyosin I,Null mutant is viable; myo3 myo5 double deletion mu\ntants exhibit loss of actin polarity, growth arrest at 37 de\ngrees or high osmotic strength, accumulation of intracellula\nr membranes, and loss of polarized cell surface growth; myo3\n myo5 double mutants have longer doubling times and thicker \ncell walls\n mVPS38:involved in vacuolar protein targeting,,\n mVTH1:vps ten homolog,potential membrane glycoprotein (putative) ,\n strong similarity to Vth2 and Pep1/Vps10,Null mutant is via\nble; overexpression partially suppresses the sorting defect \nof a pep1 null mutant.\n mYUR1:Probable glycosyltransferase of KRE2/KTR1/YUR1 family; locat\ned in the Golgi,mannosyltransferase,Null mutant is viable\n mYAP3:bZIP protein; transcription factor,,\n mYNR068C:Unknown ,, Unknown\n mATX1:antioxidant protein and metal homeostasis factor, protects a\ngainst oxygen toxicity,copper binding homeostasis protein (p\nutative),hypersensitive toward paraquat (a generator of supe\nroxide anion)\n mYLL049W:Unknown ,, Unknown\n mSEC72:protein involved in membrane protein insertion into the ER,,\nNull mutant is viable, accumulates a subset of secretory pre\ncursors\n mMAL11:Part of MAL1 complex locus; encodes funct. maltose permease \nin all strains, exhibits sign. seq. variability; shows homol\n. to functional maltose permease from S. carlsbergenesis; me\nmber of the 12 tm domain superfamily of sugar transporters,a\nlpha-glucoside transporter , hexose transporter , maltose pe\nrmease,Mutant is defective in maltose fermentation.\n mERG4:Sterol C-24 reductase,sterol C-24 reductase,Null mutant is v\niable\n mRXT3:Unknown ,, Unknown\n mVPS41:vacuolar protein sorting,,Null mutant is viable, associated \nwith fragmented vacuoles, exhibits defective high affinity t\nransport due to impaired Fet3p activity and also exhibits de\nfects in the processing and sorting of multiple vacuolar hyd\nrolases\n mMNR2:Product of gene unknown,,overexpression overcomes manganese \ntoxicity\n mYCK2:membrane-bound casein kinase I homolog,casein kinase I homol\nog,Null mutant is viable; yck1 yck2 double deletion mutant i\ns inviable\n mKIN3:protein kinase,protein kinase,Null mutant is viable\n mEND3:Required for endocytosis and organization of the cytoskeleto\nn,,Null mutant is viable and defective in endocytosis\n mMCM22:Required for maintenance of chromosomes and minichromosomes,\n,Null mutant is viable\n mECM39:ExtraCellular Mutant,,A Tn3 insertion into this gene causes \nhypersensitivity to the cell surface polymer perturbing agen\nt calcofluor white.\n mYKL136W:Unknown ,, Unknown\n mYBL086C:Unknown ,, Unknown\n mMAK3:N-acetyltransferase,N-acetyltransferase,deficient in mainten\nance of killer\n mAAT2:aspartate aminotransferase, cytosolic,aspartate aminotransfe\nrase,\n mYOR164C:Unknown ,, Unknown\n mYGL046W:Unknown ,, Unknown\n mGOT1:Golgi Transport,membrane protein,Null mutant is viable but e\nxhibits ER to Golgi transport defects in vitro. got1 is synt\nhetically lethal with mutations in sft2; the got1 sft2 doubl\ne mutant exhibits defects in transport to the Golgi complex.\n mYBR220C:Unknown ,, Unknown\n mSWR1:Sick With Rat8 ts,RNA helicase (putative) , deah box protein\n,Null mutant is viable and shows no growth defects; swr1 rat\n8-2 double mutant has a slow growth phenotype; SWR1 is a par\ntial High copy suppressor of pse1-1 kap123\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 mSWC1:Unknown ,, Unknown\n mARP1:actin-related protein of the dynactin complex,,Null mutant i\ns viable, but both null mutations and overexpression lead to\n defects in spindle orientation and nuclear migration\n mRDS2:Unknown ,, Unknown\n mYOL111C:Unknown ,, Unknown\n mARP6:actin-related protein,,\n mYPS7:Gpi-anchored aspartic protease (Yapsin 7),GPI-anchored aspar\ntic protease,\n mYOR091W:Unknown ,, Unknown\n mMDR1:Mac1-dependent regulator,GTPase activating protein (GAP) fo\nr Ypt6,Null mutant is viable\n mNHP10:Non-Histone Protein 10,HMG1-box containing protein,null muta\nnt is viable and has normal growth rate\n mWHI2:Protein involved in growth regulation,,Null mutant is viable\n mENT4:epsin N-terminal homology-containing protein,,unknown\n mFUI1:uridine permease,uridine permease,Null mutant is viable, res\nistant to 5-fluorouridine and does not grow on media contain\ning uridine as the sole source of pyrimidines\n mENT5:Unknown ,, Unknown\n mRIT1:Modifies initiator methionine tRNA to distinguish it from el\nongator methionine tRNA,initiator methionine tRNA 2'-O-ribos\nyl phosphate transferase,Abolishes requirement for elongator\n methionine tRNA\n mYNR040W:Unknown ,, Unknown\n mMRPL13:mitochondrial ribosomal protein YmL13,ribosomal protein (YmL\n13),Null mutant is viable, grows poorly on non-fermentable c\narbon sources\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 mCHS6:Involved in chitin biosynthesis and/or its regulation,,Reduc\ned levels of chitin, temperature-sensitive growth on rich me\ndium in certain genetic backgrounds\n mYDL096C:Unknown ,, Unknown\n mRPL15B:Homology to rat L15,ribosomal protein L15B (YL10) (L13B) (rp\n15R),\n mSWD1:YAR003W,,\n mSWD3:YBR175W,,\n mYJR111C:Unknown ,, Unknown\n mMAL31:Part of the complex locus MAL3; functional in S288C; highly \nhomologous to MAL61 from S. cerevisiae, MAL61 from S. carlsb\nergenesis strains JM1901 and CB11, and MAL1T from strain 405\n9,maltose permease,Defective maltose fermentation\n mBUD14:Hypothetical ORF,,Null mutant is viable; random budding in d\niploid null mutants\n mPSR2:Plasma membrane Sodium Response 2,,Mutant is sensitive to so\ndium ions.\n mTRM1:N2,N2-dimethylguanosine-specific tRNA methyltransferase,N2,N\n2-dimethylguanosine-specific tRNA methyltransferase,An uncha\nracterized allele affects a specific base modification of bo\nth cytoplasmic and mitochondrial tRNA.\n mVPS60:vacuolar protein sorting (putative),,Null mutant is viable b\nut a class E vps mutant (missorts vacuolar hydrolases and ac\ncumulates late endosomal compartment).\n mYOR325W:Unknown ,, Unknown\n mYJL064W:Unknown ,, Unknown\n mYPR050C:Unknown ,, Unknown\n mAPG10:Involved in autophagy; protein-conjugating enzyme involved i\nn the Apg12p-Apg5p conjugation pathway,protein-conjugating e\nnzyme,Defective autophagy, apg10-1 allele shows reduced viab\nlility under starvation conditions\n mYLR374C:Unknown ,, Unknown\n mAPG12:autophagy,,Null mutant is viable, defective in autophagy\n mSHR5:Involved in RAS localization and palmitoylation,,Null mutant\n is viable; exhibits normal palmityltransferase activity in \nvitro and attenuates Ras function in cells with mutant Ras2 \nproteins that are not farnesylated or palmitoylated; shr5 mu\ntation originally isolated as suppressor of Ras function\n mYKR018C:Unknown ,, Unknown\n mKRE1:cell wall beta-glucan assembly,,Null mutant is viable, exhib\nits reduction in cell wall (1--6)-beta-glucan\n mPHO13:p-nitrophenyl phosphatase,p-nitrophenyl phosphatase,Null mut\nant is viable\n mAPG16:autophagy,,Null mutant is viable, defective in autophagy\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 mPAK1:high copy suppressor of temperature sensitive cdc17 (DNA pol\nymerase alpha) mutations,,Null mutant is viable\n mYDL133W:Unknown ,, Unknown\n mSNA2: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 mARR4:Unknown ,, Unknown\n mYGR269W:Unknown ,, Unknown\n mAGE1:ADP-ribosylation factor (ARF) GTPase activating protein (GAP\n) effector,ARF GAP with effector function(s),Null mutant is \nviable\n mYDR049W:Unknown ,, Unknown\n mVPS71:Unknown ,, Unknown\n mVPS72:Unknown ,, Unknown\n mBNI4:bud neck involved,required to link Chs3p and Chs4p to the se\nptins,Null mutant is viable, shows delocalized chitin, elong\nated buds, enlarged bud necks\n mVPS73:Unknown ,, Unknown\n mMET32:Involved in methionine metabolism,highly homologous to Met31\np , transcriptional regulator of sulfur amino acid metabolis\nm , zinc finger protein,the met31 met32 double mutant is a m\nethionine auxotroph\n mSIP3:Interacts with SNF1 protein kinase,transcriptional activator\n (putative),Null mutant is viable; does not confer snf1 phen\notypes\n mBUD2:GTPase-activating protein (GAP) for Rsr1p/Bud1p,GTPase activ\nating protein (GAP) for Rsr1p/Bud1p,Null mutant is viable, w\nith random bud site selection in all cell types\n mELM1:cell morphology,protein kinase,formation of expanded, branch\ned chains of elongated cells; grow invasively under the surf\nace of agar medium\n mYJR083C:Unknown ,, Unknown\n mUBP13:similar to Ubp9p,ubiquitin carboxyl-terminal hydrolase,\n mBUD6:actin interacting rotein,,Null mutant is viable; mutants exh\nibit severe disruption of the actin cytoskeleton; deletion s\ntrains have a depolarized cytoskeleton, mitotic delay, and p\nrobable cytokinesis defects\n mBUD7:bud site selection,,Diploid-specific heterogenous bud site s\nelection\n mYGL231C:Unknown ,, Unknown\n mYGL217C:Unknown ,, Unknown\n mSCS2:Likely to be involved in regulating INO1 expression, suppres\nsor of a dominant nuclear mutation that is inositol-dependen\nt in the presence of choline,,Null mutant is viable but is a\nn inositol auxotroph above 34 deg.\n mRCY1:Unknown ,, Unknown\n mYBL089W:Unknown ,, Unknown\n mNCR1:Niemann-Pick Type C homologous gene,transmembrane protein (p\nutative),Null mutant is viable.\n mNMD2:Protein involved in decay of mRNA containing nonsense codons\n,,Null mutant is viable, exhibits stabilization of nonsense-\ncontaining mRNAs\n mYBL010C:Unknown ,, Unknown\n mNMD4:putative Upf1p-interacting protein,,\n mKSS1:Recovery from alpha factor arrest,MAP kinase , involved in p\nheromone signal transduction,\n mSHE1:Product of gene unknown,,\n mYFL049W:Unknown ,, Unknown\n mDPH2:Diptheria toxin resistance protein, required for diphthamide\n biosynthesis,,Null mutant is viable\n mAMD1:putative alpha-mannosidase,alpha-mannosidase (putative),Null\n mutant is viable\n mHOC1:Homologous to OCH1, an alpha-1,6-mannosyltransferase; Golgi-\nlocalized, type II integral membrane protein,mannosyltransfe\nrase (putative),Null mutant is viable but is hypersensitive \nto calcofluor white and hygromycin B and has lowered restric\ntive temperature in a pkc1-371 background; high copy suppres\nsor of pkc1-371\n mDFG5:Protein required for filamentous growth, cell polarity, and \ncellular elongation,,Null mutant is viable and defective in \nfilamentous growth\n mDPH5:diphthamide biosynthesis,,Null mutant is viable\n mYHR155W:Unknown ,, Unknown\n mALG5:UDP-glucose:dolichyl-phosphate glucosyltransferase,UDP-gluco\nse:dolichyl-phosphate glucosyltransferase,underglycosylation\n of carboxypeptidase Y\n mTAT2:Tryptophan permease, high affinity,tryptophan permease, high\n affinity,suppressor of chromosome segregation mutation\n mYHP1:Hypothetical ORF,,\n mYDR269C:Unknown ,, Unknown\n mALG8:adds glucose to the dolichol-linked oligosaccharide precurso\nr prior to transfer to protein,glycosyl transferase,Null mut\nant is viable, secretes under-glycosylated proteins\n mALG9:catalyzes the transfer of mannose from Dol-P-Man to lipid-li\nnked oligosaccharides,mannosyltransferase,accumulation of li\npid-linked Man6GlcNAc2; hypoglycosylation of secreted protei\nns\n mYMR029C:Unknown ,, Unknown\n mCDC50:cell division cycle mutant,,Null mutant is cold-sensitive an\nd sensitive to MMS and HU\n mCNE1:Functions in endoplasmic reticulum protein quality control,c\nalnexin and calreticulin homolog,Null mutant is viable, incr\nease of cell-surface expression of ste2-3p, increase in secr\netion of heterologously expressed mammalian alpha 1-antitryp\nsin\n mSBH2:Ssh1p-Sss1p-Sbh2p complex component, involved in protein tra\nnslocation into the endoplasmic reticulum,Sbh1p homolog,Null\n mutant is viable. sbh1 sbh2 double deletion mutants exhibit\n synthetic temperature sensitivity and accumulation of secre\ntory protein precursors\n mIRS4:Increased rDNA silencing,,Null mutant is viable and shows in\ncreased rDNA silencing\n mLHP1:Protein homologous to human La (SS-B) autoantigen,,Null muta\nnt is viable\n mYKR035C:Unknown ,, Unknown\n mYJL162C:Unknown ,, Unknown\n mYBR071W:Unknown ,, Unknown\n mCIT3:Mitochondrial isoform of citrate synthase,citrate synthase,N\null mutant shows severely reduced growth on the respiratory \nsubstrate glycerol in a delta cit1 background\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 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 mYPL261C:Unknown ,, Unknown\n mYDR357C:Unknown ,, Unknown\n mSEO1:Suppressor of Sulfoxyde Ethionine resistance,permease (putat\nive),\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mYNL122C:Unknown ,, Unknown\n mSDC1:YDR469W,,\n mURK1:converts ATP and uridine to ADP and UMP,uridine kinase,\n mPOL32:Polymerase-associated gene,55 kDa , DNA polymerase delta sub\nunit,Null mutant is viable but is cold-sensitive, hydroxyure\na-sensitive, defective for induced mutagenesis, synthetic le\nthal with pol3, pol30 and pol31\n mYPR039W:Unknown ,, Unknown\n mYOL093W:Unknown ,, Unknown\n mYCL005W:Unknown ,, Unknown\n mYPR061C:Unknown ,, Unknown\n mYBL012C:Unknown ,, Unknown\n mAPL3:clathrin Associated Protein complex Large subunit,clathrin a\nssociated protein complex large subunit,Null mutant is viabl\ne\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 mSTB3:binds Sin3p in two-hybrid assay,,Null mutant is viable\n mAPL5:Delta-like subunit of the yeast AP-3 complex which functions\n in transport of alkaline phosphatase to the vacuole via the\n alternate pathway, suppressor of loss of casein kinase 1 fu\nnction,clathrin assembly complex AP-3 adaptin component delt\na-like subunit,Null mutant is viable, rescues yck1,yck2 doub\nle mutant\n mIDP1:Mitochondrial form of NADP-specific isocitrate dehydrogenase\n,NADP-dependent isocitrate dehydrogenase,Null mutant is viab\nle\n mYBL062W:Unknown ,, Unknown\n mYGR106C:Unknown ,, Unknown\n mYOR300W:Unknown ,, Unknown\n mMCK1:Disp. for mitosis, required for chr. segregation, benomyl re\nsist., basal IME1 transcript. in mitosis, IME1 induction in \nmeiosis & ascus mat. independ. of IME1; maybe in mitotic chr\n. segregation specific to CDEIII,43.1 kDa serine/threonine/t\nyrosine protein kinase,Null mutant is viable, cold sensitive\n, temperature sensitive, and benomyl sensitive; associated w\nith delays and decreased levels of sporulation. High copy MC\nK1 acclerates early gene expression.\n mHOT1:high osmolarity induced transcription,nuclear protein,osmost\nress hypersensitivity\n mRIM13:calpain-like protease involved in proteolytic processing of \nRim1p,cysteine protease , similar to E. nidulans palB,Mutant\n shows reduced expression of IME1, defect in Rim1p C-termina\nl proteolytic processing, reduced sporulation, slow growth a\nt 17 degrees, smooth colony morphology and slow growth in al\nkaline medium (pH8.0).\n mELA1:similar to mammalian elongin A, interacts with elongin C,elo\nngin A transcription elongation factor,viable\n mYOR053W:Unknown ,, Unknown\n mTRS33:Trapp subunit of 33 kDa,,Null mutant is viable\n mYOL036W:Unknown ,, Unknown\n mDCR2:Unknown ,, Unknown\n mSNT1:,,\n mYNL043C:Unknown ,, Unknown\n mRGA2:contains a Rho-GAP domain and two LIM domains, similar to Rg\na1p and all known Rho-GAPs,Rho-GTPase Activating Protein,Nul\nl mutants are viable but increase the restrictive temperatur\ne of a cdc24-4 strain and increase the constitutive activati\non of the pheromone response pathway in conjungtion with mut\nations in RGA1 and BEM3; overexpression of RGA2 causes a dec\nrease in the restrictive temperature of a cdc42-1 strain\n mMKC7:protease involved in protein processing that shares function\ns with Yap3 and Kex2,aspartyl protease , related to Yap3p,Nu\nll mutant is viable, mkc7 yap3 double mutants are temperatur\ne sensitive, and mkc7 yap3 kex2 triple mutants are temperatu\nrea nd cold-sensitive\n mYBR219C:Unknown ,, Unknown\n mYNL319W:Unknown ,, Unknown\n mPSH1:Unknown ,, Unknown\n mPRK1:p53 regulatory kinase,serine/threonine kinase (putative),Nul\nl mutant is viable. Strains that overexpress Prk1 are inviab\nle.\n mDIP5:dicarboxylic amino acid permease,dicarboxylic amino acid per\nmease,Null mutant is viable, exhibits loss of L-aspartate an\nd L-glutamate uptake\n mAPM3:Mu3-like subunit of the yeast AP-3 complex which functions i\nn transport of alkaline phosphatase to the vacuole via the a\nlternate pathway,clathrin associated protein complex medium \nsubunit,Null mutant is viable, even combined with apm1 and a\npm2\n mSKN7:Protein with similarity to DNA-binding region of heat shock \ntranscription factors,,Null mutant is viable\n mYMR158W-A:Unknown ,, Unknown\n mAPM4:Clathrin associated protein, medium subunit,clathrin associa\nted protein complex medium subunit,\n mINP54:INositol polyphosphate 5-Phosphatase, fourth one identified;\n has homology to Type I mammalian inositol polyphosphate 5-p\nhosphatases,inositol polyphosphate 5-phosphatase,\n mYBL006C: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 mBBC1:shows synthetic fitness defect with bni1 mutants and associa\ntes with the Bee1p-Vrp1p-Myo3/5p complex,,\n mMDM39:Unknown ,, Unknown\n mVTA1:Unknown ,, Unknown\n mCWH41:Glucosidase I, involved in assembly of cell wall beta 1,6 gl\nucan; an ER type II integral membrane N-glycoprotein,glucosi\ndase I,Null mutant is viable, associated with K1 killer toxi\nn-resistant phenotype and a 50% reduction in the cell wall b\neta 1,6-glucan level\n mCWH43:,,\n mYGL242C:Unknown ,, Unknown\n mYPL176C:Unknown ,, Unknown\n mBPH1:beige protein homologue 1,,Null mutant is viable, sensitive \nto low pH\n mSNF7:Involved in derepression of SUC2 in response to glucose limi\ntation,,Null mutant is viable. Similar to disruption SNF8, S\nNF7 disruption causes a fewfold decrease in invertase derepr\nession, a growth defect on raffinose, temperature-sensitive \ngrowth on glucose, and a sporulation defect in homozygous di\nploids. Genetic interactions suggest SNF7 is different from \nSNF2, SNF5 and SNF6, members of the SNF/SWI chromatin remode\nling complex\n mSNF8:appears to be functionally related to SNF7,,Null mutant is v\niable, sporulation defective, grows poorly on raffinose as a\n carbon source, shows a five-fold decrease in invertase dere\npression\n mTHR1:homoserine kinase,homoserine kinase,Null mutant is viable, t\nhreonine auxotroph\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 mYEL059W:Unknown ,, Unknown\n mCLN3:role in cell cycle START; involved in G(sub)1 size control,G\n1 cyclin,Null mutant is viable; dominant mutation causes alp\nha-factor resistance and small cell size; chromosomal deleti\non increases cell volume\n mYDR112W:Unknown ,, Unknown\n mCCW12:Hypothetical ORF,cell wall mannoprotein,Null mutant is viabl\ne and shows decrease in mating efficiency and defect in aggl\nutination\n mCCW14:Secretory Stress Response protein,cell wall mannoprotein,Nul\nl mutant is viable\n mSIF2:Sir4p-Interacting Factor,,Null mutant is viable, exhibits in\ncreased telomeric silencing\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 mCTF3:Unknown ,, Unknown\n mYLR431C:Unknown ,, Unknown\n mSPP1:YPL138C,,\n mTOM7:Involved in mitochondrial protein import,translocase of the \nouter mitochondrial membrane,Null mutant is viable\n mYMR306C-A:Unknown ,, Unknown\n mRHO2:Gtp-binding protein of the rho subfamily of ras-like protein\ns,GTP-binding protein , rho subfamily,null is viable\n mYOR055W:Unknown ,, Unknown\n mSYT1:Suppressor of Ypt3,,\n mOPI3:Second and third steps of methylation pathway for phosphatid\nylcholine biosynthesis,methylene-fatty-acyl-phospholipid syn\nthase (unsaturated phospholipid N-methyltransferase),Null mu\ntant is viable, temperature sensitive in the presence of mon\nomethylethanolamine, exhibits an inositol secretion phenotyp\ne\n mYDL146W:Unknown ,, Unknown\n mYCR076C:Unknown ,, Unknown\n mPSY1:Unknown ,, Unknown\n mYOL046C:Unknown ,, Unknown\n mPSY3:Unknown ,, Unknown\n mUFD2:Ubiquitin fusion degradation protein,,Null mutant is viable \nbut exhibits increased sensitivity to ethanol stress.\n mYBR235W:Unknown ,, Unknown\n mAOR1:actin overexpression resistant,,Sensitive to NaCl and NaF at\n >35 deg. C.\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 mYNL089C:Unknown ,, Unknown\n mYOL003C:Unknown ,, Unknown\n mVTC1:Null mutant identified in different genetic screens both by \nits ability to reverse the Cdc42p suppression of a cdc24-4ts\n mutant and its ability to suppress the vacuolar ATPase null\n phenotype,S. pombe Nrf1p homolog (97% identical in predicte\nd amino acid sequence),Null mutant is viable, but exhibits b\noth reduced V-ATPase in the vacuolar membrane and reduced H(\n+)-ATPase(Pma1p) in the plasma membrane\n mLYP1:lysine permease,lysine permease,\n mPHO84:inorganic phosphate transporter, transmembrane protein,inorg\nanic phosphate transporter,Null mutant is viable\n mUBP7:Ubiquitin-specific protease,ubiquitin-specific protease,\n mPHO87:May collaborate with Pho86p and Pho84p in inorganic phosphat\ne uptake; protein contains 12 predicted transmembrane domain\ns,phosphate permease,Null mutant is viable; pho86 pho87 doub\nle mutant constitutively synthesizes repressible acid phosph\natase and is aresenate-resistant\n mAUA1:Involved in ammonia regulation of GAP1 activity,,Null mutant\n is viable\n mITC1:Imitation switch Two Complex 1,,Null mutant is viable, but s\nhows abnormal morphology and reduced mating efficiency when \nthe disruption is in a MATalpha background. \n mYJL123C:Unknown ,, Unknown\n mYPR064W:Unknown ,, Unknown\n mYIL158W:Unknown ,, Unknown\n mEAF6:Unknown ,, Unknown\n mSCJ1:dnaJ homolog,DnaJ homolog,Null mutant is viable but exhibits\n defects in protein sorting and sensitivity to tunicamycin.\n mCOG7:Unknown ,, Unknown\n mCOG8:Unknown ,, Unknown\n mSUR2:Suppressor of rvs161 and rvs167 mutations,sphingosine hydrox\nylase,Null mutant is viable, has altered phospholipid levels\n mEGD1:beta subunit of the nascent-polypeptide-associated complex (\nNAC); homologous to human BTF3b; GAL4 enhancer protein,pol I\nI transcribed genes regulator,Null mutant is viable; reduced\n induction of galactose-regulated genes upon shift from gluc\nose to galactose\n mDID2:Doa4-independent degradation; Rad52 Inhibitor (Fifty Two Inh\nibitor),class E vacuolar-protein sorting and endocytosis fac\ntor,Overexpression causes growth inhibition and G2 arrest in\n rad52 and cdc9 mutants; null mutants are canavanine-hyperse\nnsitive, temperature sensitive, and suppress defects associa\nted with loss of DOA4\n mYGL034C:Unknown ,, Unknown\n mCUE1:Cue1p assembles with Ubc7p. Cue1p recruits Ubc7p to the cyto\nsolic surface of the endoplasmic reticulum. Assembly with Cu\ne1p is a prerequisite for the function of Ubc7p,Ubc7p bindin\ng and recruitment protein,Null mutant is viable and shows st\nabilization of ER degradation substrates\n mDSE3:Hypothetical ORF,,\n mYND1:Yeast Nucleoside Diphosphatase,apyrase (NDPase/NTPase),Null \nmutant is viable but vanadate-resistant and hygromycin-sensi\ntive. The double mutant ynd1 gda1 exhibits slow growth and s\nubstantial defects in protein glycosylation and cell morphol\nogy.\n mRAV2:Regulator of (H+)-ATPase in Vacuolar membrane,,\n mSGN1:contains one RNA recognition (RRM) domain,,\n
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Computational Genomics Lab, Tel-Aviv uniresity