Module number 1048




Database revision : gnsdb28.10
Date : Tue Feb 25 17:35:27 2003
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mNOP1:nucleolar protein, homologous to mammalian fibrillarin,nucle\nolar protein , similar to mammalian fibrillarin,Null mutant \nis inviable. Temperature-sensitive alleles exhibit various d\nefects in rRNA processing.\n mYBR287W:Unknown ,, Unknown\n mYGR026W:Unknown ,, Unknown\n mSAM1:S-adenosylmethionine synthetase,,Null mutant is viable.\n mPAD1:Phenylacrylic acid decarboxylase,phenylacrylic acid decarbox\nylase,Null mutant is viable but is cinnamic acid-sensitive\n mPMC1:May be involved in depleting cytosol of Ca2+ ions,Ca2+ ATPas\ne (putative),Null mutant is viable but fails to grow in high\n Ca2+ medium; this death in high calcium is suppressed by mu\ntations in calcineurin (CNA1, CNA2, CNB1) and calmodulin (CM\nD1); pmc1 vcx1 double mutant is even more sensitive to Ca2+\n mSKN7:Protein with similarity to DNA-binding region of heat shock \ntranscription factors,,Null mutant is viable\n mFET3:FET3 encodes a ferro-O2-oxidoreductase that is part of the h\nigh-affinity iron transport system,multicopper oxidase,The n\null mutant is viable but defective for high affinity Fe(II) \nuptake. The null mutant is inviable when environmental iron \nis limiting.\n mTIR3:TIP1-related,cell wall mannoprotein,inviable under unaerobic\n conditions\n mMUP1:high affinity methionine permease,high affinity methionine p\nermease,Null mutant is viable but cannot perform high-affini\nty methionine update.\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 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 mPDC5:pyruvate decarboxylase,pyruvate decarboxylase,undetectable p\nyruvate decarboxylase activity in pdc1pdc5 double mutants\n mMSC3:Meiotic Sister-Chromatid recombination,,\n mAAH1:adenine aminohydrolase (adenine deaminase),adenine aminohydr\nolase (adenine deaminase),Null mutant is viable\n mPTM1:Putative membrane protein,membrane protein (putative),Null m\nutant is viable, no observable phenotype\n mYBR139W:Unknown ,, Unknown\n mYPR196W:Unknown ,, Unknown\n mARO1:pentafunctional arom polypeptide (contains: 3-dehydroquinate\n synthase, 3-dehydroquinate dehydratase (3-dehydroquinase), \nshikimate 5-dehydrogenase, shikimate kinase, and epsp syntha\nse),3-dehydroquinate dehydratase (3-dehydroquinase) , 3-dehy\ndroquinate synthase , epsp synthase , pentafunctional arom p\nolypeptide , shikimate 5-dehydrogenase , shikimate kinase,ar\nomatic amino acid requiring; lack of premeiotic DNA synthesi\ns; blocked sporulation in homozygous mutant\n mARO3:DAHP synthase; a.k.a. phospho-2-dehydro-3-deoxyheptonate ald\nolase, phenylalanine-inhibited; phospho-2-keto-3-deoxyhepton\nate aldolase; 2-dehydro-3-deoxyphosphoheptonate aldolase; 3-\ndeoxy-D-arabine-heptulosonate-7-phosphate synthase,DAHP synt\nhase; a.k.a. phospho-2-dehydro-3-deoxyheptonate aldolase, ph\nenylalanine-inhibited; phospho-2-keto-3-deoxyheptonate aldol\nase; 2-dehydro-3-deoxyphosphoheptonate aldolase; 3-deoxy-D-a\nrabine-heptulosonate-7-phosphate synthase,null mutant is via\nble\n mERG4:Sterol C-24 reductase,sterol C-24 reductase,Null mutant is v\niable\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 mPRD1:Saccharolysin (oligopeptidase yscD),,Null mutant is viable b\nut exhibits a decrease in the intracellular degradation of p\neptides\n mMCA1:Unknown ,, Unknown\n mECM33:ExtraCellular Mutant,,A Tn3 insertion into this gene causes \nhypersensitivity to the cell surface polymer perturbing agen\nt calcofluor white.\n mMNR2:Product of gene unknown,,overexpression overcomes manganese \ntoxicity\n Cond719:t4-SSD1\n mSHP1:isolated as a suppressor of the lethality caused by overexpr\nession of the phosphoprotein phosphatase 1 catalytic subuniu\nt encoded by GLC7,,Null mutant is viable; sporulation defect\nive, slow growth; is deficient in glycogen accumulation; low\n Glc7p specific activity\n mNCR1:Niemann-Pick Type C homologous gene,transmembrane protein (p\nutative),Null mutant is viable.\n Cond724:t4+SSD1,H44\n mRRD1:Resistant to Rapamycin Deletion,,Null mutant is viable but s\nhows pleiotropic phenotypes (eg. caffeine and rapamycin resi\nstance, vanadate and calcium sensitivity, etc.); synthetic l\nethal with RRD2 (YPL152w)\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 mGAS5:Unknown ,, Unknown\n mECM39:ExtraCellular Mutant,,A Tn3 insertion into this gene causes \nhypersensitivity to the cell surface polymer perturbing agen\nt calcofluor white.\n mTSA1:antioxidant enzyme that provides protection against oxidatio\nn systems capable of generating reactive oxygen and sulfur s\npecies,thioredoxin-peroxidase (TPx); reduces H2O2 and alkyl \nhydroperoxides with the use of hydrogens provided by thiored\noxin, thioredoxin reductase, and NADPH,Null mutant is viable\n, grows slower than wild-type under aerobic conditions\n mTHR1:homoserine kinase,homoserine kinase,Null mutant is viable, t\nhreonine auxotroph\n COMP.:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mADO1:adenosine kinase,adenosine kinase,\n mFPS1:Suppressor of tps1/fdp1 and member of the MIP family of tran\nsmembrane channels; may be involved in glycerol efflux,glyce\nrol channel protein,Null mutant is viable\n mTHR4:threonine synthase,threonine synthase,threonine requiring\n mDPH2:Diptheria toxin resistance protein, required for diphthamide\n biosynthesis,,Null mutant is viable\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 Cond718:t4+SSD1wt\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 mRPN3:proteasome subunit,26S proteasome regulatory module componen\nt , similar to human p58 subunit,Null mutant is inviable. RP\nN3 is a high copy suppressor of the nin1-1 temperature sensi\ntive phenotype\n mYJL016W:Unknown ,, Unknown\n mHOG1:osmoregulation,MAP kinase,Null mutant is viable and unable t\no grow in high osmolarity media\n mALG6:Required for glucosylation in the N-linked glycosylation pat\nhway,glucosyltransferase,Null mutant is viable and defective\n in protein glycosylation.\n Cond709:t0+Vec\n mTAT2:Tryptophan permease, high affinity,tryptophan permease, high\n affinity,suppressor of chromosome segregation mutation\n mSCT1:High copy suppresor of choline-transport mutants,,Null mutan\nt is viable\n mSHM1:Serine hydroxymethyltransferase, mitochondrial,,Null mutant \nis viable.\n mASK10:transcriptional activator of the SKN7 mediated 'two-componen\nt' regulatory system,transcriptional activator of the SKN7 m\nediated 'two-component' regulatory system,\n mCPR4:cyclophilin homolog,cyclophilin , peptidyl-prolyl cis-trans \nisomerase (PPIase) , cyclophilin , peptidyl-prolyl cis-trans\n isomerase (PPIase),suppressor of cdc65\n Cond717:t2-SSD1\n mRCK2:Serine/threonine protein kinase,,Null mutant is viable\n mTRP2:anthranilate synthase Component I,anthranilate synthase comp\nonent I,tryptophan requiring\n mADE5,7:glycinamide ribotide synthetase and aminoimidazole ribotide \nsynthetase,aminoimidazole ribotide synthetase , glycinamide \nribotide synthetase,Adenine requiring\n mYAL053W:Unknown ,, Unknown\n Cond720:t0+SSD1,H44\n mYJR001W:Unknown ,, Unknown\n mYLR224W:Unknown ,, Unknown\n mSGE1:multi-copy suppressor of gal11 null; member of drug-resistan\nce protein family,,Null mutant is viable; shows decreased ex\npression of galactose-inducible genes; shows increased sensi\ntivity to crystal violet\n Cond716:t2+SSD1wt\n mGDS1:involved in nuclear control of mitochondria,,Null mutant is \nviable, shows partial impairment of growth on medium contain\ning glycerol as the carbon source. Overexpxression suppresse\ns NAM9-1 glycerol deficient phenotype\n mSRV2:70-kDa adenylyl cyclase-associated protein,70 kDa adenylyl c\nyclase-associated protein,Null mutant is inviable.\n Cond708:t0+SSD1\n mYLR137W:Unknown ,, Unknown\n mYML117W:Unknown ,, Unknown\n mSTT3:Required for protein glycosylation,integral ER membrane prot\nein , oligosaccharyltransferase complex subunit (putative),N\null mutant is inviable. sst3 mutants are defective in protei\nn glycosylation, sensitive to hygromycin B, and resistant to\n sodium orthovanadate. Depletion of the STT3 protein results\n in loss of oligosaccharyl transferase activity in vivo and \na deficiency in the assembly of oligosaccharyl transferase c\nomplex.\n mILV1:threonine deaminase,threonine deaminase,Isoleucine-plus-vali\nne requiring\n mIMD3:Hypothetical ORF,IMP dehydrogenase homolog,\n mYNL321W:Unknown ,, Unknown\n mMID2:Protein required for mating,,Null mutant is viable, dies whe\nn exposed to mating pheromone\n mYNL045W:Unknown ,, Unknown\n mYBR246W:Unknown ,, Unknown\n mYLR257W:Unknown ,, Unknown\n mYPL014W: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 mADE3:Required for the biosynthesis of purines, thymidylate, methi\nonine, histidine, pantothenic acid and formylmethionyl-tRNA,\nC1-tetrahydrofolate synthase,Null mutant is viable, adenine \nauxotroph, histidine auxotroph\n mLYP1:lysine permease,lysine permease,\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mMVD1:involved in the polyisoprene biosynthesis pathway,mevalonate\n pyrophosphate decarboxylase,Null mutant is inviable; a sing\nle leucine to proline mutation causes temperature sensitivit\ny.\n mPSR2:Plasma membrane Sodium Response 2,,Mutant is sensitive to so\ndium ions.\n mUBP6:deubiquitinating enzyme (putative),,\n mCYS3:cystathionine gamma-lyase,cystathionine gamma-lyase,Null mut\nant is viable, cysteine auxotroph\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 mCYS4:Cystathionine beta-synthase,cystathionine beta-synthase,Null\n mutant is viable, exhibits vacuolar acidification defects; \ncys2 and cys4 mutations are linked together and co-operative\nly confer cysteine dependence\n mYNL190W:Unknown ,, Unknown\n Cond723:t2-SSD1,M31\n mSED1:putative cell surface glycoprotein,cell surface glycoprotein\n (putative),Null mutant is viable; during stationary phase, \nnull mutants exhibit increased sensitivity to Zymolyase.\n mOST6:Putative new 37kDa subunit of N-oligosaccharyltransferase co\nmplex,N-oligosaccharyltransferase complex 37kDa subunit (put\native),\n mIML2:Similar to Ykr018p,,\n Cond714:t0+SSD1wt\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 mGDA1:converts nucleoside diphosphates to nucleoside monophosphate\ns to recycle nucleosides and promote transport of additional\n nucleotide sugars into golgi,guanosine diphosphatase of Gol\ngi membrane,Null mutant is viable and has partial block in m\nannosylation of proteins and sphingolipids\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 mKRE2:N-glycosylation,alpha-1,2-mannosyltransferase,have altered N\n-linked glycosylation of proteins and grow slowly at 30 degr\nees; unable to grow at 37 degrees\n mSXM1:Suppressor of mRNA export mutant; Importin-beta like gene,ka\nryopherin beta family member,Null mutant is viable, does not\n exhibit growth defects at any temperature examined or exhib\nit marked defects in tRNA processing\n mTEF4:Translation elongation factor EF-1gamma,translation elongati\non factor EF-1gamma,\n mIDP1:Mitochondrial form of NADP-specific isocitrate dehydrogenase\n,NADP-dependent isocitrate dehydrogenase,Null mutant is viab\nle\n mPHO13:p-nitrophenyl phosphatase,p-nitrophenyl phosphatase,Null mut\nant is viable\n mSUR2:Suppressor of rvs161 and rvs167 mutations,sphingosine hydrox\nylase,Null mutant is viable, has altered phospholipid levels\n mHXT2:hexose transporter,high affinity hexose transporter-2,Null m\nutant is viable\n mYDR539W:Unknown ,, Unknown\n Cond721:t0-SSD1,M31\n mGPD1:glycerol-3-phosphate dehydrogenase,glycerol-3-phosphate dehy\ndrogenase,lethal under conditions of osmotic stress, unable \nto grow on glycerol\n mGPD2:Involved in glycerol production via conversion of glyerol-3-\nphosphate and NAD+ to glycerol phosphate and NADH,glycerol-3\n-phosphate dehydrogenase (NAD+),Null mutant is viable\n mFRS1:Phenylalanyl-tRNA synthetase, alpha subunit, cytoplasmic,phe\nnylalanine-tRNA ligase subunit,\n mKRE9:cell wall beta-glucan assembly,,Null mutant is viable, assoc\niated with growth defects, altered cell wall, aberrant multi\nply budded morphology, mating defects; exhibits double mutan\nt lethality in combination with knh1, kre1, kre6, or kre11 m\nutants; killer toxin resistant; reduction in cell wall (1---\n-6)-beta-glucan\n mHMG2:3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase is\nozyme,3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reduct\nase isozyme,Null mutant is viable, sensitive to compactin, a\n competitive inhibitor of HMG-CoA reductase; hmg1 hmg2 doubl\ne deletion mutants are inviable\n mYMR237W:Unknown ,, Unknown\n mGSC2:Highly similar to FKS1 (GSC1). GSC2 and FKS1 encode redundan\nt catalytic components of 1,3-beta-glucan synthase. Deletion\n of both is lethal,1,3-beta-D-glucan synthase catalytic comp\nonent,Null mutant is viable and shows partially reduced 1,3-\nbeta-glucan synthase activity\n Cond710:t2+SSD1\n mCCT2:cytoplasmic chaperonin of the Cct ring complex related to Tc\np1p; subunit beta,,Null mutant is inviable; some mutant alle\nles exhibit defects in microtubule and actin assembly.\n mCRN1:coronin, an actin-binding protein originally identified in D\nictyostelium,Dictyostelium and human actin-binding protein c\noronin homolog,Null mutant is viable\n mYDL046W:Unknown ,, Unknown\n mHOG1 mRCK2
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Computational Genomics Lab, Tel-Aviv uniresity