Module number 3267




Database revision : gnsdb28.10
Date : Tue Feb 25 17:22:29 2003
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mMAF1:Mod5 protein sorting,,Mislocalizes Mod5p to the nucleus\n mAGE2:ADP-ribosylation factor (ARF) GTPase activating protein (GAP\n) effector ,ARF GAP with effector function(s),Null mutant is\n viable\n mCPT1:Phospholipid biosynthesis,sn-1,2-diacylglycerol cholinephosp\nhotransferase,Null mutant is viable, cpt1 ept1 double deleti\non mutants are viable\n mSET3:,,\n mBCK1:bypass requirement for protein kinase C homolog,MEKK,Null mu\ntants are temperature-sensitive and exhibit cell lysis, whic\nh can be rescued by 1M sorbitol; null mutants grow very poor\nly even at the permissive temperature. Some dominant alleles\n suppress a pkc1 null mutant.\n mBRE1:Hypothetical ORF,,null mutant is sensitive to brefeldin A\n mYKL037W:Unknown ,, Unknown\n mGYP1:Gtpase activating protein for Ypt1p,GTPase activating protei\nn (GAP),Null mutant is viable and shows no phenotype\n mBRE2:Product of gene unknown,,null mutant is sensitive to brefeld\nin A\n mSNX4:Sorting NeXin,,\n mTKL1:Transketolase 1,transketolase 1,Null mutant is viable; growt\nh on fermentable carbon sources, but not gluconeogenic carbo\nn sources, is reduced; tkl1 tkl2 mutants are auxotrophic for\n aromatic amino acids\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 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 mBRE5:Product of gene unknown,,null mutant is sensitive to brefeld\nin A\n mORM2:Unknown ,, Unknown\n mYLR171W:Unknown ,, Unknown\n mURA4:Third step in pyrimidine biosynthesis pathway,dihydrooratase\n,Null mutant is viable and requires uracil\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 mUBP13:similar to Ubp9p,ubiquitin carboxyl-terminal hydrolase,\n mLST4:involved in regulated secretion/recycling of nitrogen regula\nted permeases,,very low activity of the nitrogen-regulated p\nermeases Gap1p and Put4p on poor nitrogen sources; lst4-1 be\nhaves as a complete kanMX knockout for the phenotypes tested\n so far\n mUBP15:putative deubiquitinating enzyme,deubiquitinating enzyme (pu\ntative),\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 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 mYPL013C:Unknown ,, Unknown\n mRCY1:Unknown ,, Unknown\n mADO1:adenosine kinase,adenosine kinase,\n mYOR342C:Unknown ,, Unknown\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 mRTF1:Directly or indirectly regulates the DNA-binding properties \nof Spt15p, the TATA box-binding protein, and the relative ac\ntivities of different TATA elements,nuclear protein,Null mut\nant is viable and can suppress TATA box-binding protein muta\nnts (SPT15) in an allele-specific fashion\n mERD1:Protein required for retention of luminal ER proteins,,disru\nption of the retention system for ER proteins; defects in th\ne Golgi-dependent modification of glycoproteins\n mOPT1:Oligopeptide transporter; Opt1p transports tetra- and pentap\neptides, including the endogenous opioid pentapeptide leucin\ne enkephalin.,glutathione transporter , peptide transporter,\nNull mutant is viable, exhibits loss of plasma membrane glut\nathione transport\n mSAC2:May interact with actin as a component or controller of the \nassembly or stability of the actin cytoskeleton,,Null mutant\n is viable, cold-sensitive growth phenotype, suppressor of a\nctin mutation; aberrant organization of intracellular actin \nand deposition of chitin at the cell surface\n mYHR162W:Unknown ,, Unknown\n mPEP8:Plays a role in delivery of proteins to the vacuole,vacuolar\n protein similar to mouse gene H<beta>58,Null mutant is viab\nle but is defective in processing of soluble vacuole proteas\nes due to inability of soluble vacuolar hydrolase to reach t\nhe vacuole\n mSAP190:190 kDa protein that associates with the SIT4 phosphatase in\n a cell cycle dependent manner,type 2A-related protein phosp\nhatase,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 mTAT1:Amino acid transport protein for valine, leucine, isoleucine\n, and tyrosine,amino acid transport protein for valine, leuc\nine, isoleucine, and tyrosine,\n mRMD5:Unknown ,, Unknown\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 mSCT1:High copy suppresor of choline-transport mutants,,Null mutan\nt is viable\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 mCDC50:cell division cycle mutant,,Null mutant is cold-sensitive an\nd sensitive to MMS and HU\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 mYDR008C:Unknown ,, Unknown\n mSHM2:serine hydroxymethyltransferase,,Null mutant is viable\n mCSM1:Hypothetical ORF,,missegregates chromosomes in meiosis\n mGIS4:GIG3 suppressor,CAAX box containing protein,\n mGCN2:Derepression of GCN4 expression,eukaryotic initiation factor\n 2 alpha (eIF2-alpha) kinase,Null mutant is viable, unable t\no grow on medium containing 3-aminotriazole (3-AT), a compet\nitive inhibitor of histidine biosynthesis, because it cannot\n derepress GCN4 and its target genes in the histidine biosyn\nthetic pathway\n mGRH1:Yeast (GR)ASP65 (H)omologue,mammalian GRASP protein homolog,\nNull mutation is viable, exhibits defects in spindle checkpo\nint\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 mGCN3:34 KD alpha subunit of eIF2B,eIF2B 34 kDa alpha subunit,null\n mutants fail to derepress amino acid-regulated genes under \nconditions of amino acid starvation\n mGCN4:transcriptional activator of amino acid biosynthetic genes,t\nranscriptional activator of amino acid biosynthetic genes,Th\ne null mutant is viable but requires arginine on minimal med\nium and issensitive to 3-amino-1,2,4-triazole. General contr\nol of amino acid synthesis non-derepressible in the null mut\nant.\n mYER119C-A:Unknown ,, Unknown\n mIRS4:Increased rDNA silencing,,Null mutant is viable and shows in\ncreased rDNA silencing\n mYBL083C:Unknown ,, Unknown\n mMLF3:Protein of unknown function,,Null mutant is viable and hyper\nsensitive to leflunomide\n mTRP1:Note that the sequence of TRP1 from strain S228C, which is t\nhe sequence stored in SGD, contains an ochre mutation at cod\non 67.,N-(5'-phosphoribosyl)-anthranilate isomerase,tryptoph\nan requiring\n mYGL007W:Unknown ,, Unknown\n mTRP2:anthranilate synthase Component I,anthranilate synthase comp\nonent I,tryptophan requiring\n mYDR290W:Unknown ,, Unknown\n mADE5,7:glycinamide ribotide synthetase and aminoimidazole ribotide \nsynthetase,aminoimidazole ribotide synthetase , glycinamide \nribotide synthetase,Adenine requiring\n mTRP3:anthranilate synthase Component II and indole-3-phosphate (m\nultifunctional enzyme),anthranilate synthase component II , \nindole-3-phosphate,Null mutant is viable, tryptophan auxotro\nph\n mTRP4:anthranilate phosphoribosyl transferase,anthranilate phospho\nribosyl transferase,tryptophan requiring\n mSTP2:Involved in pre-tRNA splicing and in uptake of branched-chai\nn amino acids,,\n mTRP5:tryptophan synthetase,tryptophan synthetase,Null mutant is v\niable and requires tryptophan\n mYLR224W:Unknown ,, Unknown\n mSTP4:Involved in pre-tRNA splicing and in uptake of branched-chai\nn amino acids,,\n mMOT3:High Copy Suppressor of MOT1-SPT3 synthetic lethality,2 Cys2\n-His2 zinc fingers at c-terminus, glutamine and asparagine r\nich,Null mutant is viable, displays modest increase in Ty mR\nNA levels; mot3 deletion can partially suppress mutations in\n mot1 and spt3\n mSPT8:transcription factor, probable member of histone acetyltrans\nferase SAGA complex,probable member of histone acetyltransfe\nrase SAGA complex , transcription factor,Null mutant is viab\nle, no growth defects, exhibits suppression of Ty insertion \nmutations, defects in Ty transcription\n mYDL172C:Unknown ,, Unknown\n mTIS11:Zinc finger containing homolog of mammalian TIS11, glucose r\nepressible gene,,Null mutant is viable but alters metabolism\n that is reflected by a pH change on YPD plates.\n mRTT103:Regulator of Ty1 Transposition,,Gene disruption causes Ty1 h\nypertransposition phenotype\n mYHL044W:Unknown ,, Unknown\n mPTK2:Putative serine/threonine protein kinase that enhances sperm\nine uptake,,Mutant shows reduced spermine and putrescine upt\nake and is resistant to toxic polyamine analogs and Li+ and \nNa+ ions; ptk1 ptk2 double mutant shows virtaully abolished \nhigh-affinity spermidine transport\n mILV1:threonine deaminase,threonine deaminase,Isoleucine-plus-vali\nne requiring\n mRTT106:Regulator of Ty1 Transposition - same phenotype as RTT101 - \nRTT105, disruption causes increase in Ty1 transposition. Iso\nlated from the same screen as the other named RTT genes.,,Nu\nll mutant is viable, but Ty1 retrotransposition is increased\n.\n mRRM3:involved in rDNA replication and Ty1 transposition,DNA helic\nase,Null mutant is viable and causes increased Ty1 transposi\ntion, rDNA breakage, and accumulation of rDNA circles\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mYLR065C:Unknown ,, Unknown\n mAPS3:sigma3-like subunit of the yeast AP-3 complex which function\ns in transport of alkaline phosphatase to the vacuole via th\ne alternate pathway, suppressor of loss of casein kinase 1 f\nunction,,Null mutant is viable, rescues yck1,yck2 double mut\nant\n mSDC1:YDR469W,,\n mCYS3:cystathionine gamma-lyase,cystathionine gamma-lyase,Null mut\nant is viable, cysteine auxotroph\n mARG80:Regulator of arginine-responsive genes with ARG81 and ARG82,\ntranscription factor,Arginine requiring\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 mYMR073C:Unknown ,, Unknown\n mECM17:ExtraCellular Mutant,sulfite reductase (putative),loss of fu\nnction mutants are methionine requiring and sensitive to the\n cell wall perturbing agent calcoflour white.\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 mSBE22:functionally redundant and similar in structure to SBE2,,syn\nthetic lethal with sbe2 mutation\n mAUT1:Protein involved in autophagocytosis during starvation,,Null\n mutant is viable, defective in starvation-induced bulk flow\n transport of cytoplasmic proteins to the vacuole, exhibits \ndecreased survival rates during starvation, defective in pro\ntein degradation in the vacuoles induced by nitrogen starvat\nion, homozygous diploids fail to sporulate\n mYBL012C:Unknown ,, Unknown\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 mLGE1:Unknown ,, Unknown\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 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 mMET6:vitamin B12-(cobalamin)-independent isozyme of methionine sy\nnthase (also called N5-methyltetrahydrofolate homocysteine m\nethyltransferase or 5-methyltetrahydropteroyl triglutamate h\nomocysteine methyltransferase),vitamin B12-(cobalamin)-indep\nendent isozyme of methionine synthase (also called N5-methyl\ntetrahydrofolate homocysteine methyltransferase or 5-methylt\netrahydropteroyl triglutamate homocysteine methyltransferase\n),Null mutant is viable, and is a methionine auxotroph\n mYGL080W:Unknown ,, Unknown\n mSTB5:binds Sin3p in two-hybrid assay,,Null mutant is viable\n mIXR1:intrastrand crosslink recognition protein,intrastrand crossl\nink recognition protein,Null mutant is viable; exhibits decr\neased sensitivity to the anticancer drug, cisplatin\n mAPL6:beta3-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 beta adaptin component (put\native),Null mutant is viable, null rescues yck1 yck2 double \nmutant\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 mYOL138C: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 mYOR068C:Unknown ,, Unknown\n mYOL087C: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 mMUD1:U1 snRNP A protein,U1 snRNP A protein,Null mutant is viable\n mYJL200C:Unknown ,, Unknown\n mYOL036W:Unknown ,, Unknown\n mYDR220C:Unknown ,, Unknown\n mSNT1:,,\n mYGR004W:Unknown ,, Unknown\n mNBP2:interacts with Nap1, which is involved in histone assembly,,\n mYIL039W:Unknown ,, Unknown\n mVPS35:Protein involved in vacuolar sorting,retromer complex compon\nent,Null mutant is viable, exhibits defects in sorting of va\ncuolar carboxypeptidase Y, proteinase A, proteinase B, and a\nlkaline phosphatase\n mYDL173W:Unknown ,, Unknown\n mARG1:arginosuccinate synthetase,arginosuccinate synthetase,Argini\nne requiring\n mARG2:First step in ornithine biosynthesis pathway,acetylglutamate\n synthase,\n mARG4:argininosuccinate lyase,argininosuccinate lyase,Arginine req\nuiring\n mYPR076W:Unknown ,, Unknown\n mYDR271C:Unknown ,, Unknown\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 mINP53:Synaptojanin-like protein,inositol polyphosphate 5-phosphata\nse,Null mutant is viable but has abnormal vacuoles\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 mYKL077W:Unknown ,, Unknown\n mMDM38:Unknown ,, Unknown\n mYKL063C:Unknown ,, Unknown\n mSTE50:involved in pheromone signal transduction pathway; interacts\n with G protein and Ste11p,contains SAM (sterile alpha motif\n),Null mutant is viable, sterile, has a modulated sensitivit\ny to alpha-pheromone\n mECM1:putative transmembrane domain protein involved in cell wall \nbiogenesis,,A Tn3 insertion into ECM1 causes hypersensitivit\ny to the cell surface polymer perturbing agent calcofluor wh\nite.\n mFTR1:Plasma membrane iron permease,iron permease,Lacks high affin\nity iron uptake\n mERG2:sterol biosynthesis,C-8 sterol isomerase,Null mutant is viab\nle\n mARO2:Chorismate synthase,chorismate synthase,aromatic amino acid \nrequiring; lack of premeiotic DNA synthesis; blocked sporula\ntion in homozygous mutant\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 mTRK1:180 kDa high affinity potassium transporter,180 kDa high aff\ninity potassium transporter,Null mutant is viable, requires \nadded potassium; trk1 trk2 double mutants are viable\n mARO7:chorismate mutase,chorismate mutase,Aromatic amino acid requ\niring; Low osmotic pressure sensitive\n mECM30:ExtraCellular Mutant,,A Tn3 insertion into this gene causes \nhypersensitivity to the cell surface polymer perturbing agen\nt calcofluor white.\n mMGA2:Product of gene unknown,,Null mutant is viable, shows subtle\n effects on growth, UV sensitivity, and galactose utilizatio\nn; mga2 spt23 double deletion mutants are inviable\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 mYPT31:probably involved in intra-Golgi transport or in the formati\non of transport vesicles at the most distal Golgi compartmen\nt,GTPase , YPT32 homolog , ras homolog,YPT1 is required for \nviability in some strain backgrounds but not others; ypt31 y\npt32 double deletion mutants are inviable\n mTHR4:threonine synthase,threonine synthase,threonine requiring\n mAAT2:aspartate aminotransferase, cytosolic,aspartate aminotransfe\nrase,\n mYDR149C:Unknown ,, Unknown\n mYDR279W:Unknown ,, Unknown\n mSIF2:Sir4p-Interacting Factor,,Null mutant is viable, exhibits in\ncreased telomeric silencing\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 mYGR071C: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 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 mSPP1:YPL138C,,\n mTOM7:Involved in mitochondrial protein import,translocase of the \nouter mitochondrial membrane,Null mutant is viable\n mOPI1:Negative regulator of phospholipid biosynthesis,,The null mu\ntant is viable but constitutively accumulates INO1 mRNA.\n mYPL184C:Unknown ,, Unknown\n mSER1:phosphoserine transaminase,phosphoserine transaminase,Null m\nutant is viable, serine-requiring\n mSER2:phosphoserine phosphatase,phosphoserine phosphatase,serine-r\nequiring\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 mTLG2:member of the syntaxin family of t-SNAREs,tSNARE that affect\ns a late Golgi compartment,Null mutant is viable in SEY6210,\n exhibits endocytosis defect and loss of Kex2p\n mPKR1:Pichia farinosa Killer toxin Resistance,,Confers resistance \nto Pichia farinosa killer toxin (SMK toxin) when overexpress\ned\n mKSP1:Serine/threonine kinase similar to casein kinase II and othe\nr serine/threonine protein kinases,,Null mutant is viable\n mAPG7:autophagy,,Null mutant is viable, defective in autophagy\n mSRC1:Spliced mRNA and Cell cycle regulated gene,,Null mutant is v\niable and shows normal growth in standard media; expression \nis induced at G2/M transition.\n mCHS3:Required for chitin synthesis,chitin synthase 3,Null mutant \nis viable; reduced chitin levels; lack chitin synthase III a\nctivity in vitro; Derepressed INO1 transcription\n mLEU3:Reg. express. of genes involved in branched chain aa biosynt\nh. & in ammonia assimilation. Mod. by alpha-isopropylmalate,\n intermediate in leu biosynth. With alpha-isopropylmalate be\ncomes transcript. act.,zinc finger transcription factor of t\nhe Zn(2)-Cys(6) binuclear cluster domain type,Null mutant is\n viable, leaky leucine auxotroph\n mYML117W-A:Unknown ,, Unknown\n mYMR258C: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 mYML117W:Unknown ,, Unknown\n mGDH1:NADP-specific glutamate dehydrogenase,NADP-specific glutamat\ne dehydrogenase,Null mutant is viable\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 mVAM7:Regulator of vacuolar morphogenesis,heptad repeat motif , hy\ndrophilic protein,Null mutant is viable, exhibits prominent \nlarge vacuoles\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 mUBP3:Possible role for UBP3 in controlling the activity or assemb\nly of the SIR protein complex.,ubiquitin-specific protease,N\null mutant is viable. Null yuh1 ubp1 ubp2 ubp3 quadruple mut\nants are viable and retain the ability to deubiquitinate ubi\nquitin fusions. Deletion of the UBP3 gene results in markedl\ny improved silencing of genes inserted either near a telomer\ne or at one of the silent mating type loci.\n mADE4:phosphoribosylpyrophosphate amidotransferase,phosphoribosylp\nyrophosphate amidotransferase,Adenine requiring\n mADE6:5'-phosphoribosylformyl glycinamidine synthetase,5'-phosphor\nibosylformyl glycinamidine synthetase,Adenine requiring\n mMET22:Putative phosphatase gene involved in salt tolerance and met\nhionine biogenesis; halotolerance,3'(2')5'-bisphosphate nucl\neotidase,Methionine requiring; lacks 3'-phosphoadenylylsulfa\nte (PAPS) reductase activity; unable to grow on sulfate as s\nole sulfur source\n mPCL6:PHO85 cyclin,,Null mutant is viable. A Ty insertion mutant e\nxhibits slow growth.\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 mGCS1:Zn-finger-containing protein that functions as ADP-ribosylat\nion factor GTPase-activating protein and is involved in regu\nlating vesicle transport,ADP-ribosylation factor GTPase-acti\nvating protein (ARF GAP),Null mutant is cold-sensitive for r\neentry into mitotic cell cycle from stationary phase and sho\nws inefficient secretion of invertase\n mYDL162C:Unknown ,, Unknown\n mBAP2:contains 12 predicted transmembrane domains,amino acid perme\nase for leucine, valine, and isoleucine (putative),reduced u\nptake of leucine, isoleucine, and valine\n mYJR119C:Unknown ,, Unknown\n mAPG14:Required for autophagy,,Null mutant is viable but defective \nin autophagy.\n mSUR2:Suppressor of rvs161 and rvs167 mutations,sphingosine hydrox\nylase,Null mutant is viable, has altered phospholipid levels\n mYOR246C:Unknown ,, Unknown\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 mLEO1:Product of gene unknown,,Null mutant is viable\n mSKY1:SRPK1-like Kinase in Yeast (SRPK1 is a human serine kinase t\nhat specifically phosphoryates arginine-serine rich domains \nfound in the SR family of splicing factors.),,Slow growth; D\necreased in vivo phosphorylation of npl3p\n mYMR209C:Unknown ,, Unknown\n mECM1 mSXM1 mSIF2 mSNT1 mAPM3 mAPL5 mBRE1 mLGE1 mSDC1 mBRE2 mTRP2 mTRP3 mTRP5 mGCN3 mKSP1 mBCK1 mARP1 mJNM1 mAPG7 mAUT1 mPEP8 mVPS35 mVPS5 mVPS17
this is an automaticly generated SAMBA report
Computational Genomics Lab, Tel-Aviv uniresity