Module protein_modification




Database revision : gnsdb28.10
Date : Fri Feb 28 01:36:32 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
mYBR022W:Unknown ,, Unknown\n mHSE1:Unknown ,, Unknown\n mYPR109W:Unknown ,, Unknown\n mMET30:F-box protein involved in sulfur metabolism and protein ubiq\nuitination,contains five copies of WD40 motif and interacts \nwith and regulates Met4p,Null mutant is inviable\n mCOS7:Protein with strong similarity to other subtelomerically-enc\noded proteins such as Cos5p, Ybr302p, Cos3p, Cos1p, Cos4p, C\nos8p, Cos6p, Cos9p,,\n mHAP5:Regulates respiratory functions; subunit of a heterotrimeric\n complex required for CCAAT binding,CCAAT-binding transcript\nion factor component (along with Hap2p and Hap3p),Null mutan\nt is viable\n Jelinski.Jelinski:Regulatory networks revealed by transcriptional profiling of\n damaged Saccharomyces cerevisiae cells: Rpn4 links base exc\nision repair with proteasomes.  Mol Cell Biol. 2000 Nov;20(2\n1):8157-67.\n mYHR121W:Unknown ,, Unknown\n mVPS75:Unknown ,, Unknown\n mCEG1:mRNA guanylyltransferase (mRNA capping enzyme), alpha subuni\nt,mRNA capping enzyme alpha subunit , mRNA guanylyltransfera\nse,Null mutant is inviable\n mATE1:arginyl-tRNA-protein transferase,arginyl-tRNA-protein transf\nerase,Null mutant is viable, but unable to degrade substrate\ns of the N-end rule pathway that start with residues recogni\nzed by the Arg-transferase\n mYBL009W:Unknown ,, Unknown\n mSTE11:involved in the mating signalling pathway,,Null mutant is vi\nable but sterile\n mMOG1:Required for nuclear-protein import,nuclear protein that int\neracts with GTP-Gsp1p,Null mutant is viable, temperature sen\nsitive, exhibits defects in nuclear-protein import; MOG1 ove\nrexpression supresses the temperature sensitivity of gsp1 st\nrains; overexpression of NTF2 or GSP1 can suppress the ts ph\nenotype of mog1\n Cond711:t2+Vec\n mMUP3:methionine uptake,very low affinity methionine permease,\n mYDR115W:Unknown ,, Unknown\n mCLB4:Involved in mitotic induction,B-type cyclin,Null mutant is v\niable\n mMRPL38:mitochondrial ribosomal protein L14,ribosomal protein L14,\n mYLR077W:Unknown ,, Unknown\n mXPT1:Xanthine Phosphoribosyl Transferase,xanthine phosphoribosyl \ntransferase,Cannot utilize xanthine as a source of GMP\n mYEL015W:Unknown ,, Unknown\n mYGL085W:Unknown ,, Unknown\n mMSG1:Unknown ,, Unknown\n mMNN5:mannan synthesis,golgi alpha-1,2-mannosyltransferase (putati\nve),Null mutant is viable but defective in addition of the a\nlpha-1,3-linked mannose branch to the mannan structure found\n on N-linked glycans.\n mYKR051W:Unknown ,, Unknown\n mSPO7:dispensable for mitosis, but required for a normal mutation \nrate, required for premeiotic DNA synthesis, recombination, \nmeiosis I, meiosis II, glycogen degradation and spores,,Null\n mutant is viable, sporulation defective\n Cond719:t4-SSD1\n mSSP120:secretory protein,,Null mutant is viable\n mSNF4:involved in release from glucose repression, invertase expre\nssion, and sporulation,associates with Snf1p,Null mutant is \nviable, sucrose nonfermenting; high copy MSI1 and PDE2 parti\nally suppress sporulation defect\n mYGL024W:Unknown ,, Unknown\n Cond724:t4+SSD1,H44\n mYGL198W:Unknown ,, Unknown\n mYIR003W:Unknown ,, Unknown\n mARH1:adrenodoxin oxidoreductase homolog,adrenodoxin oxidoreductas\ne homolog,Null mutant is inviable\n mTAF10:TFIID subunit (TBP-associated factor) with predicted molecul\nar weight of 23 kD.,TFIID subunit,Null mutant is inviable\n Cond713:t4+Vec\n mYMR115W:Unknown ,, Unknown\n mHEM4:catalyzes the fourth step in the heme biosynthesis pathway,u\nroporphyrinogen III synthase,respiratory deficiency, accumul\nation of porphyrins, and heme auxotrophy\n mNUP84:component of nuclear pores; Part of complex with Nup120p, Nu\np85p, Sec13p, and a Sec13p homolog,similar to mammalian Nup1\n07p,Null mutant is viable but has defects in nuclear membran\ne and nuclear pore complex organization and in poly(A)+ RNA \ntransport\n COMP.:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mNUP85:Protein in nuclear pore complex; may function in nuclear env\nelope integrity; may also be involved in tRNA biogenesis,,Nu\nll mutant is viable but is temperature-sensitive; at nonperm\nissive temperature, null mutant accumulates poly(A)+ RNA and\n has fragmented nucleolus; at permissive temperature, nuclea\nr envelope of null mutant detaches from nucleus\n mTAF14:Protein required for actin cytoskeleton assembly or function\n,transcription initiation factor TFIIF small subunit,Null mu\ntant is viable but has a depolarized actin cytoskeleton.\n mSEY1:Unknown ,, Unknown\n mYLR252W:Unknown ,, Unknown\n mYPT32:probably involved in intra-Golgi transport or in the formati\non of transport vesicles at the most distal Golgi compartmen\nt,GTPase , YPT31 homolog , ras homolog,Null mutant is viable\n; ypt31 ypt32 double deletion mutants are inviable\n mCKB1:beta (38kDa) subunit of casein kinase II (CKII),casein kinas\ne II beta subunit,Null mutant is viable, exhibits salt sensi\ntivity specific to NaCl and LiCl\n mCKB2:Casein kinase II, beta' subunit,Casein kinase II beta' subun\nit,Null mutant is viable\n mMRPL40:Mitochondrial ribosomal protein MRPL40 (YmL40),ribosomal pro\ntein (YmL40),\n mMRP51:Mitochondrial Ribosomal Protein,mitochondrial ribosome small\n subunit component,Null mutant is viable, exhibits completel\ny blocked mitochondrial gene expression; missense mutations \nsuppress 5'-UTL mutations in at least 2 mitochondrial mRNAs\n Cond718:t4+SSD1wt\n mMRPS5:Probable mitochondrial ribosomal protein S5,ribosomal protei\nn S5 (putative),\n mSIF2:Sir4p-Interacting Factor,,Null mutant is viable, exhibits in\ncreased telomeric silencing\n mYGL082W:Unknown ,, Unknown\n mYNL026W:Unknown ,, Unknown\n mYME1:Mitochondrial protein of the CDC48/PAS1/SEC18 family of ATPa\nses,,Null mutant is viable, exhibits an elevation in the rat\ne at which copies of TRP1 and ARS1, integrated into the mito\nchondrial genome, escape to the nucleus; a heat-sensitive re\nspiratory-growth defect; a cold-sensitive growth defect on r\nich glucose medium; and synthetic lethality in rho- (cytopla\nsmic petite) cells; yme1 (osd1) mutants fail to degrade newl\ny synthesized subunits of cytochrome c\n mYGR165W:Unknown ,, Unknown\n mMUB1:Homolog of samB gene of Aspergillus nidulans (deletion of sa\nmB results in mislocalization of septa,,Null mutant is viabl\ne but shows multi-budding\n mYDR061W:Unknown ,, Unknown\n mHRB1:an ORF of unknown function located in a centromeric region d\nuplicated between chromosomes III and XIV,hypothetical RNA-b\ninding protein,\n Cond709:t0+Vec\n mPPG1:Serine/threonine protein phosphatase involved in glycogen ac\ncumulation,,Null mutant is viable but accumulates less glyco\ngen\n mYGR111W:Unknown ,, Unknown\n mYLR031W:Unknown ,, Unknown\n mUBS1:General positive regulator of CDC34; Suppress some cdc34 mut\nations when over-expressed,,Null mutant is viable but exhibi\nts a synthetic phenotype with temperature-sensitive alleles \nof cdc34.\n mYNL335W:Unknown ,, Unknown\n mYGR031W:Unknown ,, Unknown\n mRET3:vesicle coat component,vesicle coat component,ret3-1 mutant \nis thermosensitive and shows defects in retrieval of dilysin\ne-tagged proteins from the Golgi back to the ER\n mSEC4:Involved in transport and fusion of post-Golgi secretory ves\nicles to the plasma membrane,ras homolog , small GTP binding\n protein,null is inviable; conditional mutants show defects \nin secretion and accumulation of post-Golgi vesicles under n\non-permissive conditions\n mARE2:Acyl-CoA cholesterol acyltransferase (sterol-ester synthetas\ne),acyl-CoA cholesterol acyltransferase (sterol-ester synthe\ntase),Null mutant is viable; greatly reduces in vivo and in \nvitro ergosterol esterification (to 15 - 35 % of wild-type).\n Deletion of both ARE1 and ARE2 completely eliminates in viv\no and in vitro ergosterol esterification\n mMNS1:specific alpha-mannosidase,alpha-mannosidase,Null mutant is \nviable\n mNUP53:Component of karyopherin docking complex of the nuclear pore\n complex,karyopherin docking complex component of the nuclea\nr pore complex,Null mutant is viable but disrupts Kap121 loc\nalization to the nuclear envelope.\n mYMR210W:Unknown ,, Unknown\n mRSM27:mitochondrial ribosome small subunit component,mitochondrial\n ribosome small subunit component,\n mYPL144W:Unknown ,, Unknown\n Cond717:t2-SSD1\n mSIN4:involved in positive and negative regualtion of transcriptio\nn, possibly via changes in chromatin structure,RNA polymeras\ne II holoenzyme/mediator subunit,Null mutant is viable, temp\nerature sensitive, displays defects in both positive and neg\native regulation of transcription, suppresses Ty insertion m\nutations (Spt-), exhibits decreased superhelical density of \ncircular DNA molecules, exhibits expression from promoters l\nacking UAS elements; associated with a defect in RME1-depend\nent repression and a methionine or cysteine requirement, exh\nibits flocculant/lacy colony morphology, suppressor of snf/s\nwi mutations\n mCPR8:Shows similarity to the secretory pathway cyclophilin Cpr4,c\nyclophilin , peptidyl-prolyl cis-trans isomerase (PPIase),Nu\nll mutant is viable\n mSSU72:functionally related to TFIIB, affects start site selection \nin vivo,,Null mutant is inviable\n mREX3:RNA EXonuclease; member of 3'->5' exonuclease family. See Mo\nser et al. 1997 Nucleic acids Res. 25:5110-5118,,Mutants exh\nibit RNase MRP RNA processing defect; functions redundantly \nwith REX1 and REX2 in U5 snRNA and RNase P RNA processing\n mYLR224W:Unknown ,, Unknown\n mYFL046W:Unknown ,, Unknown\n Cond878:MNNG\n mYOR291W:Unknown ,, Unknown\n mSEC11:signal peptidase subunit,,Null mutant is inviable\n Cond716:t2+SSD1wt\n mYBR206W:Unknown ,, Unknown\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 Cond708:t0+SSD1\n Cond725:t4-SSD1,M31\n mYPR100W:Unknown ,, Unknown\n mYLR253W:Unknown ,, Unknown\n mYDR287W:Unknown ,, Unknown\n mMNN10:Required for mannan synthesis and for polarized growth and b\nud emergence,galactosyltransferase,Null mutant is viable, is\n larger than wild-type cells, is deficient in bud emergence,\n and depends upon an intact morphogenesis checkpoint control\n to survive\n mCBC2:cap binding complex,nuclear cap binding complex subunit,muta\nnts exhibit promiscuous 3'-end formation; sae-1 mutation cau\nses temporary cell cycle arrest in meiotic prophase\n mYOR223W:Unknown ,, Unknown\n Cond712:t4+SSD1\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mMTF1:Mitochondrial RNA polymerase specificity factor,mitochondria\nl RNA polymerase specificity factor,Null mutant is viable, d\nefective in respiration, and lacks mtDNA.\n mYPR140W:Unknown ,, Unknown\n mFOL1:folic acid synthesis,dihydro-6-hydroxymethylpterin pyrophosp\nhokinase , dihydroneopterin aldolase , dihydropteroate synth\netase,essential, induces pseudohyphal growth\n mVPS24:involved in secretion,,Null mutant missorts vacuolar hydrola\nses and accumulates a late endosomal compartment; Class E vp\ns mutant\n mRFC1:RFC is a DNA binding protein and ATPase that acts as a proce\nssivity factor for DNA polymerases delta and epsilon and loa\nds proliferating cell nuclear antigen (PCNA) on DNA,replicat\nion factor C subunit 1 , similar to human RFC 140 kDa subuni\nt,Null mutant is inviable, rfc1 conditional mutants arrest b\nefore mitosis\n mYHR192W:Unknown ,, Unknown\n mGLO2:Cytoplasmic glyoxylase-II,glyoxylase-II,Null mutant is viabl\ne but shows increased sensitivity to methylglyoxal\n mYKL123W:Unknown ,, Unknown\n mPHO86:May collaborate with Pho87p and Pho84p in phosphate uptake,i\nnorganic phosphate transporter (putative),Null mutant is via\nble and expresses repressible acid phosphatase in high phosp\nhate medium; pho86 pho87 double mutant and pho86 pho88 doubl\ne mutant constituvely synthesize repressible acid phosphatas\ne and are arsenate-resistant; pho84 pho86 pho87 triple mutan\nt grows more slowly than pho84 mutant\n Cond723:t2-SSD1,M31\n mMRL1:Mannose 6-phosphate Receptor Like,,\n mGRX5:Member of a glutaredoxin subfamily in Sc together with GRX3 \n& GRX4. Significant sequence diff. with the other glutaredox\nin subfamily, formed by the previously described GRX1 & GRX2\n glutaredoxins (Luikenhuis MBC 9:1081, 1998),glutaredoxin,Nu\nll mutant is viable and shows high sensitivity to oxidative \nstress and increased sensitivity to osmotic stress, and incr\neased oxidation levels of cell proteins; grx5 is synthetical\nly lethal with grx2.\n mTAF9:TFIID subunit (TBP-associated factor) with predicted molecul\nar weight of 17 kD.,TFIID subunit,Null mutant is inviable\n mMRP1:shows allele-specific genetic interactions with pet122 and p\net123,37 kDa mitochondrial ribosomal protein,defective mitoc\nhondrial protein synthesis; absence of a and b type cytochro\nmes; reduced levels of mitochondrial 15 S rRNA; defective pr\nocessing of apocytochrome b intron; convert to rho- and rho0\n at high frequency\n mSEH1:Nuclear pore protein, homologous to sec13,,\n mKTR3:Putative alpha-1,2-mannosyltransferase,alpha-1,2-mannosyltra\nnsferase (putative),\n mNVJ1:Vac8p binding protein; nucleus-vacuole junction,,Null mutant\n is viable; cells do not form nucleus-vacuole junctions\n mPSK1:contains serine/threonine protein kinase domain and shows ho\nmology with the SNF1 serine/threonine protein kinase,,Null m\nutant is viable\n mUFE1:t-SNARE that resides on the endoplasmic reticulum and mediat\nes retrograde traffic from the Golgi complex,t-SNARE (ER),Nu\nll mutant is inviable\n mRVB2:RUVB-like protein, TIP49b Homologue,transcriptional regulato\nr,Null mutant is inviable\n mUSA1:Identified by its interaction with the U1 snRNP-specific pro\ntein, Snp1p.,pre-mRNA splicing factor (putative),\n mYMR160W:Unknown ,, Unknown\n mPNG1:de-N-glycosylation enzyme,peptide:N-glycanase,Null mutant is\n viable and shows no growth or viability defect under experi\nmental conditions\n mMAK32:Protein necessary for structural stability of L-A double-str\nanded RNA-containing particles,,\n mYGR011W:Unknown ,, Unknown\n mPTP1:phosphotyrosine-specific protein phosphatase,phosphotyrosine\n-specific protein phosphatase,viable\n Cond710:t2+SSD1\n mYKL033W:Unknown ,, Unknown\n mYSP3:subtilisin-like protease III,subtilisin-like protease III,\n mMSY1:Tyrosyl-tRNA synthetase,tyrosine-tRNA ligase,\n mYBR178W:Unknown ,, Unknown\n mNUP84 mSEH1 mPHO86 mNUP85 mTAF10 mTAF9 mTAF14 mYEL015W mMET30 mMNS1 mCKB1 mCKB2
mSPC1:Homolog of the SPC12 subunit of mammalian signal peptidase c\nomplex. Protein is important for efficient signal peptidase \nactivity.,,Null mutant is viable; synthetically lethal with \na conditional mutation in sec11; high copy Spc1 suppresses t\nhe conditional sec11 mutation\n mCOS6:Protein with strong similarity to other subtelomerically-enc\noded proteins such as Cos5p, Ybr302p, Cos3p, Cos1p, Cos4p, C\nos8p, Cos6p, Cos9p,,\n mCPT1:Phospholipid biosynthesis,sn-1,2-diacylglycerol cholinephosp\nhotransferase,Null mutant is viable, cpt1 ept1 double deleti\non mutants are viable\n mTIM17:Mitochondrial inner membrane protein involved in protein imp\nort,16.5 kDa inner membrane protein required for import of m\nitochondrial precursor proteins,Null mutant is inviable\n Jelinski.Jelinski:Regulatory networks revealed by transcriptional profiling of\n damaged Saccharomyces cerevisiae cells: Rpn4 links base exc\nision repair with proteasomes.  Mol Cell Biol. 2000 Nov;20(2\n1):8157-67.\n mKRE27:Killer toxin REsistant,,K1 killer toxin resistance\n mERG12:mevalonate catabolism,mevalonate kinase,Null mutant is invia\nble and unable to grow vegetatively or germinate spores; mut\nants exhibit increased mitotic stability of plasmids with we\nak ARS elements.\n mYGR026W:Unknown ,, Unknown\n mPPM1:carboxy methyl transferase for protein phosphatase 2A cataly\ntic subunit,carboxy methyl transferase for protein phosphata\nse 2A catalytic subunit,Mutant is rapamycin resistant, benom\nyl supersensitive, and nocodazole sensitive.\n mYNL156C:Unknown ,, Unknown\n mAPM1:medium subunit of the clathrin-associated protein complex,cl\nathrin associated protein complex medium subunit,Null mutant\n is viable, enhances the slow growth and late Golgi sorting \ndefects of a chc1-ts mutant\n Cond887:t-BuOOH\n mDFG10:Protein required for filamentous growth, cell polarity, and \ncellular elongation,,Null mutant is viable and defective in \nfilamentous growth\n mAPM4:Clathrin associated protein, medium subunit,clathrin associa\nted protein complex medium subunit,\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 mYDR319C:Unknown ,, Unknown\n mLAP3:aminopeptidase of cysteine protease family; bleomycin hydrol\nase,aminopeptidase of cysteine protease family,Null mutant i\ns viable with no obvious growth defects but is leucine amino\npeptidase deficient and hypersensitive to bleomycin; overexp\nression confers resistance to bleomycin\n mYJL084C:Unknown ,, Unknown\n mVMA21:Protein involved in vacuolar H-ATPase assembly or function,,\nNull mutant is viable but grows slowly and exhibits increase\nd calcium sensitivity. Null mutants also cannot grow on glyc\nerol or at pH 7.5\n mCLB5:role in DNA replication during S phase; additional functiona\nl role in formation of mitotic spindles along with Clb3 and \nClb4,B-type cyclin,Null mutant is viable, but has an extende\nd S phase\n mERG2:sterol biosynthesis,C-8 sterol isomerase,Null mutant is viab\nle\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 mSYS1:Multicopy suppressor of ypt6 null mutation,,Null mutant is v\niable. sys1 ypt6 double mutant displays enhanced defects in \nvacuolar sorting and cell growth\n Cond892:S\n Cond883:5\n mZRC1:Zinc- and cadmium-resistance protein,,Null mutant is viable \nand sensitive to zinc\n mHNM1:choline transport protein; may also control uptake of nitrog\nen mustard,transporter (permease) for choline and nitrogen m\nustard; share homology with UGA4,Null mutant is viable, but \nhyper-resistant to nitrogen mustard; ctr1,cho1 double null i\ns inviable\n Cond889:4NQO_2\n mYGR024C:Unknown ,, Unknown\n mYIL059C: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 mDFG5:Protein required for filamentous growth, cell polarity, and \ncellular elongation,,Null mutant is viable and defective in \nfilamentous growth\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 Cond888:MNNG_2\n mYMR221C:Unknown ,, Unknown\n mBGL2:Cell wall endo-beta-1,3-glucanase,cell wall endo-beta-1,3-gl\nucanase,Null mutant is viable\n mCCC1:Functions in the homeostasis of both calcium and manganese i\nons,transmembrane Ca2+ transporter (putative),Wild-type comp\nlements csg1 (calcium sensitive-group) mutants when overexpr\nessed\n mTAT2:Tryptophan permease, high affinity,tryptophan permease, high\n affinity,suppressor of chromosome segregation mutation\n mTOM7:Involved in mitochondrial protein import,translocase of the \nouter mitochondrial membrane,Null mutant is viable\n mYGL159W: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 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 mMRPL9:Mitochondrial ribosomal protein MRPL9 (YmL9) (E. coli L3) (h\numan MRL3),ribosomal protein (YmL9) (E. coli L3) (human MRL3\n),Null mutant is viable\n Cond895:G2MMS\n mSEC11:signal peptidase subunit,,Null mutant is inviable\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 Cond882:zero3\n mCHS7:The seventh gene identified that is involved in chitin synth\nesis; involved in Chs3p export from the ER,,Null mutant is v\niable but exhibit reduced chitin synthesis due to a severe r\neduction of Chitin Synthase III activity.\n mYIL041W:Unknown ,, Unknown\n mPAU7:similar to Pau3, member of Pau1 family,,\n mERV14:ER-derived vesicles,14 kDa protein found on ER-derived vesic\nles,Null mutant is viable but exhibits defects in sporulatio\nn (diploids) and bud site selection (haploids). Null mutants\n also retain the bud site selection marker, Axl2p, in the ER\n and exhibit slow recovery from selective to rich media.\n Cond886:g-ray\n mDPM1:dolichol phosphate mannose synthase,dolichol phosphate manno\nse synthase,Null mutant is inviable\n mSWD1:YAR003W,,\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mYNL122C:Unknown ,, Unknown\n mYDR107C:Unknown ,, Unknown\n mGSF2:Glucose Signaling Factor,,A Tn3 insertion into this gene cau\nses hypersensitivity to the cell surface polymer perturbing \nagent calcofluor white; Defective in glucose repression; mut\nants decrease transcriptional repression by MIG1; alter gluc\nose-regulated subunit interactions within the Snf1 protein k\ninase complex; the effects of eff1 and eff2 on SUC2 repressi\non are strongly synergistic.\n mYMR073C:Unknown ,, Unknown\n mOST6:Putative new 37kDa subunit of N-oligosaccharyltransferase co\nmplex,N-oligosaccharyltransferase complex 37kDa subunit (put\native),\n mYPL098C:Unknown ,, Unknown\n mYNL100W:Unknown ,, Unknown\n mYPL170W:Unknown ,, Unknown\n mYMR157C:Unknown ,, Unknown\n mMRP2:14 kDa mitochondrial ribosomal protein; homologous to E. col\ni S14 protein,14 kDa mitochondrial ribosomal protein , simil\nar to E. coli S14 protein,defective mitochondrial protein sy\nnthesis; absence of a and b type cytochromes; reduced levels\n of mitochondrial 15 S rRNA; defective processing of apocyto\nchrome b intron; convert to rho- and rho0 at high frequency\n mIMP1:Inner membrane protease (mitochondrial protein),inner membra\nne protease,petite; unable to grow on non-fermentable carbon\n sources\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 mYMR160W:Unknown ,, Unknown\n mYGR033C:Unknown ,, Unknown\n mYGL080W:Unknown ,, Unknown\n mSWP1:oligosaccharyl transferase glycoprotein complex, delta subun\nit,oligosaccharyl transferase glycoprotein complex, delta su\nbunit,lethal\n mSPS19:late sporulation specific gene which may function during spo\nre wall formation,2,4-dienoyl-CoA reductase,Null mutant is v\niable. SPS19 is dispensable for growth and sporulation on so\nlid acetate and oleate media, but is essential for these pro\ncesses to occur on petroselineate.\n mYMC1:putative mitochondrial carrier protein,carrier protein (puta\ntive),\n mYGR106C: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 mYMR099C: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 mATP15:nuclear gene for ATP synthase epsilon subunit,ATP synthase e\npsilon subunit , nuclear encoded,unable to grow on glycerol \nmedium; no detectable oligomycin-sensitive ATPase activity; \noligomycin-sensitive uncoupling of the mitochondrial respira\ntion rate\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 mYJL178C:Unknown ,, Unknown\n mERV29:ER Vesicle protein of 29 kDa (apparent MW),ER-Golgi transpor\nt vesicle protein,Null mutant is viable.\n mESBP6:Protein with similarity to mammalian monocarboxylate transpo\nrters MCT1 and MCT2,monocarboxylate permease (putative),\n mYHL046C:Unknown ,, Unknown\n

this is an automaticly generated GENESYS report
Computational Genomics Lab, Tel-Aviv uniresity