Module number 1038




Database revision : gnsdb28.10
Date : Tue Feb 25 17:34:21 2003
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mSPC2:subunit of signal peptidase complex, homologous to mammalian\n protein SPC25,signal peptidase complex subunit , similar to\n mammalian protein SPC25,Null mutant is viable. spc1 spc2 do\nuble deletion mutants grow relatively well as compared to wi\nld-type. spc2 sec11 double deletion mutant is inviable. Spc2\np is important for cell viability and signal peptidase activ\nity at high temperatures (42 degrees celsius).\n mYBR287W:Unknown ,, Unknown\n mSML1:Suppressor of mec lethality,,Null mutant is viable and suppr\nesses mec1 and rad53 lethality; suppresses mip1-1 at 37 C, s\nuppresses dun1 DNA damage sensitivity; increased resistance \nto DNA damage; increased dNTP pools\n mASH1:Zinc-finger inhibitor of HO transcription which is asymmetri\ncally localized to the daughter cell nucleus,,Mutant ash1 da\nughters can transcribe HO and switch mating type\n mURA3:orotidine-5'-phosphate decarboxylase,orotidine-5'-phosphate \ndecarboxylase,Null mutant is viable, uracil auxotroph\n mTIR1:cold-shock induced protein of the Srp1p/Tip1p family of seri\nne-alanine-rich proteins,,\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 mSEC31:involved in protein transport from endoplasmic reticulum to \nGolgi,COPII coat of secretory pathway vesicles component (p1\n50),Null mutant is inviable\n mVCX1:Similar to sodium/calcium exchangers, including bovine Na+/C\na2+,K+ antiporter; putative vacuolar transmembrane protein,v\nacuolar H+/Ca2+ exchanger,Null mutant is viable, sensitive t\no high Ca2+ conditions\n mTIR3:TIP1-related,cell wall mannoprotein,inviable under unaerobic\n conditions\n mEGT2:cell-cycle regulation protein, may be involved in the correc\nt timing of cell separation after cytokinesis,,\n mTIR4:Hypothetical ORF,cell wall mannoprotein,inviable under anaer\nobic conditions\n mRPS14B:Homology to human S14 and rat S14, E. coli S11,ribosomal pro\ntein S14B (rp59B),Null mutant is viable\n mYBL081W:Unknown ,, Unknown\n mHRP1:Putative polyadenylated-RNA-binding protein located in nucle\nus; similar to vertebrate hnRNP A/B protein family,,Null mut\nant is inviable; mutants can suppress temperature-sensitive \nalleles of npl3 (but not npl3 null mutants)\n mYGL245W:Unknown ,, Unknown\n mPRO3:delta 1-pyrroline-5-carboxylate reductase,delta 1-pyrroline-\n5-carboxylate reductase,proline requiring\n mYPR196W:Unknown ,, Unknown\n mDYS1:Deoxyhypusine synthase carries out the first step in hypusin\ne biosynthesis, converting lysine and spermidine into deoxyh\nypusine.,deoxyhypusine synthase,Null mutant is inviable\n mPWP1:Protein with periodic trytophan residues that resembles memb\ners of beta-transducin superfamily because of presence of WD\n-40 repeats,,Null mutants are viable but show severely retar\nded growth\n mRHR2:DL-glycerol-3-phosphatase,DL-glycerol-3-phosphatase,\n mRSP5:involved in ubiquitin-mediated protein degradation,,Null mut\nant is inviable; an rsp5 mutation was isolated as a suppress\nor of mutations in SPT3; certain rsp5 mutants also exhibit h\nypersensitivity to stresses such as cadmium and canavanine, \nand sporulation defects\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 mDNF2:Drs2 Neo1 Family,Potential aminophospholipid translocase,via\nble\n mAUR1:involved in phospolipid metabolism,,Null mutant is inviable;\n mutant exhibits dominant resistance to aureobasidin A. Wild\n type (sensitive) is recessive.\n Cond713:t4+Vec\n COMP.:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mGND1:6-phosphogluconate dehydrogenase, decarboxylating; converts \n6-phosphogluconate + NADP to ribulose-5-phosphate + NADPH + \nCO2,,cannot grow on media containing D-glucono-delta-lactone\n as the sole carbon source\n mASI1:Amino acid Sensor-Independent (ASI) genes encode membrane pr\noteins Asi1p, Asi2p and Asi3p. Asi1p and Asi3p have conserve\nd ubiquitin ligase-like RING domains at their C-termini,,\n mRPA14:14 kDa subunit of RNA polymerase I,RNA polymerase I subunit,\nNull mutant is viable but is temperature sensitive\n mDAN3:delayed anaerobic gene,putative cell wall protein,unknown\n mCWP1:cell wall protein, involved in O and N glycosylation, accept\nor of B1-6 glucan.,cell wall mannoprotein,Null mutant is via\nble, has increased sensitivities to calcoflour white and con\ngo red\n Cond718:t4+SSD1wt\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 mSAC1:integral membrane protein localizing to the ER and Golgi,int\negral membrane protein,suppressor of actin mutations, suppre\nssor of sec14 alleles, inositol auxotrophy\n mSUT2:Involved in sterol uptake; homologous to SUT1,,\n mYOR1:multispecific organic anion transporter important for tolera\nnce against toxic environmental organic anions,ABC transport\ner,Null mutant is viable but exhibits a slight growth defect\n; null mutant is hypersensitive to reveromycin A and fumonis\nin B1. Overexpression increases resistance to fumonisin B, s\nphingosine, and reveromycin A.\n mSHM1:Serine hydroxymethyltransferase, mitochondrial,,Null mutant \nis viable.\n mFKS1:Required for viability of calcineurin mutants,1,3-beta-D-glu\ncan synthase,Null mutant is viable, demonstrates slow growth\n, hypersensitivity to FK506 and cyclosporin A, sensitivity t\no echinocandin and a reduction in 1,3-beta-D-glucan synthase\n activity in vitro; sensitivity to papulacandin B\n mADH3:alcohol dehydrogenase isoenzyme III,alcohol dehydrogenase is\noenzyme III,Null mutant is viable\n mCHO2:First step in the methylation pathway for phosphatidylcholin\ne biosynthesis,phosphatidyl-ethanolamine N-methyltransferase\n,Null mutant is viable and accumulates phosphatidylethanolam\nine and has reduced levels of phosphatidylcholine\n mADH4:Alcohol dehydrogenase type IV,alcohol dehydrogenase isoenzym\ne IV,Null mutant is viable\n mLOC1:Localization of mRNA,,Mutant exhibits slow growth at 30C\n mYDL237W:Unknown ,, Unknown\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 mPAU4:member of the seripauperin protein/gene family (see Gene_cla\nss PAU),,\n mGCV2:Glycine CleaVage system,glycine cleavage system P subunit , \nglycine decarboxylase complex P subunit , glycine synthase P\n subunit,Inability to convert glycine to serine (ser1 backgr\nound); Inability to utilize glycine as a nitogen source.\n mPAU6:member of the seripauperin protein/gene family,,\n mNOG1:Nucleolar G-protein 1; LPG15w (working nomenclature),homolog\ns identified in human and Trypanosoma brucei , nucleolar G-p\nrotein (putative),Null mutant is inviable.\n mBOP1:bypass of PAM1,,\n mYBR246W:Unknown ,, Unknown\n mNCL1:Nuclear protein 1, similar to NOP2 and human proliferation a\nssociated nucleolar protein p120,tRNA:m5C-methyltransferase,\nNull mutant is viable, sensitive to paromomycin, lacks m5C m\nethylation in total yeast tRNA\n mSIK1:homology to microtubule binding proteins and to X90565_5.cds\n,similar to microtubule binding proteins and to X90565_5.cds\n,wild-type gene suppresses toxicity of GAL4-I-Kappa-B alpha \nin yeast\n mTPO1:Polyamine transport protein,,\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 mIDH2:NAD+-dependent isocitrate dehydrogenase,NAD-dependent isocit\nrate dehydrogenase,Null mutant is viable\n mOST4:May be subunit or accessory component of oligosaccharyltrans\nferase,3.6 kDa protein, probably membrane-located,Null mutan\nt is viable but is cold- and heat-sensitive; vanadate-resist\nant, hygromycin B-sensitive; defective in oligosaccharyltran\nsferase activity in vivo and in vitro\n mFAS2:Trifunctional enzyme,fatty acid synthase alpha subunit,Fatty\n acid synthetase deficient\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 mOST6:Putative new 37kDa subunit of N-oligosaccharyltransferase co\nmplex,N-oligosaccharyltransferase complex 37kDa subunit (put\native),\n mRAD51:Involved in processing ds breaks, synaptonemal complex forma\ntion, meiotic gene conversion and reciprocal recombination.,\nRad51p colocalizes to ~ 65 spots with Dmc1p prior to synapsi\ns (independently of ZIP1 and DMC1), and interacts with Rad52\np and Rad55p; human Rad51p homolog interacts with Brca2 prot\nein which has been implicated in causing breast cancer , Rec\nA homolog,Null mutant is viable; accumulates meiosis-specifi\nc double strand breaks at a recombination hotspot and reduce\ns the formation of physical recombinants and processed doubl\ne strand breaks with long heterogeneous tails; rad51 mutants\n are also defective for X-ray damage repair and gene convers\nions; rad51 rad27 mutants are inviable.\n mECM19:ExtraCellular Mutant,,A Tn3 insertion into this gene causes \nhypersensitivity to the cell surface polymer perturbing agen\nt calcofluor white.\n mHEK2:Unknown ,, Unknown\n mZRT1:High-affinity zinc transport protein,,disruption viable\n mYAR028W:Unknown ,, Unknown\n mSPF1:Sensitivity to a killer toxin (SMK toxin) produced by Pichia\n farinosa,P-type ATPase,The null mutant is viable and resist\nant to the SMK toxin, but grows slowly and has glycosylation\n defects.\n mZRT3:Hypothetical ORF,,\n mKEX2:prohormone processing; golgi localization marker, dispensabl\ne for meiotic recombination but partially required for meios\nis I and/or meiosis II,Ca2+-dependent serine protease,Null m\nutant is viable and defective in killer expression\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 mRSC9:Remodels the Structure of Chromatin,,Null: Lethal.\n mYJL097W:Unknown ,, Unknown\n mRNR2:small subunit of ribonucleotide reductase,ribonucleotide red\nuctase subunit , ribonucleotide reductase, small (R2) subuni\nt,Null mutant is inviable\n mYAL069W:Unknown ,, Unknown\n mPIN3:[PSI+] induction,,Other phenotypes: overexpression of PIN3 a\nllows for the induction of the [PSI+] prion in strains cured\n of [PIN+].\n mGUA1:GMP synthase,GMP synthase,Null mutant is viable but is a gua\nnine auxotroph\n Cond710:t2+SSD1\n mAPE3:Aminopeptidase yscIII,aminopeptidase yscIII,Null mutant is v\niable but exhibited reduced vacuolar aminopeptidase activiti\nes and could not hydrolyze Lys-Ala-MCA to Lys and Ala-MCA.\n mBMH2:Brain Modulosignalin Homolog,member of conserved eukaryotic \n14-3-3 gene family,Null mutant is viable; bmh1 bmh2 double m\nutant is inviable; (in strain Sigma-1278b, required for pseu\ndohyphal development but not for viability)\n mYIL039W:Unknown ,, Unknown\n mMXR1:peptide Methionine sulfoXide Reductase 1,peptide methionine \nsulfoxide reductase,Null mutant is viable; shows weaker grow\nth on methionine sulfoxide as only sulfur source, increased \nresistance to ethionine sulfoxide, and inability to form dim\nethylsulfide (DMS) from dimethylsulfoxide (DMSO).\n mKRE22:Killer toxin REsistant,,Null mutant is K1 killer toxin resis\ntent\n mSRP1:karyopherin alpha homolog of 60 kDa,karyopherin alpha,supres\nsor of rpb1, cold-sensitive\n mVAC8:An armadillo repeat-containing protein localized on the vacu\nolar membrane,armadillo repeat-containing protein,Defective \nin vacuole inheritance and aminopeptidase I targeting to the\n vacuole\n mYNL101W:Unknown ,, Unknown\n mHOM2:threonine and methionine pathway,aspartic beta semi-aldehyde\n dehydrogenase,Homoserine requiring\n mLYS20:homocitrate synthase, highly homologous to YDL131W,YDL131W (\nLYS21) homolog , homocitrate synthase,Null mutant is viable,\n is able to grow on minimal media, and exhibits reduced but \nsignificant homocitrate synthase activity\n mLYS21:homocitrate synthase, highly homologous to YDL182W,YDL182W (\nLYS20) homolog , homocitrate synthase,\n mGPA2:homologous to mammalian G proteins; potential role in regula\ntion of cAMP levels,nucleotide binding regulatory protein,Nu\nll mutant is viable\n Cond711:t2+Vec\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 mTUB2:beta subunit of tubulin monomer; involved in chromosome segr\negation and nuclear migration,beta-tubulin,null is inviable;\n conditional mutants show block of mitotic nuclear migration\n and chromosome segregation and defects in spindle and/or cy\ntoplasmic microtubules at non-permissive conditions; some mu\ntants are benomyl-hypersensitive\n mNEW1:This gene encodes a protein with an Q/N-rich amino terminal \ndomain that acts as a prion, termed [NU]+.,,Null mutant is v\niable\n mRPL25:Homology to E. coli L23 and rat L23a,ribosomal protein L25 (\nrpl6L) (YL25),\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 mARO2:Chorismate synthase,chorismate synthase,aromatic amino acid \nrequiring; lack of premeiotic DNA synthesis; blocked sporula\ntion in homozygous mutant\n mHIP1:histidine permease,histidine permease,requires supplementati\non with large amounts of histidine for growth\n mERG4:Sterol C-24 reductase,sterol C-24 reductase,Null mutant is v\niable\n mPRS1:ribose-phosphate pyrophosphokinase,ribose-phosphate pyrophos\nphokinase,\n mARO8:aromatic amino acid aminotransferase,aromatic amino acid ami\nnotransferase,Null mutant is viable\n mYHR020W: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 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 mECM39:ExtraCellular Mutant,,A Tn3 insertion into this gene causes \nhypersensitivity to the cell surface polymer perturbing agen\nt calcofluor white.\n mHSP150:Heat shock protein, secretory glycoprotein,heat shock protei\nn , secretory glycoprotein , heat shock protein , secretory \nglycoprotein , heat shock protein , secretory glycoprotein,N\null mutant is viable\n mHEM1:First enzyme in heme biosynthetic pathway,5-aminolevulinate \nsynthase,Null mutant is viable; auxotroph for heme and methi\nonine\n mALR1:aluminium resistance ,ion transporter (putative),Null mutant\n is inviable; overexpression increases resistance to aluminu\nm and gallium toxicity\n mMAK5:Necessary for maintenance of dsRNA killer plasmids. Is predi\ncted to encode an DEAD-box RNA helicase,,deficient in mainte\nnance of killer\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 mYER004W:Unknown ,, Unknown\n mZEO1:Overexpression yields resistance to Zeocin,,Null mutant is v\niable and exhibits slow growth in galactose\n mYJR015W:Unknown ,, Unknown\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 mYMR148W:Unknown ,, Unknown\n mYPR114W:Unknown ,, Unknown\n mGLN1:glutamine synthetase,glutamine synthetase,Glutamine syntheta\nse non-derepressible\n mCLG1:cyclin-like protein that interacts with Pho85p in affinity c\nhromatography,,Null mutant is viable\n mPRE1:Required for mitotic division and sporulation,22.6 kDa prote\nasome subunit,Null mutant is inviable, pre1 mutants accumula\nte ubiquitin-protein conjugates\n mBDF2:bromodomain protein, homolog of BDF1,BDF1 homolog , bromodom\nain protein,Null mutant is viable in FY1679, RAY3A-D, and CE\nN.PK2 backgrounds, and synthetic lethal with bdf1\n mCDC19:Required for START A in the cell cycle and sporulation,pyruv\nate kinase,Null mutant is inviable. cdc19 mutants are pyruva\nte kinase deficient and show cell division cycle blocked at \n36 degrees C\n mCBF5:major low affinity 55 kDa Centromere/microtubule binding pro\ntein,major low affinity 55 kDa centromere/microtubule bindin\ng protein,Null mutant is inviable\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 mPRE3:Proteasome subunit necessary for hydrolysis of peptidylgluta\nmyl-peptide,20S proteasome subunit,Null mutant is inviable\n mSSO1:SSO1 and SSO2 encode syntaxin homologs (post-Golgi t-SNAREs)\n; act in late stages of secretion,t-SNARE,SSO1, SSO2 double \nnull mutant is inviable; high copy number of either SSO1 or \nSSO2 suppresses mutations in late-acting sec genes (sec1,3,5\n,9,15)\n Cond717:t2-SSD1\n mKRS1:lysyl-tRNA synthetase,lysine-tRNA ligase,Null mutant is invi\nable; mutants can show resistance to 5-methyltryptophan, 5-f\nluorotryptophan and canavanine; constitutive derepression an\nd slow growth; posttranscriptional increase in histidine bio\nsynthetic enzyme activity\n mCST13:Chromosome STability,,Null mutant is viable, but grows slowl\ny and shows increased sensitivity to copper ions\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 mPDA1:alpha subunit of pyruvate dehydrogenase (E1 alpha),pyruvate \ndehydrogenase alpha subunit (E1 alpha),Null mutant is viable\n, exhibits reduced growth on glucose and increased formation\n of petites\n mPMT1:Transfers mannose residues from dolichyl phosphate-D-mannose\n to specific serine/threonine residues of proteins in the se\ncretory pathway; acts in complex with Pmt2p,dolichyl phospha\nte-D-mannose:protein O-D-mannosyltransferase,Null mutant is \nviable but shows decrease by 40-50% of in vivo protein O-man\nnosylation; pmt1 pmt2 double mutant shows severe growth defe\nct but residual O-mannosylation activity; the pmt1 pmt2 pmt3\n pmt4 quadruple mutant is inviable\n Cond725:t4-SSD1,M31\n mSPT15:TATA-binding protein (tfIId),TFIID subunit,Null mutant is in\nviable\n mNHP2:HMG-like nuclear protein,HMG-like protein,Null mutant is inv\niable\n mSPT16:global regulator of transcription,,suppression of Ty inserti\non mutations\n mALD5:Utilizes NADP+ as the preferred coenzyme. Activated by K+.,a\nldehyde dehydrogenase,\n mSOL3:weak multicopy suppressor of los1-1,,Null mutant is viable\n mMIS1:mitochondrial C1-tetrahydroflate synthase,C1-tetrahydrofolat\ne synthase,Null mutant is viable, exhibits no apparent defec\nts in cell growth\n mDBP2:ATP-dependent RNA helicase of DEAD box family,ATP dependent \nRNA helicase , dead box protein,Null mutant is inviable\n mMID2:Protein required for mating,,Null mutant is viable, dies whe\nn exposed to mating pheromone\n mYHM2:Yeast suppressor gene of HM mutant (abf2),DNA binding protei\nn , mtDNA stabilizing protein, mitochondrial inner membrane \nprotein with low homology to RIM2,Null mutant is viable but \nshows slow growth in the presence of non-fermentable carbon \nsources; mutant shows mitochondrial genome unstability\n mYGP1:may be involved in cellular adaptations prior to stationary \nphase,gp37, a glycoprotein synthesized in response to nutrie\nnt limitation which is homologous to the sporulation-specifi\nc SPS100 gene,\n mASN1:Asn1p and Asn2p are isozymes,asparagine synthetase,Null muta\nnt is viable; L-asparagine auxotrophy occurs upon mutation o\nf both ASN1 and ASN2\n mMRH1:Membrane protein related to Hsp30p; Localized by immunofluor\nescence to membranes, mainly the plasma membr. punctuate imm\nunofluorescence pattern observed in buds. The nuclear envelo\npe, but not vacuole or mitochondrial membranes also stained,\n,Null mutant is viable\n mASN2:Asn1p and Asn2p are isozymes,asparagine synthetase,Null muta\nnt is viable; L-asparagine auxotrophy occurs upon mutation o\nf both ASN1 and ASN2\n mSWD2:YKL018W,,\n mDBP6:Dead Box Protein 6,RNA helicase (putative),Null mutant is in\nviable; Dbp6p depletion leads to decreased production of the\n 27S and 7S precursors, resulting in a depletion of the matu\nre 25S and 5.8S rRNAs\n mIRA2:Negatively regulates cAPK by antagonizing CDC25,GTPase activ\nating protein , highly homologous to Ira1p , neurofibromin h\nomolog , GTPase activating protein , highly homologous to Ir\na1p , neurofibromin homolog,Null mutant is viable, exhibits \nincreased sensitivity to heat shock and nitrogen starvation,\n sporulation defects, and suppression of the lethality of a \ncdc25 mutants\n mYIL056W:Unknown ,, Unknown\n mNCP1:NADP-cytochrome P450 reductase,NADP-cytochrome P450 reductas\ne,Null mutant is viable\n mAFG1:ATPase family gene,ATPase family,\n mYJL217W:Unknown ,, Unknown\n mTRM5:tRNA modification enzyme,,\n mRPL4B:Highly similar to ribosomal protein L4A,ribosomal protein L4\nB (L2B) (rp2) (YL2),\n mEXG1:Exo-1,3-beta-glucanase,exo-1,3-beta-glucanase,Null mutant is\n viable, displays modest increase in killer toxin sensitivit\ny and beta 1,6-glucan levels\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 mTEF4:Translation elongation factor EF-1gamma,translation elongati\non factor EF-1gamma,\n mIMP4:Interacts With Mpp10. Imp4p is a specific component of the U\n3 snoRNP and is required for pre-18S rRNA processing.,,Null \nmutant is inviable\n mYPL229W:Unknown ,, Unknown\n mKRE6:cell wall beta-glucan assembly,beta-glucan synthase (putativ\ne),Null mutant is viable, slow growing, killer toxin-resista\nnt, possesses half the normal level of wild-type cell wall (\n1-->6) beta-glucan)\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 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 mYRF1-4:Y'-helicase protein 1,Y'-helicase protein 1,\n mGDI1:Regulates vesicle traffic in secretory pathway by regulating\n dissociation of GDP from Sec4/Ypt/rab family of GTP-binding\n proteins,GDP dissociation inhibitor,Null mutant is inviable\n mYMR237W:Unknown ,, Unknown\n mYOR108W:Unknown ,, Unknown\n mYDR063W:Unknown ,, Unknown\n mUTP22:Unknown ,, Unknown\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 mYDL046W:Unknown ,, Unknown\n mHTB2:Histone H2B (HTB1 and HTB2 code for nearly identical protein\ns),histone H2B (HTB1 and HTB2 code for nearly identical prot\neins),Null mutant is viable. Deletion of the HTA2-HTB2 (TRT2\n) locus has no reported observable phenotypes, presumably be\ncause HTA1-HTB1 (TRT1) expression is upregulated and can com\npensate in the absence of TRT2\n mPIR3:Protein containing tandem internal repeats,contains tandem i\nnternal repeats,Null mutant is viable; pir1 hsp150 (pir2) pi\nr3 triple mutant is slow-growing on agar slab and sensitive \nto heat shock\n mPDR10:Putative ABC transporter highly similar to Pdr5p,ABC transpo\nrter (putative) , highly similar to Pdr5p,\n mYJL218W:Unknown ,, Unknown\n mYKL146W:Unknown ,, Unknown\n mORM1:Product of gene unknown,,\n mHYR1:Hydroperoxide resistance conferring gene,glutathione-peroxid\nase (putative),Null mutant is hypersensitive to oxidative st\nress\n mNSP1:Nucleoskeletal protein found in nuclear pores and spindle po\nle body,nuclear pore complex subunit,Null mutant is inviable\n.\n mNSA1:Nop seven associated,ribosome biogenesis,\n mYDR492W:Unknown ,, Unknown\n mPDR5:multidrug resistance transporter,multidrug resistance transp\norter,pleiotropic drug resistance\n mPDC5:pyruvate decarboxylase,pyruvate decarboxylase,undetectable p\nyruvate decarboxylase activity in pdc1pdc5 double mutants\n mAAH1:adenine aminohydrolase (adenine deaminase),adenine aminohydr\nolase (adenine deaminase),Null mutant is viable\n mUTR4:Product of gene unknown,,\n mPBI2:Proteinase inhibitor that inhibits protease Prb1p (yscB),pro\nteinase inhibitor I2B (PBI2),Null mutant is viable but shows\n 50% elevation of protein degradation rate when cells are su\nbject to nutritional stress\n mLAT1:Dihydrolipoamide acetyltransferase component (E2) of pyruvat\ne dehydrogenase complex,pyruvate dehydrogenase complex dihyd\nrolipoamide acetyltransferase component (E2),Null mutant is \nviable\n mNPY1:hydrolyzes the pyrophosphate linkage in NADH and related nuc\nleotides,NADH pyrophosphatase 1,No readily detected phenotyp\ne\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 mSMT3:may be involved in function and/or structure of the eukaryot\nic kinetochore,,isolated as suppressor of mif2 (centromeric \nprotein) mutation\n mASP1:Asparaginase I, intracellular isozyme,asparaginase I , intra\ncellular isozyme,Aspartic acid requiring\n mPIS1:phosphatidylinositol synthase,phosphatidylinositol synthase,\nNull mutant is inviable\n mRPS13:Homology to rat S13,ribosomal protein S13 (S27a) (YS15),\n mLSM5:Like Sm-E protein,snRNP protein,Null mutant is viable.\n mGAS5:Unknown ,, Unknown\n mNMD3:putative Upf1p-interacting protein,factor required for a lat\ne assembly step of the 60S subunit,Null mutant is inviable, \nat nonpermissive temperature, nmd3 ts mutants exhibit decrea\nsed levels of 60S subunits resulting in formation of half-me\nr polysomes; nmd3 xrn1(kem1) double mutants are inviable\n mNUP49:localizes to discrete spots in the nuclear envelope,nuclear \npore complex subunit,Null mutant is inviable; some nsp1 nsp4\n9 alleles exhibit synthetic lethality\n mADO1:adenosine kinase,adenosine kinase,\n mDPH2:Diptheria toxin resistance protein, required for diphthamide\n biosynthesis,,Null mutant is viable\n mYOR385W:Unknown ,, Unknown\n mRPN11:Suppressor of mutant (ts on glycerol) tRNA gene deficient in\n the processing of its 3'-end; homologous to S. pombe PAD1 g\nene - global positive regulator of nuclear transcription and\n is involved in maintenance of chromatin structure,,Null mut\nant is inviable\n mABF2:HMG-1 homolog, mitochondrial,HMG-1 homolog,\n mYJL016W:Unknown ,, Unknown\n mALG6:Required for glucosylation in the N-linked glycosylation pat\nhway,glucosyltransferase,Null mutant is viable and defective\n in protein glycosylation.\n mSNC1:Involved in mediating targeting and transport of secretory p\nroteins; forms a complex with Snc2p and Sec9p,Snc2p homolog \n, synaptobrevin homolog,Null mutant is viable; snc1 snc2 mut\nants are deficient in normal bulk secretion, accumulate larg\ne numbers of post-Golgi vesicles, and display a variety of c\nonditional lethal phenotypes; snc1 mutations suppress loss o\nf cap in strains possessing an activated ras2 allele\n mYFL006W:Unknown ,, Unknown\n mYPR125W:Unknown ,, Unknown\n mARE1:Acyl-CoA cholesterol acyltransferase (sterol-ester synthetas\ne),acyl-CoA cholesterol acyltransferase (sterol-ester synthe\ntase),Null mutant is viable, slightly reduces in vivo and in\n vitro ergosterol esterification. Deletion of both ARE1 and \nARE2 completely eliminates of in vivo and in vitro ergostero\nl esterification\n mYOL092W:Unknown ,, Unknown\n mTRP4:anthranilate phosphoribosyl transferase,anthranilate phospho\nribosyl transferase,tryptophan requiring\n mYAL053W:Unknown ,, Unknown\n mSTP3:Involved in pre-tRNA splicing and in uptake of branched-chai\nn amino acids,,\n mGLC7:Glycogen accumulation,protein phosphatase type I,Null mutant\n is inviable\n Cond716:t2+SSD1wt\n mYLR413W:Unknown ,, Unknown\n mCTR2:Putative low-affinity copper transport protein,,ctr2 mutants\n display a high level of resistance to toxic copper concentr\nations. CTR2 overexpression provides increased resistance to\n copper starvation and is also associated with an increased \nsensitivity to copper toxicity.\n Cond708:t0+SSD1\n mSRV2:70-kDa adenylyl cyclase-associated protein,70 kDa adenylyl c\nyclase-associated protein,Null mutant is inviable.\n mGPI12:N-acetylglucosaminylphosphatidylinositol de-N-acetylase,N-ac\netylglucosaminylphosphatidylinositol de-N-acetylase,Null mut\nation is inviable\n mFUM1:Fumarase converts l-malate to fumarate as part of the TCA cy\ncle,fumarase (fumarate hydralase),respiratory defective\n mRTT102:Regulator of Ty1 Transposition,,Null mutant is viable and ca\nuses increase in Ty1 transposition\n mIMD3:Hypothetical ORF,IMP dehydrogenase homolog,\n mILV1:threonine deaminase,threonine deaminase,Isoleucine-plus-vali\nne requiring\n mPDE1:3',5'-Cyclic-nucleotide phosphodiesterase, low affinity,3',5\n'-cyclic-nucleotide phosphodiesterase, low affinity,Null mut\nant is viable\n mRPL40A:Homology to rat L40,ribosomal protein L40A,Null mutant is vi\nable\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n Cond712:t4+SSD1\n mSUP35:altered form creates [PSI] prion,translation termination fac\ntor eRF3,accumulation of large budded cells and substantial \narrest of DNA synthesis at the nonpermissive temperature (ar\nrests at G(sub)1/S transition); omnipotent suppressor of non\nsense mutations\n mCDC60:cytosolic leucyl tRNA synthetase,leucine--tRNA ligase,arrest\n at START point of cell cycle upon shift to restrictive temp\nerature\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 mNPL3:involved as a protein carrier in mRNA export, involved in mi\ntochondrial protein targeting,contains RNA recognition motif\n , nuclear shuttling protein , contains RNA recognition moti\nf , nuclear shuttling protein , contains RNA recognition mot\nif , nuclear shuttling protein,Null mutant is inviable, npl3\n mutants are temperature-sensitive for growth, but do not ex\nhibit a defect in localization of nuclear proteins\n mYDR531W:Unknown ,, Unknown\n mSUN4:Protein involved in the aging process,,\n mEPS1:Hypothetical ORF,,\n mGCN20:Positive effector of the EIF-2-alpha kinase activity of GCN2\n; component of a heteromeric complex that includes GCN1 and \nGCN20,ATP-binding cassette (ABC) family,Null mutant is viabl\ne and shows impaired derepression of GCN4 translation and re\nduced levels of eIF-2 alpha phosphorylation\n mGCD11:Negative regulator of GCN4 expression,translational initiati\non factor eIF-2 gamma subunit,Null mutant is inviable, gcd11\n mutants have slower growth rate under nonstarvation conditi\nons\n mYHR033W:Unknown ,, Unknown\n mCUP5:vacuolar ATPase V0 domain subunit c (17 kDa),17 kDa , VO sec\ntor subunit , dicyclohexylcarbodiimide binding subunit , pro\nteolipid , vacuolar ATP synthase proteolipid C , vacuolar AT\nPase V0 domain subunit c (dicyclohexylcarbodiimide binding s\nubunit) (17 kDa) , 17 kDa , VO sector subunit , dicyclohexyl\ncarbodiimide binding subunit , proteolipid , vacuolar ATP sy\nnthase proteolipid C , vacuolar ATPase V0 domain subunit c (\ndicyclohexylcarbodiimide binding subunit) (17 kDa) , 17 kDa \n, VO sector subunit , dicyclohexylcarbodiimide binding subun\nit , proteolipid , vacuolar ATP synthase proteolipid C , vac\nuolar ATPase V0 domain subunit c (dicyclohexylcarbodiimide b\ninding subunit) (17 kDa),Null mutant is viable, petite, copp\ner sensitive\n mPPA1:vacuolar ATPase V0 domain subunit c'',proteolipid , vacuolar\n ATPase V0 domain subunit c'',Null mutant is inviable in som\ne genetic backgrounds, in others, exhibits no V-ATPase activ\nity and failure to assemble V-ATPase subunits onto the vacuo\nlar membrane\n mBAT1:branched-chain amino acid transaminase, highly similar to ma\nmmalian ECA39, which is regulated by the oncogene myc,branch\ned-chain amino acid transaminase , highly similar to mammali\nan ECA39, which is regulated by the oncogene myc , branched-\nchain amino acid transaminase , highly similar to mammalian \nECA39, which is regulated by the oncogene myc,Null mutant is\n viable; ILV auxotrophy in bat1 bat2 double mutant\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 mTCP1:chaperonin subunit alpha,chaperonin subunit alpha,Null mutan\nt is inviable\n mATP16:ATP synthase delta subunit,ATP synthase delta subunit,cells \nare entirely cytoplasmic petite\n mCPA1:Carbamoyl phosphate synthetase, arginine specific,arginine s\npecific , carbamoyl phosphate synthetase,Null mutant is viab\nle\n mELP6:ELongator Protein 6; 30kD subunit,RNA polymerase II Elongato\nr protein subunit,Null:Slow adaptation to growth on new medi\na; <br> ts- (39 oC); sensitive to 1 M NaCl; insensitive to p\nGKL killer toxin\n mLCB2:Involved in sphingolipid biosynthesis; may catalyze the firs\nt step in biosynthesis of long-chain sphingolipids,serine pa\nlmitoyltransferase component (putative),Auxotrophic for long\n-chain component of sphingolipids; some mutations can suppre\nss the Ca2+-sensitive mutant csg2\n mSNT1:,,\n mATP1:mitochondrial F1F0-ATPase alpha subunit,F1F0-ATPase alpha su\nbunit,null mutant is viable; grows slowly on fermentable car\nbon sources; exhibits delayed kinetics of protein import for\n several mitochondrial precursors\n mHAP1:Activator of CYC1 and CYP3 transcription; positive regulator\n of cytochrome C genes CYC1 and CYC7,zinc finger transcripti\non factor of the Zn(2)-Cys(6) binuclear cluster domain type,\nEssential for anaerobic or heme deficient growth; Null mutan\nt is viable, deficient in expression of CYC1 and CYC7\n mISC1:Hypothetical ORF,ISC1 encodes phospholipase C type enzyme wh\nich hydrolyzes inositolphosphosphingolipids (IPC, MIPC, M(IP\n)2C) as well as sphingomyelin.,Null mutant is viable and con\ntains more inositolphosphosphingolipids.\n mPUB1:poly(A)+ RNA-binding protein,poly(A) binding protein,Null mu\ntant is viable\n mRRP12:Required for normal pre-rRNA processing,,Null: lethal.\n mNEO1:ATPase that leads to neomycin-resistant protein when overexp\nressed,P-type ATPase,Null mutant is inviable. When overexpre\nssed, Neo1 confers neomycin resistance.\n 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 mNOP2:May participate in nucleolar function during the transition \nfrom stationary phase to rapid growth,90 kDa protein homolog\nous to a human proliferation-associated nucleolar protein, p\n120,Null mutant is inviable; overexpression leads to changes\n in nucleolar morphology\n mNOP4:RNA recognition motif-containing protein,RNA binding protein\n (putative),Null mutant is inviable; conditional mutant show\ns diminished accumulation of 60S ribosomal subunits due to a\n lack of production of mature 25S rRNA from 27S precursor rR\nNA\n mYGR026W:Unknown ,, Unknown\n mSKN1:Involved in (1->6)-beta-glucan biosynthesis,highly homologou\ns to Kre6p , type II membrane protein (putative),Null mutant\n is viable; exhibits no alterations in killer sensitivity, g\nrowth, or (1->6)-beta-glucan levels; skn1 kre6 double deleti\non mutants show a dramatic reduction in both (1-->6)-beta-gl\nucan levels and growth rate compared with either single disr\nuptant\n mTRR1:Thioredoxin reductase,thioredoxin reductase,Null mutant is v\niable but grow slowly; trr1 mutations are sensitive to hydro\ngen peroxide and activate Mlu1 cell cycle box (MCB)- and Swi\n4/Swi6 cell cycle box (SCB)-dependent reporter genes in swi6\n null mutants.\n mDIA1:may be involved in invasive growth, pseudohyphal growth,,Nul\nl mutant is viable and causes invasive growth in haploids an\nd pseudohyphal growth in diploids\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 mSKN7:Protein with similarity to DNA-binding region of heat shock \ntranscription factors,,Null mutant is viable\n mSSU1:sensitive to sulfite,major facilitator superfamily,Null muta\nnt is viable; sulfite sensitive\n mYKL084W:Unknown ,, Unknown\n mRAS1:ras proto-oncogene homolog,ras homolog,\n mPPQ1:May play role in regulation of translation,protein phosphata\nse Q,Null mutants are viable, show an altered morophology, h\nave a slight growth defect on several carbon sources, have l\nower cell density in stationary phase in the absence of an e\nssential amino acid, show a reduced rate of protein synthesi\ns in exponential phase, are hypersensitive to protein synthe\nsis inhibitors, and have an allosuppressor phenotype in supp\nressor strain backgrounds (i.e. enhanced efficiency of trans\nlational suppressors),\n mHSP12:induced by heat shock, entry into stationary phase, depletio\nn of glucose, and addition of lipids (fatty acids),heat shoc\nk protein 12,Null mutant is viable, but shows induction of h\neat shock response under conditions normally associated with\n low-level HSP12 expression\n mYNR046W:Unknown ,, Unknown\n mECM3:ExtraCellular Mutant,,A Tn3 insertion into this gene causes \nhypersensitivity to the cell surface polymer perturbing agen\nt calcofluor white.\n mNST1:Unknown ,, Unknown\n mYJR116W:Unknown ,, Unknown\n mFIT2:Facilitator of iron transport,Cell wall protein involved in \niron transport,impaired siderophore-iron uptake, activation \nof the major iron -dependent transcription factor, AFT1\n mYIL090W:Unknown ,, Unknown\n Cond719:t4-SSD1\n mSNU13:RNA binding protein (putative), similar to Nhp2p,U4/U6.U5 sn\nRNP component,the null mutant is inviable\n mTHR1:homoserine kinase,homoserine kinase,Null mutant is viable, t\nhreonine auxotroph\n mEFT1:translation elongation factor 2 (EF-2),translation elongatio\nn factor 2 (EF-2),Null mutant is viable (eft1 eft2 double mu\ntant is lethal)\n mTHR4:threonine synthase,threonine synthase,threonine requiring\n mMPT5:Product of gene unknown,,Null mutant is viable, temperature \nsensitive\n mHEM13:Oxygen-repressed, sixth step in heme biosynthetic pathway,co\nproporphyrinogen III oxidase,Null mutant is viable; auxotrop\nh for heme and methionine\n mYOR302W:Unknown ,, Unknown\n mTOM1:Temperature dependent Organization in Mitotic nucleus,hect-d\nomain-containing protein, containing kinase motifs , similar\n to Rsp5,Null mutant is viable and temperature sensitive, an\nd arrests at the G2/M boundary of the cell cycle\n mYMR191W:Unknown ,, Unknown\n mTNA1:Transporter of Nicotinic Acid,high affinity nicotinic acid p\nlasma membrane permease,Null mutant is viable; the deletion \nof both YGR260W and YJR025C/BNA1 is lethal at low external n\nicotinic acid concentration\n Cond709:t0+Vec\n mYMR010W:Unknown ,, Unknown\n mMKT1:Protein involved in propagation of M2 dsRNA satellite of L-A\n virus,retroviral protease signature protein,Null mutant is \nviable\n mHRR25:Similar to YCK1 and YCK2, two other casein kinase I isoforms\n; found primarily in nucleus; may be involved in DNA-damage \nrepair,casein kinase I isoform,Null mutant is viable but sho\nws slow growth; hrr25-1 mutation results in sensitivity to c\nontinuous expression of HO endonuclease, to methylmethanesul\nfonate, and to x-irradiation; homozygous hrr25-1 mutants are\n unable to sporulate\n mHXK2:Glucose phosphorylation,hexokinase II (PII) (also called hex\nokinase B),Null mutant is viable and can ferment fructose, b\nut fails to show glucose repression at SUC2, CYC1, GAL10. hx\nk1, hxk2 double null mutant cannot ferment fructose\n mUTH1:Youth, involved in determining yeast longevity,,extension of\n yeast lifespan\n mCPR4:cyclophilin homolog,cyclophilin , peptidyl-prolyl cis-trans \nisomerase (PPIase) , cyclophilin , peptidyl-prolyl cis-trans\n isomerase (PPIase),suppressor of cdc65\n mCDC91:member of major facilitator superfamily,,\n mYJR001W:Unknown ,, Unknown\n mFUN12:Function unknown now,97 kDa protein,Null mutant is inviable\n mYIL121W: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 mYIL041W:Unknown ,, Unknown\n mPRM9:pheromone-regulated membrane protein,,\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 mYHR181W:Unknown ,, Unknown\n mALG11:Specifies addition of the terminal alpha 1,2-Man to the Man5\nGlcNAc2-PP-dolichol N-Glycosylation intermediate,,Null mutan\nt displays poor growth and temperature-sensitive lethality\n mVTC2:Phosphate metabolism; transcription is regulated by PHO syst\nem,polyphosphate synthetase (putative),Null nutant is viable\n; no polyphosphate accumulation in a vtc2(phm1)/vtc3(phm2) d\nouble disruptant\n 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 mUBA1:ubiquitin activating enzyme, similar to Uba2p,ubiquitin acti\nvating enzyme, similar to Uba2p,Null mutant is inviable\n mLYP1:lysine permease,lysine permease,\n mRSN1:overexpression Rescues sro7/sop1 in NaCl,,viable in both hig\nh and low salinity\n mUBP6:deubiquitinating enzyme (putative),,\n mSPB1:Suppressor of PaB1 mutant; involved in 60S ribosomal subunit\n biogenesis,methyltransferase (putative),Null mutant is invi\nable. The spb1-1 mutant is an extragenic suppressor of a pab\n1 null mutation.\n mFSH1:Unknown ,, Unknown\n mYBR293W:Unknown ,, Unknown\n mSES1:seryl-tRNA synthetase,serine-tRNA ligase,Null mutant is invi\nable.\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 mPCL5:PHO85 cyclin,,Null mutant is viable.\n mGAL80:inhibits transcription activation by Gal4p in hte absence of\n galactose,transcriptional regulator,Null mutant is viable a\nnd cannot utilize galactose.\n mRRP40:Ribosomal RNA Processing,,The null mutant is inviable and de\nfective in 3' processing of 5.8S rRNA\n Cond715:t0-SSD1\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 mGCD1:general control of amino acid biosynthesis and cell cycle in\nitiation,gamma subunit , negative regulator in the general c\nontrol of amino acid biosynthesis , translation initiation f\nactor eIF2B subunit,affect growth rate under nonstarvation c\nonditions\n mSEC21:non-clathrin coat protein involved in transport between ER a\nnd Golgi,PEST sequence-containing protein , non-clathrin coa\nt protein,Null mutant is inviable\n mSUR2:Suppressor of rvs161 and rvs167 mutations,sphingosine hydrox\nylase,Null mutant is viable, has altered phospholipid levels\n mWTM1:WD repeat containing transcriptional modulator 1,transcripti\nonal modulator,Null mutant is viable\n mFCY1:cytosine deaminase highly homologous to Candida albicans cyt\nosine deaminase,cytosine deaminase,Mutant is resistant to 5-\nfluorocytosine and shows total loss of cytosine deaminase ac\ntivity\n mSEC28:Part of a heptameric protein complex that regulates retrogra\nde Golgi-to-ER protein traffic in eukaryotic cells; coatomer\n forms the COP I vesicle coat whose functions are essential,\nepsilon-COP coatomer subunit,Null mutant is viable, shows te\nmperature sensitivity; high copy suppressor of ret1-3\n mCAF40:Hypothetical ORF,,Null mutant is viable\n mSRL1:Suppressor of rad53 lethality,,\n mVTS1: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 mRIM101:Rim101p is similar to the Aspergillus Phenotype-response reg\nulator PacC and the Yarrowia proteinase YlRim1010p; transcri\nptional activator required for entry into meiosis,,Poor grow\nth at low temperature, altered colony morphology, inefficien\nt sporulation due to reduced expression of the meiotic activ\nator IME1, and defective invasive growth\n mFAA4:acyl-CoA synthetase (long-chain fatty acid CoA ligase) (fatt\ny acid activator 2), activates imported fatty acids and prov\nides substrates for N-myristoylation,long chain fatty acyl:C\noA synthetase , long-chain fatty acid:CoA ligase,Not essenti\nal for vegetative growth when fatty acid synthase (fas) is a\nctive\n mYKL051W:Unknown ,, Unknown\n mSNC1 mSSO1 mSPB1 mGLC7 mNOP1 mSIK1 mNOP2 mBDF2 mSES1 mHRR25 mNSA1 mADH4 mPDC5 mLOC1 mCYS4 mNMD3 mCBF5 mSRP1 mFCY1 mHEM13 mSED1 mTCP1 mCCT2 mPWP1 mWTM1 mSXM1 mNSP1 mRPL25 mPRE1 mYHR033W mPRE3 mGPA2 mYGL245W mGCD11 mGCD1 mSML1 mADH3 mNST1 mCAF40 mGDS1 mYPL229W
this is an automaticly generated SAMBA report
Computational Genomics Lab, Tel-Aviv uniresity