Module number 819




Database revision : gnsdb28.10
Date : Tue Feb 25 17:04:56 2003
How to read this figure?


mYMR316C-A:Unknown ,, Unknown\n Cond217:yer050c\n mYLR346C:Unknown ,, Unknown\n mYPR015C:Unknown ,, Unknown\n mYOL083W:Unknown ,, Unknown\n mXKS1:Xylulokinase,xylulokinase,Null mutant is viable and cannot g\nrow on media containing xylulose as the sole carbon source\n mYOR152C:Unknown ,, Unknown\n mPDR15:similar to Pdr5p and Pdr10p,multidrug resistance transporter\n (putative),\n mPDR16:involved in pleiotropic drug resistance by controlling lipid\ns in various cellular compartments; positively regulated by \nPDR1,Pdr17p homolog , Sec14p homolog,Null mutant is viable, \nexhibits hypersensitivity to azole inhibitors of ergosterol \nbiosynthesis, alterations in sterol composition of the plasm\na membrane; pdr16 pdr17 double deletion mutants exhibit addi\ntive exacerbated phenotypes\n mMRPL31:15.5 kDa mitochondrial ribosomal protein YmL31,ribosomal pro\ntein (YmL31),Null mutant is viable; unable to grow on non-fe\nrmentable carbon sources\n mMCH5:Unknown ,, Unknown\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 mYER079W:Unknown ,, Unknown\n mPDR3:Zinc-finger transcription factor related to Pdr1p,,pleiotrop\nic drug resistance\n mPDR5:multidrug resistance transporter,multidrug resistance transp\norter,pleiotropic drug resistance\n mYNL200C:Unknown ,, Unknown\n mYDR115W:Unknown ,, Unknown\n mMRPL37:Probable mitochondrial protein L37,ribosomal protein L37 (pu\ntative),\n Cond4:afg3(haploid)\n mBUD9:among a group of genes whose products are necessary for bud-\nsite selection; likely involvement in positioning the proxim\nal pole signal,,In null mutants bipolar-budding cells bud pr\neferentially at distal pole\n mMRPL38:mitochondrial ribosomal protein L14,ribosomal protein L14,\n mFRE1:Ferric (and cupric) reductase,cupric reductase , ferric redu\nctase,Null mutant is viable, fre1-1 mutants are deficient in\n the uptake of ferric iron and are extremely sensitive to ir\non deprivation\n mFRE2:Ferric reductase, similar to Fre1p,ferric reductase,\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 mSNQ2:ABC transporter,ABC transporter,null mutant is viable; overe\nxpression confers multi-drug resistance\n mFRE3:similar to FRE2,,\n mDLD1:mitochondrial enzyme D-lactate ferricytochrome c oxidoreduct\nase,D-lactate ferricytochrome c oxidoreductase,Null mutant i\ns viable and cannot grow on media containing lactate as the \nsole carbon source\n mCYB2:Expression is repressed by glucose and anaerobic conditions,\n is induced by L-lactate and is regulated by GRR1, ROX3, HAP\n1, HXK2 and CYC8,L-lactate cytochrome c oxidoreductase , cyt\nochrome b2,Null mutant is viable but is deficient in cytochr\nome b2 and L-lactate dehydrogenase activity and is unable to\n use L-lactate as a sole carbon source\n mFRE5:similar to FRE2,,\n mRSM10:mitochondrial ribosome small subunit component,mitochondrial\n ribosome small subunit component,\n mFRE6:similar to FRE2,,\n mTSL1:123 kD regulatory subunit of trehalose-6-phosphate synthase/\nphosphatase complex; homologous to TPS3 gene product,similar\n to TPS3 gene product , trehalose-6-phosphate synthase/phosp\nhatase complex 123 kDa regulatory subunit,Null mutant is via\nble\n mSCS7:Required for the hydroxylation of the very long chain fatty \nacid (VLCFA), located in the endoplasmic reticulum,desaturas\ne , hydroxylase,Null mutant is viable, suppresses the Ca2+-s\nensitive phenotype of csg2 delta mutants\n mPST2:Protoplasts-SecreTed protein; the gene product was detected \namong the proteins secreted by regenerating protoplasts,,\n mYDR116C:Unknown ,, Unknown\n mCTF13:58 kd component (Cbf3c) of the multisubunit 'Cbf3' kinetocho\nre protein complex, which binds to the CDE III element of ce\nntromeres,,Null mutant is inviable\n mHSF1:heat shock transcription factor,heat shock transcription fac\ntor,Null mutant is inviable\n mYKL169C:Unknown ,, Unknown\n mRSM19:mitochondrial ribosome small subunit component,mitochondrial\n ribosome small subunit component,\n mINO1:involved in the rate limiting step of inositol biosynthesis,\nL-myo-inositol-1-phosphate synthase,Null mutant is viable, i\nnositol auxotroph\n mYHR140W:Unknown ,, Unknown\n mAMS1:vacuolar alpha mannosidase,alpha mannosidase,null mutant is \nviable\n mPEP4:vacuolar proteinase A,vacuolar proteinase A,Null mutant is v\niable, proteinase deficient, phosphatase deficient; pep4 mut\nants exhibit a 60-70% reduction in total protein degradation\n during sporulation\n mYMR188C:Unknown ,, Unknown\n mVID24:also involved in vacuolar protein targeting,peripheral vesic\nle membrane protein,Null mutant is viable, defective in fruc\ntose-1,6-bisphosphatase dergadation\n mSKS1:multicopy suppressor of snf3 and grr1 mutants,,Null mutant i\ns viable; Sks1 lacking the consensus ATP binding site cannot\n suppress snf3 mutants when overexpressed\n mMRPL44:Mitochondrial ribosomal protein MRPL44 (YmL44),ribosomal pro\ntein (YmL44),\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 mDDR48:DNA damage inducible; implicated in the production or recove\nry of mutations,contains >35 repeats of the amino acid seque\nnce NNNDSYGS , flocculent specific protein,Null mutant is vi\nable, displays reduced spontaneous mutation rate\n mYKR049C:Unknown ,, Unknown\n mYNL208W:Unknown ,, Unknown\n mAPC2:subunit of the Anaphase Promoting Complex; all known APC sub\nunit co-immunoprecipitate with epitope-tagged Apc2. Apc2 sho\nws similarity to cullins.,anaphase promoting complex (APC) s\nubunit,Null mutant is inviable at 25 deg. C; ts mutants arre\nst in metaphase due to defect in the degradation of Pds1; ex\ntracts from G1-arrested apc2 mutants are defective in the ub\niquitination of mitotic cyclins\n mPEX21:Peroxin; Pex18p and Pex21p are partially functionally redund\nant.,peroxin,Null mutant is viable.\n mICY1:Interacting with the cytoskeleton,,\n mPTR2:Functions in transport of small peptides into the cell,pepti\nde transporter,Null mutant is viable\n mSMF3:Putative metal transporter, Nramp homolog, homolog of SMF1 a\nnd SMF2,Nramp homolog , SMF1 and SMF2 homolog , metal transp\norter (putative),Viable\n mMAM33:33-kDa mitochondrial acidic matrix protein,,\n mRSM25:mitochondrial ribosome small subunit component,mitochondrial\n ribosome small subunit component,Null mutant is viable, but\n unable to respire.\n mYMR181C:Unknown ,, Unknown\n mFTH1:FTS3 Homolog 1,,none observed\n mYOR052C:Unknown ,, Unknown\n mRSB1:Unknown ,, Unknown\n mCOX14:mitochondrial membrane protein,mitochondrial membrane protei\nn,Nuclear respiration deficient, lack cytochromes a and a3 a\nnd detectable cytochrome oxidase activity\n mGLC3:Glycogen branching enzyme,1,4-glucan-6-(1,4-glucano)-transfe\nrase,Null mutant is viable, glycogen deficient\n mYGR257C:Unknown ,, Unknown\n mAKR1:Negative regulator of pheromone response pathway; required f\nor endocytosis of pheromone receptors; involved in cell shap\ne control,ankyrin repeat-containing protein,Null mutant is v\niable, exhibits slow growth, abnormal morphology, and partia\nl activation of pheromone response; defective for endocytosi\ns of Ste2p and Ste3p\n mCOX17:Involved in copper metabolism and assembly of cytochrome oxi\ndase,cysteine-rich protein,Null mutant is viable, respirato\nry defective, rescued by addition of copper to growth media \nand/or high copy expression of SCO1 and SCO2 genes\n mYJL067W:Unknown ,, Unknown\n mSNZ1:Snooze: stationary phase-induced gene family; may be involve\nd in cellular response to nutrient limitation and growth arr\nest,highly conserved 35 kDa protein that shows increased exp\nression after entry into stationary phase,Null mutant is via\nble, sensitive to 6-azauracil and methylene blue.\n mMRP21: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 mYMR102C:Unknown ,, Unknown\n mCIT1:citrate synthase. Nuclear encoded mitochondrial protein.,cit\nrate synthase,Null mutant is viable; disruption of both CIT1\n and CIT2 result in glutamate auxotrophy and poor growth on \nrich medium containing lactate\n mODC2:Hypothetical ORF,mitochondrial 2-oxodicarboxylate transport \nprotein,\n mCIT2:non-mitochondrial citrate synthase,citrate synthase,Null mut\nant is viable; disruption of both CIT1 and CIT2 result in gl\nutamate auxotrophy and poor growth on rich medium containing\n lactate.\n mGCV1:Required for metabolizing glycine as a nitrogen source,glyci\nne decarboxylase complex T subunit,Null mutant is viable but\n cannot use glycine as sole nitrogen source\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 mHPA3:Histone and other Protein Acetyltransferase; Has sequence ho\nmology to known HATs and NATs,,Null mutant is viable and doe\ns not show any detectable phenotype\n mGCV3:H-protein subunit of the glycine cleavage system,glycine cle\navage system H-protein subunit,Null mutant is viable but doe\ns not grow if glycine is the sole nitrogen source\n mGLK1:Glucose phosphorylation,glucokinase,Null mutant is viable wi\nth no discernible difference from wild-type; hxk1, hxk2, glk\n1 triple null mutants are unable to grow on any sugar except\n galactose and fail to sporulate\n Cond20:bub3(haploid**2)\n mGPG1:Unknown ,, Unknown\n mRME1:mediates cell type control of sporulation; negatively regula\ntes IME1 and sporulation,negative regulator of meiosis; dire\nctly repressed by a1-a2 regulator , zinc finger protein,Null\n mutant is viable, rme1 allows alpha/alpha and a/a diploids \nto sporulate, and a and alpha haploids to form viable spores\n in the presence of spo13\n mPRB1:dispensable for haploidization and sporulation, but needed f\nor full protein degradation during sporulation, and proper s\npore morphology,vacuolar protease B,Null mutant is viable, p\nrotease B deficient, has smaller spores than wild-type embed\nded in a thick matrix\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mYLR218C:Unknown ,, Unknown\n mYNL115C:Unknown ,, Unknown\n mECM13:ExtraCellular Mutant,,A Tn3 insertion into this gene causes \nhypersensitivity to the cell surface polymer perturbing agen\nt calcofluor white.\n Cond91:kim4\n mIDH1:alpha-4-beta-4 subunit of mitochondrial isocitrate dehydroge\nnase 1,isocitrate dehydrogenase 1 alpha-4-beta-4 subunit,Nul\nl mutant is viable, grows at a reduced rate on glycerol, lac\ntate, and acetate\n mIDH2:NAD+-dependent isocitrate dehydrogenase,NAD-dependent isocit\nrate dehydrogenase,Null mutant is viable\n mENB1:Siderophore transporter for enterobactin; AFT1 regulon,enter\nobactin transporter,Null mutants are viable but are unable t\no take up and utilize iron from enterobactin\n mYMR244C-A:Unknown ,, Unknown\n mSFT2:similar to mammalian syntaxin 5,,Null mutant is viable; got1\n sft2 double mutant exhibits defects in transport to the Gol\ngi complex.\n mYAL061W:Unknown ,, Unknown\n mPRY1:Pathogen Related in Sc, contains homology to the plant PR-1 \nclass of pathogen related proteins. The protein sequence is \nover 60% identical with the Pry2p & Pry3p over 145 resid. PR\nY1 is >35% identical (50% similar) to tobacco PR-1c protein.\n,,\n mYER053C:Unknown ,, Unknown\n mPCA1:Putative P-type Cu(2+)-transporting ATPase,P-type ATPase Cu(\n2+)-transporting (putative),Null mutant is viable but ceases\n growth earlier when grown in minimal medium with high coppe\nr concentration; overexpression of PCA1 causes poor growth; \nmulticopy PCA1 results in slower growth on synthetic medium \nwith 0.3 mM CuSO4\n mCTS1:Endochitinase,endochitinase,Null mutant is viable; exhibits \na defect in cell separation\n mYOR285W:Unknown ,, Unknown\n mYDR539W:Unknown ,, Unknown\n mATP11:essential for assembly of a functional F1-ATPase; binds the \nbeta subunit of F1-ATPase.,,greatly reduced ATPase activity;\n alpha and beta subunits of F1-ATPase accumulate in mitochon\ndria as inactive aggregates\n mARN1:Product of gene unknown,,\n mARN2:Siderophore transporter for triacetylfusarinine C,triacetylf\nusarinine C transporter,YHL047c disrupted cells are unable t\no take up and utilize iron from triacetylfusarinine C und fu\nsigen\n mAGP1:broad substrate range permease which transports asparagine a\nnd glutamine with intermediate specificity,amino acid permea\nse,Null mutant is viable; resistant to the amino acid analog\n gamma-hydroxyaspartate, decreased growth on asn, gln and so\nme other amino acids in strains in which Gap1 and Gnp1 are a\nlso missing.\n mAGP2:General amino acid permease with broad substrate specificity\n,amino acid permease,Null mutant is viable; loss of growth o\nn some amino acids as nitrogen source (leu, thr) in a strain\n which has no Gap1p or Agp1p function\n mGPH1:Releases glucose-1-phosphate from glycogen,glycogen phosphor\nylase,Null mutant is viable; haploid cells contain higher le\nvels of intracellular glycogen\n mTGL2:Triglyceride Lipase,triglyceride lipase,Null mutant is viabl\ne, exhibits no apparent phenotype\n mYBR262C:Unknown ,, Unknown\n mURA10:Fifth step in pyrimidine bio5,orotate phosphoribosyltransfer\nase 2,Null mutant is viable\n Cond101:mrpl33\n mYLR168C:Unknown ,, Unknown\n Cond3:aep2\n mTOS5:Hypothetical ORF,,\n mTYE7:may be involved in glycolytic gene expression,33 kDa , serin\ne-rich protein, is a potential member of the bHLH/leucine-zi\npper protein family,Null mutant is viable; expression of eno\nlase genes is reduced three-fivefold in null mutant; gcr1 ty\ne7 double deletion mutants exhibit additive defects in enola\nse expression. TYE7 was isolated as a dominant suppressor of\n gcr1 mutations\n mYOL153C:Unknown ,, Unknown\n mSIT1:Siderophore Iron Transport,ferrioxamine B permease,Viable. C\nells deleted from the gene are unable to take up ferrioxamin\ne B\n Cond130:rml2(**13)\n mMDM35:Unknown ,, Unknown\n mPGM2:Phosphoglucomutase,phosphoglucomutase,Null mutant is viable,\n pgm1 pgm2 deletion mutants fail to grow on galactose\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 mMSC1:Meiotic Sister-Chromatid recombination,,\n mICT1:Increased Copper Tolerance; Similar to Ecm18p,,\n mSCO2:Originally identified as a multicopy suppressor of a respira\ntory defective mutant; homolog of Sco1p,,\n mFTR1:Plasma membrane iron permease,iron permease,Lacks high affin\nity iron uptake\n mCAF17:CCR4 associated factor,CCR4 transcriptional complex componen\nt,Null mutant is viable, shows petite phenotype\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 mFIT3: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 mYMR002W:Unknown ,, Unknown\n mGTT1:Glutathione Transferase,glutathione transferase,Null mutant \nis viable, heat shock sensitive at stationary phase\n mARO9:aromatic amino acid aminotransferase II,aromatic amino acid \naminotransferase II,Null mutant is viable\n mPET117:Required for assembly of active cytochrome c oxidase,,petite\n; unable to grow on non-fermentable carbon sources\n mNCE103:involved in secretion of proteins that lack classical secret\nory signal sequences,,An uncharacterized allele exhibits def\nects in the export of the mammalian protein galectin-1.\n mCMK2:Calmodulin-dependent protein kinase,calmodulin-dependent pro\ntein kinase,Null mutant is viable, exhibits slow rate of spo\nre germination\n mYOR135C:Unknown ,, Unknown\n mYOR338W:Unknown ,, Unknown\n mYML087C:Unknown ,, Unknown\n mYKL151C:Unknown ,, Unknown\n mYGR035C:Unknown ,, Unknown\n mMRPS9:Probable mitochondrial ribosomal protein S9,ribosomal protei\nn S9 (putative),Null mutant is viable, respiration deficient\n, exhibits defects in mitochondrial protein synthesis as ind\nicated by a loss of cytochrome c oxidase activity\n Cond180:top1(haploid)\n mPDH1:Prpd homolog (ie the propionate operon of many prokary. spec\nifically prpD); close homologs (known to be essential for pr\nopionate utilization) in prokaryotes (several of these homol\nogs are called prpD), & it is transcribed in yeast.,,\n mCCC2:copper-transporting P-type ATPase with similarity to human M\nenkes and Wilsons genes,,Null mutant is viable, exhibits def\nects in respiration and iron uptake\n mHSP26:heat shock protein 26,heat shock protein 26,Null mutant is v\niable; hsp26 hsp42 double deletion mutants are viable\n Cond229:yhr011w(**14)\n mHXK1:Glucose phosphorylation,hexokinase I (PI) (also called hexok\ninase A),Null mutant is viable, is able to ferment fructose,\n and has little or no effect on glucose repression; hxk1, hx\nk2 double null mutant cannot ferment fructose and fails to s\nhow glucose repression at SUC2, CYC1, GAL10\n mSER3:catalyzes the first step in serine biosynthesis; isozyme of \nSER33,3-phosphoglycerate dehydrogenase,enzyme activity of 3P\n-glycerate dehydrogenase is decreased in null mutant compare\nd to wildtype and abolished in ser3 ser33 double deletion mu\ntant\n mYHR138C:Unknown ,, Unknown\n mYGL069C:Unknown ,, Unknown\n mACO1:Aconitase, mitochondrial,aconitase,glutamate auxotrophy\n mUGA2:involved in utilization of GABA as a nitrogen source,succina\nte semialdehyde dehydrogenase,Null mutant is viable but cann\not grow with GABA as the only nitrogen source.\n mYKL137W:Unknown ,, Unknown\n mNDE1:Unknown ,, Unknown\n mSPI1:Stationary Phase Induced; strongly expressed during stationa\nry phase, and trancription is dependent on MSN2/MSN4.,,\n mYPR100W:Unknown ,, Unknown\n COMP.KO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n Cond24:cem1\n mYGR043C:Unknown ,, Unknown\n mPRM5:pheromone-regulated membrane protein,,\n mSNO1:SNZ1 proximal ORF, stationary phase induced gene,,Null mutan\nt is viable, sensitive to 6-azauracil and methylene blue.\n mYER158C:Unknown ,, Unknown\n mLAC1:Longevity-assurance gene 1 cognate (LAG1 cognate),LAG1 longe\nvity gene homolog,Null mutant is viable but exhibits synthet\nic lethality with mutations in lag1.\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 mYKL195W:Unknown ,, Unknown\n mYLR177W:Unknown ,, Unknown\n mGRE2:induced by osmotic stress; similar to dihydroflavonol 4-redu\nctase from plants,,\n mYGR021W:Unknown ,, Unknown\n mYIL056W:Unknown ,, Unknown\n mYTP1:Yeast putative Transmembrane Protein,,Null mutant is viable\n mYLR149C:Unknown ,, Unknown\n mPHO89:Probable Na+/Pi symporter,Na+/Pi symporter (putative),Null m\nutant is viable\n mBIO5:transmembrane regulator of KAPA/DAPA transport,transmembrane\n regulator of KAPA/DAPA transport,\n mNCA3:With NCA2, regulates proper expression of subunits 6 (Atp6p)\n and 8 (Atp8p ) of the Fo-F1 ATP synthase,,Null mutant is vi\nable\n mYML030W:Unknown ,, Unknown\n mISU1:Iron-sulfur cluster nifU-like protein,,Null mutant is viable\n on YPD at 30 degrees C, and is synthetically lethal with is\nu2 null.\n Cond103:msu1\n Cond265:ymr293c\n mEMI5:Unknown ,, Unknown\n mBUR6:Homolog of DRAP1 (NC2alpha),transcriptional regulator,Null m\nutant is viable, but grows very poorly\n mMRP8:mitochondrial ribosomal protein,ribosomal protein,\n mYNR020C:Unknown ,, Unknown\n mDUR1,2:Urea amidolyase (contains urea carboxylase and allophanate h\nydrolase),urea amidolyase (contains urea carboxylase and all\nophanate hydrolase),Null mutant is viable; urea degradation \ndeficient\n mDSE1:Hypothetical ORF,,\n mHXT3:Low-affinity glucose transporter,low affinity glucose transp\norter,Null mutant is viable but grows slowly on galactose; s\nome mutant alleles confer sodium hypersensitivity.\n mYBR047W:Unknown ,, Unknown\n mDSE2:Hypothetical ORF,,\n mYMR251W:Unknown ,, Unknown\n mYMR041C:Unknown ,, Unknown\n mHXT4:hexose transporter,high affinity glucose transporter,Null mu\ntant is viable\n mSTF1:ATPase stabilizing factor,,\n mMRPL27:essential for mitochondrial function,ribosomal protein (YmL2\n7),Null mutant is viable, fails to grow on nonfermentable ca\nrbon sources\n mSTF2:ATPase stabilizing factor,ATPase stabilizing factor,\n mDSE4:Hypothetical ORF,,\n mYDC1:Yeast dihydro-ceramidase,alkaline dihydroceramidase with min\nor reverse activity,Null mutant is viable.\n mHXT6:Repression of HXT6 expression by glucose requires SNF3,hexos\ne transporter,Null mutant is viable; snf3 hxt1 hxt2 hxt3 hxt\n4 hxt6 hxt7 mutant cannot grow on media containing glucose a\ns sole carbon source\n mHXT7:Hexose transporter,hexose transporter,Null mutant is viable;\n snf3 hxt1 hxt2 hxt3 hxt4 HXT7 hxt7 mutant cannot grow on me\ndia containing glucose as sole carbon source\n mYGL157W:Unknown ,, Unknown\n mYOR289W:Unknown ,, Unknown\n mYHL035C:Unknown ,, Unknown\n mSCW11:Soluble Cell Wall protein,soluble cell wall protein,Null mut\nant is viable but exhibits defects in separation after divis\nion and displays flocculant growth.\n mYPL222W:Unknown ,, Unknown\n mYDR115W mMRP8 mCCC2 mATX1 mMAM33 mCYB2 mYPR015C mPGM2 mSNO1 mSNZ1
this is an automaticly generated SAMBA report
Computational Genomics Lab, Tel-Aviv uniresity