Module number 920




Database revision : gnsdb28.10
Date : Tue Feb 25 17:11:08 2003
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mYJL211C:Unknown ,, Unknown\n mSFB2:binds to Sed5p and Sec23p by distinct domains,zinc finger pr\notein (putative),\n mYNL134C:Unknown ,, Unknown\n mYNR071C:Unknown ,, Unknown\n mCPT1:Phospholipid biosynthesis,sn-1,2-diacylglycerol cholinephosp\nhotransferase,Null mutant is viable, cpt1 ept1 double deleti\non mutants are viable\n mYNL010W:Unknown ,, Unknown\n mYNL047C:Unknown ,, Unknown\n mBRE5:Product of gene unknown,,null mutant is sensitive to brefeld\nin A\n mMSN4:multicopy suppressor of snf1 mutation,zinc finger protein,Nu\nll mutant is viable; msn2 msn4 double deletion mutants exhib\nit higher sensitivity to different stresses, including carbo\nn source starvation, heat shock and severe osmotic and oxida\ntive stresses\n mPUF4:member of the PUF protein family,,\n mFYV2:Function required for Yeast Viability on toxin exposure,,K1 \nkiller toxin hypersensitivity\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 mYJR097W:Unknown ,, Unknown\n mEGT2:cell-cycle regulation protein, may be involved in the correc\nt timing of cell separation after cytokinesis,,\n mYNL011C:Unknown ,, Unknown\n mSTV1:Stv1p and Vph1p may be equivalent subunits for vacuolar-type\n H(+)-ATPases located on different organelles,110 kDa subuni\nt; not in vacuole membrane , vacuolar H-ATPase,Null mutant i\ns viable, displays additive phenotypes in combination with v\nph1 null mutations\n mCLB3:Involved in mitotic induction and perhaps in DNA replication\n and spindle assembly,B-type cyclin,Null mutant is viable\n mYLL053C:Unknown ,, Unknown\n mMDM1:Intermediate filament protein involved in organelle inherita\nnce,intermediate filament protein,Null mutant is inviable; t\nemperature sensitive mutants display defective transfer of n\nuclei and mitochondria into developing buds at the non-permi\nssive temperature\n mYNL127W:Unknown ,, Unknown\n mDAL82:Positive regulator of allophanate inducible genes,positive t\nranscriptional regulator,loss of induction for allantoin deg\nradation pathways\n mPEX14:Peroxisomal peripheral membrane protein (peroxin) involved i\nn import of peroxisomal matrix proteins,,Null mutant is viab\nle but is unable to grow on oleate and lacks peroxisomes\n mBUL2:a homologue of BUL1,,Null mutant is viable; the bul1 bul2 do\nuble disruptant is sensitive to various stresses\n mCSL4:Represses the replication of double-stranded RNA viruses, pr\notecting the host from the otherwise lethal effects of the v\nirus,,Null mutant is inviable, csl4-1 exhibits double mutant\n inviability in combination with cbf1(cep1) deletion mutants\n mYPL150W:Unknown ,, Unknown\n mZRC1:Zinc- and cadmium-resistance protein,,Null mutant is viable \nand sensitive to zinc\n mMSO1:multicopy suppressor of sec1; small hydrophilic protein, enr\niched in microsomal membrane fraction, interacts with Sec1p,\n,Null mutant is viable, exhibits accumulation of secretory v\nesicles in the bud; mso1 null mutants exhibit double mutant \ninviability in combinaiton with sec1, sec2, and sec4 mutants\n mSMM1:Suppressor of Mitochondrial Mutation in the tRNAasp gene; Di\nhydrouridine synthase 2,tRNA dihydrouridine synthase,Overexp\nression weakly suppresses a mutation affecting the maturatio\nn of mitochondrial tRNA-Asp.\n mASI3: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 mDAN3:delayed anaerobic gene,putative cell wall protein,unknown\n mMAK10:Glucose-repressible protein,,Null mutant is viable, grows po\norly on nonfermentable carbons sources\n mIES2:Hypothetical ORF,,Null mutant is viable\n mSSK1:Two-component signal transducer that with Sln1p regulates os\nmosensing MAP kinase cascade(suppressor of sensor kinase),tw\no-component signal transducer that with Sln1p regulates osmo\nsensing MAP kinase cascade(suppressor of sensor kinase),Null\n mutant is viable; suppresses the lethality of sln1 or ypd1 \ndisruption mutants\n mMPA43:Overexpression leads to increased levels of the lyase PDC1,,\nNull mutant is viable with no specific phenotype and normal \nexpression of PDC1; but overexpression causes higher basal l\nevels of PDC1\n mWSC2:cell wall integrity and stress response component 2,contains\n novel cysteine motif , integral membrane protein (putative)\n , similar to SLG1 (WSC1), WSC3 and WSC4,Null mutant is viab\nle and shows no phenotypes; slg1 (wsc1)-null wsc2-null doubl\ne mutant shows a lysis defect on YPD at room temperature and\n heat shock sensitivity; overexpression of WSC genes suppres\nses heat shock sensitivity of hyperactivated ras mutant; hea\nt shock sensitivity of wsc mutant strain is suppressed by de\nletion of ras2\n mSSK2:Suppressor of Sensor Kinase (SLN1),MAP kinase kinase kinase \n, activator of Pbs2p,Suppresses sln1 lethality. Syntheticall\ny high-osmolarity sensitive when it is combined with both ss\nk22 and sho1 mutations\n mYKR100C:Unknown ,, Unknown\n mGIS2:GIG3 suppressor,,\n mCAF120:Hypothetical ORF,,Null mutant is viable\n mPEX6:Required for peroxisome assembly,AAA ATPase,lack of peroxiso\nme biogenesis\n mRIA1:RIbosome Assembly,,Null: quasi essential. Other phenotypes: \nDepletion of Ria1p leads to modification of the polysome pro\nfile, with the apperance of halfmers and a reduced level of \n60S subunits.\n mLYS9:Seventh step in lysine biosynthesis pathway,,lysine auxotrop\nh\n mYNR066C: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 mYDL172C:Unknown ,, Unknown\n mYLR137W:Unknown ,, Unknown\n mYKL033W-A:Unknown ,, Unknown\n mPTK1:Putative serine/threonine protein kinase,,Mutant shows decre\nase in total polyamine accumulation and resistance to polyam\nine analogs; ptk1 ptk2 double mutant shows virtually abolish\ned high-affinity spermidine transport\n mYNL274C:Unknown ,, Unknown\n mBOP2:bypass of PAM1,,\n mYBR246W:Unknown ,, Unknown\n mYNL063W:Unknown ,, Unknown\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 mYNL136W:Unknown ,, Unknown\n mRAD50:coiled-coil protein, contains a purine-binding domain, two h\neptad repeats and a hydrophobic tail,Mre11-Rad50-Xrs2 protei\nn complex member involved in joining double-stranded breaks \nand DNA recombination,Null mutant is viable but defective fo\nr X-ray damage repair, sporulation, chromosome pairing, form\nation and processing of DS breaks, gene conversion and recip\nrocal recombination in non-rDNA, tripartite synaptonemal com\nplexes and heteroduplex DNA. Exhibits blocked meiotic recomb\nination and formation of synaptonemal complex at early stage\ns. rad50-1 or null is rescued by spo13 and rescues rad52 spo\n13.\n mPPH3:protein phosphatase type 2A,protein phosphatase type 2A,Null\n mutant is viable, pph3 pph21 pph22 mutants are inviable\n mYBR174C:Unknown ,, Unknown\n mHOL1:Putative ion transporter similar to the major facilitator su\nperfamily of transporters,ion transporter (putative) , simil\nar to the major facilitator superfamily of transporters,Null\n mutant is viable, unable to uptake histidinol or Na+. Gain-\nof-function mutations confer non-selective cation transport \nand abolish translational repression by a small upstream ope\nn reading frame\n mYNL100W:Unknown ,, Unknown\n mFCY21:identical to FCY2,purine-cytosine permease,\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 mMAI1:Unknown ,, Unknown\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 mAUT7:Forms a protein complex with Aut2p to mediate attachment of \nautophagosomes to microtubules. Defective in maturation of t\nhe vacuolar protein, aminopeptidase I,similar to LC3, a micr\notubule-associated protein from rat,Null mutant is viable bu\nt lacks autophagocytosis and is unable to sporulate. AUT7 is\n a suppressor of mutant phenotypes of aut2-1 cells. Uptake o\nf precursor Aminopeptidase I into the vacuole depends on Aut\n2p and Aut7p.\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 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 mESC8:Unknown ,, Unknown\n mYNL217W:Unknown ,, Unknown\n mYJL178C:Unknown ,, Unknown\n mYDL203C:Unknown ,, Unknown\n mESBP6:Protein with similarity to mammalian monocarboxylate transpo\nrters MCT1 and MCT2,monocarboxylate permease (putative),\n mYDL050C:Unknown ,, Unknown\n mYHL046C:Unknown ,, Unknown\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 mDOM34:an ORF of unknown function located in a centromeric region d\nuplicated between chromosomes III and XIV (DOM34 homologue o\nn chromosome III is a pseudogene),,\n mYLL049W:Unknown ,, Unknown\n mYNL022C:Unknown ,, Unknown\n mERG4:Sterol C-24 reductase,sterol C-24 reductase,Null mutant is v\niable\n mARO3:DAHP synthase; a.k.a. phospho-2-dehydro-3-deoxyheptonate ald\nolase, phenylalanine-inhibited; phospho-2-keto-3-deoxyhepton\nate aldolase; 2-dehydro-3-deoxyphosphoheptonate aldolase; 3-\ndeoxy-D-arabine-heptulosonate-7-phosphate synthase,DAHP synt\nhase; a.k.a. phospho-2-dehydro-3-deoxyheptonate aldolase, ph\nenylalanine-inhibited; phospho-2-keto-3-deoxyheptonate aldol\nase; 2-dehydro-3-deoxyphosphoheptonate aldolase; 3-deoxy-D-a\nrabine-heptulosonate-7-phosphate synthase,null mutant is via\nble\n mYNR025C:Unknown ,, Unknown\n mYCK2:membrane-bound casein kinase I homolog,casein kinase I homol\nog,Null mutant is viable; yck1 yck2 double deletion mutant i\ns inviable\n mEND3:Required for endocytosis and organization of the cytoskeleto\nn,,Null mutant is viable and defective in endocytosis\n mMCM22:Required for maintenance of chromosomes and minichromosomes,\n,Null mutant is viable\n mECM39:ExtraCellular Mutant,,A Tn3 insertion into this gene causes \nhypersensitivity to the cell surface polymer perturbing agen\nt calcofluor white.\n mYKL136W:Unknown ,, Unknown\n mMAK3:N-acetyltransferase,N-acetyltransferase,deficient in mainten\nance 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 mYBR220C:Unknown ,, Unknown\n Cond229:yhr011w(**14)\n mCLG1:cyclin-like protein that interacts with Pho85p in affinity c\nhromatography,,Null mutant is viable\n mARP5:actin-related protein,actin related protein,\n mAPG5:Involved in autophagy,,reduced viability upon nutrient starv\nation; defective in autophagy\n mKSP1:Serine/threonine kinase similar to casein kinase II and othe\nr serine/threonine protein kinases,,Null mutant is viable\n mSIN4:involved in positive and negative regualtion of transcriptio\nn, possibly via changes in chromatin structure,RNA polymeras\ne II holoenzyme/mediator subunit,Null mutant is viable, temp\nerature sensitive, displays defects in both positive and neg\native regulation of transcription, suppresses Ty insertion m\nutations (Spt-), exhibits decreased superhelical density of \ncircular DNA molecules, exhibits expression from promoters l\nacking UAS elements; associated with a defect in RME1-depend\nent repression and a methionine or cysteine requirement, exh\nibits flocculant/lacy colony morphology, suppressor of snf/s\nwi mutations\n mYNL081C:Unknown ,, Unknown\n mAPG7:autophagy,,Null mutant is viable, defective in autophagy\n mYNL227C:Unknown ,, Unknown\n mSGE1:multi-copy suppressor of gal11 null; member of drug-resistan\nce protein family,,Null mutant is viable; shows decreased ex\npression of galactose-inducible genes; shows increased sensi\ntivity to crystal violet\n mENT5:Unknown ,, Unknown\n mYNR040W:Unknown ,, Unknown\n mYGR268C:Unknown ,, Unknown\n mMRPL13:mitochondrial ribosomal protein YmL13,ribosomal protein (YmL\n13),Null mutant is viable, grows poorly on non-fermentable c\narbon sources\n COMP.KO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mALD4:Glucose repressed. Utilizes NADP+ or NAD+ as a coenzyme equa\nlly well. (sold by SIGMA under the catalogue number A5550, a\nccording to A. Blomberg).,aldehyde dehydrogenase,\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 mYNL024C:Unknown ,, Unknown\n mSWD3:YBR175W,,\n mYJR111C:Unknown ,, Unknown\n mDSL1:dsl1 mutations are suppressed by a dominant allele of SLY1, \ncalled sly1-20,,inviable\n mYOR325W:Unknown ,, Unknown\n mYHL012W:Unknown ,, Unknown\n mAPG10:Involved in autophagy; protein-conjugating enzyme involved i\nn the Apg12p-Apg5p conjugation pathway,protein-conjugating e\nnzyme,Defective autophagy, apg10-1 allele shows reduced viab\nlility under starvation conditions\n mAPG12:autophagy,,Null mutant is viable, defective in autophagy\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 mAPG13:autophagy,,Defective in autophagy\n mSHR5:Involved in RAS localization and palmitoylation,,Null mutant\n is viable; exhibits normal palmityltransferase activity in \nvitro and attenuates Ras function in cells with mutant Ras2 \nproteins that are not farnesylated or palmitoylated; shr5 mu\ntation originally isolated as suppressor of Ras function\n mAPG16:autophagy,,Null mutant is viable, defective in autophagy\n mHXT2:hexose transporter,high affinity hexose transporter-2,Null m\nutant is viable\n mYGR058W:Unknown ,, Unknown\n mHXT14:High-affinity hexose transporter,hexose transporter,\n mSNA2:Unknown ,, Unknown\n mYGR269W:Unknown ,, Unknown\n mYBR280C:Unknown ,, Unknown\n mLRO1:Lecithin cholesterol acyl transferase (LCAT) Related Orf,,Nu\nll mutant is viable\n mBNI4:bud neck involved,required to link Chs3p and Chs4p to the se\nptins,Null mutant is viable, shows delocalized chitin, elong\nated buds, enlarged bud necks\n mSIP3:Interacts with SNF1 protein kinase,transcriptional activator\n (putative),Null mutant is viable; does not confer snf1 phen\notypes\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 mBUD2:GTPase-activating protein (GAP) for Rsr1p/Bud1p,GTPase activ\nating protein (GAP) for Rsr1p/Bud1p,Null mutant is viable, w\nith random bud site selection in all cell types\n mYJR083C:Unknown ,, Unknown\n mBUD6:actin interacting rotein,,Null mutant is viable; mutants exh\nibit severe disruption of the actin cytoskeleton; deletion s\ntrains have a depolarized cytoskeleton, mitotic delay, and p\nrobable cytokinesis defects\n mBUD7:bud site selection,,Diploid-specific heterogenous bud site s\nelection\n mYNL200C:Unknown ,, Unknown\n mAAH1:adenine aminohydrolase (adenine deaminase),adenine aminohydr\nolase (adenine deaminase),Null mutant is viable\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 mFRE3:similar to FRE2,,\n mSNQ2:ABC transporter,ABC transporter,null mutant is viable; overe\nxpression confers multi-drug resistance\n mFRE4:similar to FRE2,,\n mYPL034W:Unknown ,, Unknown\n mCYB5:cytochrome b5,cytochrome b5,Null mutant is viable, cyb5 muta\ntions suppress ketoconazole hypersensitivity of a P450 reduc\ntase deficient strain\n mYNR029C:Unknown ,, Unknown\n mYBL089W:Unknown ,, Unknown\n mNCR1:Niemann-Pick Type C homologous gene,transmembrane protein (p\nutative),Null mutant is viable.\n mNMD2:Protein involved in decay of mRNA containing nonsense codons\n,,Null mutant is viable, exhibits stabilization of nonsense-\ncontaining mRNAs\n mIPI3:Unknown ,, Unknown\n mYBL010C:Unknown ,, Unknown\n mNMD4:putative Upf1p-interacting protein,,\n mYJR149W:Unknown ,, Unknown\n mARC35:Arp complex subunit,,Null mutant is viable, but exhibits sev\nere growth defects\n mDPH2:Diptheria toxin resistance protein, required for diphthamide\n biosynthesis,,Null mutant is viable\n mAMD1:putative alpha-mannosidase,alpha-mannosidase (putative),Null\n mutant is viable\n mDPH5:diphthamide biosynthesis,,Null mutant is viable\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 mVID27:Vacuole import and degradation,,Null mutant is viable but ex\nhibits vacuole degradation of cytosolic proteins\n mHCH1:high copy Hsp90 supressor,,Null mutant is viable; when overe\nxpressed, HCH1 is an allele-specific suppressor of hsp82 ts \nmutants\n mYKL031W:Unknown ,, Unknown\n mTAT2:Tryptophan permease, high affinity,tryptophan permease, high\n affinity,suppressor of chromosome segregation mutation\n mYNL114C:Unknown ,, Unknown\n mALG9:catalyzes the transfer of mannose from Dol-P-Man to lipid-li\nnked oligosaccharides,mannosyltransferase,accumulation of li\npid-linked Man6GlcNAc2; hypoglycosylation of secreted protei\nns\n mYMR029C:Unknown ,, Unknown\n mPTR2:Functions in transport of small peptides into the cell,pepti\nde transporter,Null mutant is viable\n mYNL157W:Unknown ,, Unknown\n mYNL077W:Unknown ,, Unknown\n mSIR1:repressor of silent mating loci,silent mating loci repressor\n,\n mDIN7:DNA-damage inducible gene,,\n mMDG1:multicopy suppressor of bem1 mutation, may be involved in G-\nprotein mediated signal transduction; binds cruciform DNA,,N\null mutant is viable. Deletion of MDG1 causes sterility in c\nells in which the wild-type G beta has been replaced by part\nly defective G beta derivatives\n mYBR071W:Unknown ,, Unknown\n mANB1:hypusine containg protein; ANB1 is expressed under anaerobic\n conditions and repressed under aerobic conditions whereas i\nts homolog HYP2 is inversely regulated,translation initiatio\nn factor eIF-5A, anaerobically expressed form,null mutant is\n viable; a double mutant containing disruptions of both ANB1\n and and the highly homologous HYP2 is inviable\n mIMD3:Hypothetical ORF,IMP dehydrogenase homolog,\n mYGR018C:Unknown ,, Unknown\n mYPL261C:Unknown ,, Unknown\n mSEO1:Suppressor of Sulfoxyde Ethionine resistance,permease (putat\nive),\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mYNL122C:Unknown ,, Unknown\n mURK1:converts ATP and uridine to ADP and UMP,uridine kinase,\n mYPR039W:Unknown ,, Unknown\n mYOL093W:Unknown ,, Unknown\n mGCD10:First identified as negative regulator of GCN4 expression,RN\nA-binding protein , translation initiation factor 3 (eIF-3) \nzeta subunit,Null mutant is inviable. There are mutants avai\nlable that show constitutive HIS4 transcription and slow gro\nwth\n mYNL326C:Unknown ,, Unknown\n mYBL012C:Unknown ,, Unknown\n mAPL3:clathrin Associated Protein complex Large subunit,clathrin a\nssociated protein complex large subunit,Null mutant is viabl\ne\n mYBL062W:Unknown ,, Unknown\n mYMC1:putative mitochondrial carrier protein,carrier protein (puta\ntive),\n mYOR300W:Unknown ,, Unknown\n mMCK1:Disp. for mitosis, required for chr. segregation, benomyl re\nsist., basal IME1 transcript. in mitosis, IME1 induction in \nmeiosis & ascus mat. independ. of IME1; maybe in mitotic chr\n. segregation specific to CDEIII,43.1 kDa serine/threonine/t\nyrosine protein kinase,Null mutant is viable, cold sensitive\n, temperature sensitive, and benomyl sensitive; associated w\nith delays and decreased levels of sporulation. High copy MC\nK1 acclerates early gene expression.\n 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 mELA1:similar to mammalian elongin A, interacts with elongin C,elo\nngin A transcription elongation factor,viable\n mYOR053W:Unknown ,, Unknown\n mMUD1:U1 snRNP A protein,U1 snRNP A protein,Null mutant is viable\n mTRS33:Trapp subunit of 33 kDa,,Null mutant is viable\n mYOL036W:Unknown ,, Unknown\n mYNL253W:Unknown ,, Unknown\n mRGA2:contains a Rho-GAP domain and two LIM domains, similar to Rg\na1p and all known Rho-GAPs,Rho-GTPase Activating Protein,Nul\nl mutants are viable but increase the restrictive temperatur\ne of a cdc24-4 strain and increase the constitutive activati\non of the pheromone response pathway in conjungtion with mut\nations in RGA1 and BEM3; overexpression of RGA2 causes a dec\nrease in the restrictive temperature of a cdc42-1 strain\n mYBR219C:Unknown ,, Unknown\n mYNL319W:Unknown ,, Unknown\n mYNL086W:Unknown ,, Unknown\n mFOB1:The gene product is essential for both DNA replication fork \nblocking and recombinational hotspot activities.,DNA replica\ntion fork blocking protein,Loss of replication fork blocking\n and recombinational hotspot activities.\n mYNL254C:Unknown ,, Unknown\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 mAPM4:Clathrin associated protein, medium subunit,clathrin associa\nted protein complex medium subunit,\n mYMR158W-A:Unknown ,, Unknown\n mYBL006C:Unknown ,, Unknown\n mYNL123W:Unknown ,, Unknown\n mRAS2:Ras proto-oncogene homolog. Ras2 is involved in growth on no\nn-fermentable carbon sources, the starvation response, sporu\nlation, pseudohyphal growth and aging.,small GTP-binding pro\ntein,Loss of function mutants grow poorly on nonfermentable \ncarbon sources, sporulate in rich media, are unable to diffe\nrentiate into a pseudohyphal form and exhibit an increased l\nife span.\n mSSF2:high copy suppressor of G beta subunit temperature sensitive\n mutation,,Null mutant is viable; displays double mutant let\nhality with ssf1 null mutations. Ssfp depletion is associate\nd with arrest of cell division and decreased mating\n mYJL084C:Unknown ,, Unknown\n mCRZ1:calcineurin responsive zinc-finger,transcription factor (put\native),Null mutant is viable\n mFTR1:Plasma membrane iron permease,iron permease,Lacks high affin\nity iron uptake\n mNIS1:Hypothetical ORF,,\n mMKS1:Pleiotropic regulatory factor involved in Ras-CAMP and lysin\ne biosynthetic pathways and nitrogen regulation,negative tra\nnsctiptional regulator,Null mutant is viable, fails to grow \non galactose media containing ethidium bromide at 25 degrees\n and on YPglycerol media at 37 degrees\n mYNL181W:Unknown ,, Unknown\n mYNL247W:Unknown ,, Unknown\n mSKO1:Suppressor of PKA overexpression; bZIP protein that binds to\n CRE motifs, interacts with Mig1p,CREB like trancsriptional \nrepressor,Null mutant is viable, associated with partial der\nepression of the SUC2 gene; associated with increased transc\nription through ATF/CREB sites. SKO1 is a multicopy suppress\nor of the lethality caused by overexpressing cAMP-dependent \nprotein kinase and of the toxicity caused by overexpressing \nRap1p\n mYEL059W:Unknown ,, Unknown\n mYDR112W:Unknown ,, Unknown\n mSTD1:interacts with the SNF1 protein kinase and TBP in two-hybrid\n and in in vitro binding studies,MTH1 homolog,Null mutant is\n viable, no defects in mating or sporulation. Suppressor of \nTBP deletion; multicopy suppressor of SNF; std1-mth1 has def\nective glucose derepression and sporulation\n mRLR1:Required for LacZ RNA expression from certain plasmids; supp\nressor of the Transcriptional (T) defect of Hpr1 (H) by Over\nexpression (O); plays a role in transcription elongation by \nRNA polymerase II,,Null mutant is viable but shows poor grow\nth and a temperature-sensitive phenotype.Increased frequenci\nes of recombination between direct repeats (>1000-fold above\n wild-type levels) that is linked to transcriptional elongat\nion defects. General defects in RNA polII transcription. Inc\napacity to transcribe lacZ. Overexpression of RLR1 suppresse\ns the ts phenotype and the incapacity to transcribe lacZ seq\nuences of hpr1-delta mutants\n mYNL095C:Unknown ,, Unknown\n mPPR1:Positive regulator of URA1 and URA3,zinc finger transcriptio\nn factor of the Zn(2)-Cys(6) binuclear cluster domain type,N\null mutant is viable, deficient in pyrimidine biosynthetic p\nathway\n mSRY1:Serine Racemase homolog in Yeast,pyridoxal-5'phosphate-depen\ndent enzyme , similar to mouse glial serine racemase,Null mu\ntant is viable\n mLEM3:Product of gene unknown,,null mutant is sensitive to brefeld\nin A and shows increased glucocorticoid receptor activity in\n response to dexamethasone\n mSPP1:YPL138C,,\n mORC5:May be subunit of origin recognition complex (ORC) that medi\nates the ATP-dependent binding to origins; the ORC binds to \norigins of replication and thereby directs DNA replication a\nnd is also involved in transcriptional silencing,ATP-binding\n site (putative) , origin recognition complex fifth largest \nsubunit,orc5-1 mutant is temperature-sensitive, has defects \nin transcriptional silencing, has elevated rate of plasmid l\noss and inefficient initiation of DNA replication at the per\nmissive temperature, and arrests at the nonpermissive temper\nature; CDC6 is multicopy suppressor of orc5-1\n mNAM9:putative mitochondrial S4 ribosomal protein,mitochondrial S4\n ribosomal protein (putative),Null mutant is viable but is r\nespiration-deficient and loses mitochondrial DNA integrity\n mMKT1:Protein involved in propagation of M2 dsRNA satellite of L-A\n virus,retroviral protease signature protein,Null mutant is \nviable\n mTOM7:Involved in mitochondrial protein import,translocase of the \nouter mitochondrial membrane,Null mutant is viable\n mYMR306C-A:Unknown ,, Unknown\n mSYT1:Suppressor of Ypt3,,\n mYOR055W:Unknown ,, Unknown\n mRHO2:Gtp-binding protein of the rho subfamily of ras-like protein\ns,GTP-binding protein , rho subfamily,null is viable\n Cond271:yor051c(**14)\n mYNL335W:Unknown ,, Unknown\n mPUS4:catalyzes formation of Psi55 (modified uridine) in mitochond\nrial and cytoplasmic tRNAs,pseudouridine synthase,Null mutan\nt is viable; mutant is available that is defective in exit f\nrom late anaphase/early telophase (Raymond, Wendy E.)\n mYCR076C:Unknown ,, Unknown\n mYOL046C:Unknown ,, Unknown\n mPSY2:Unknown ,, Unknown\n mSEC12:Required for recruitment of Sar1p and vessicle formation at \nthe endoplasmic reticulum.,guanine nucleotide exchange facto\nr for Sar1p,Null mutant is inviable. Defective in endoplasmi\nc reticulum to Golgi transport.\n mUGA4:GABA-specific transport protein,GABA-specific transport prot\nein,Null mutant is viable.\n mYNL176C:Unknown ,, Unknown\n mYBR235W:Unknown ,, Unknown\n mIDS2:IME2-Dependent Signalling,,Null mutations reduce or abolish \nthe ability of IME2p to activate expression of early, middle\n, and late meiotic genes. Recessive and null ids2 mutants pr\nevent toxicity of Ime2p expression in rad52 haploids, but do\n not affect Ime2p polypeptide accumulation.\n mYNL089C:Unknown ,, Unknown\n mYNL045W:Unknown ,, Unknown\n mYOL003C: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 mLYP1:lysine permease,lysine permease,\n mCOX5A:One of two genes (COX5A and COX5B, both nuclear-encoded) cod\ning for subunit V of cytochrome c oxidase; COX5A gene produc\nt is the predominantform of subunit V found in holocytochrom\ne c oxidase under normal growth conditions,cytochrome c oxid\nase chain Va,Null mutant is viable, respires at 10-15% of th\ne wild-type rate due to the presence of COX5B; cox5a cox5b d\nouble deletion mutants are completely non-respiratory\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 mABZ1:para-aminobenzoate synthase, PABA synthase,para-aminobenzoat\ne synthase (PABA synthase),Null mutant is viable and PABA au\nxotroph\n mMVD1:involved in the polyisoprene biosynthesis pathway,mevalonate\n pyrophosphate decarboxylase,Null mutant is inviable; a sing\nle leucine to proline mutation causes temperature sensitivit\ny.\n mUBP7:Ubiquitin-specific protease,ubiquitin-specific protease,\n mYPL004C:Unknown ,, Unknown\n mPHO87:May collaborate with Pho86p and Pho84p in inorganic phosphat\ne uptake; protein contains 12 predicted transmembrane domain\ns,phosphate permease,Null mutant is viable; pho86 pho87 doub\nle mutant constitutively synthesizes repressible acid phosph\natase and is aresenate-resistant\n mBIO4:dethiobiotin synthetase,dethiobiotin synthetase,\n mFIG4:FIG4 expression is induced by mating factor.,,Null mutant is\n viable, mating defective\n mYJL123C:Unknown ,, Unknown\n mYPR064W:Unknown ,, Unknown\n mCOG6:Unknown ,, Unknown\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 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 mYNL184C:Unknown ,, Unknown\n mAPP1:Unknown ,, Unknown\n mDSE3:Hypothetical ORF,,\n mDSE4:Hypothetical ORF,,\n mTRF5:TRF4 homolog; TRF4/5 function is required for proper mitosis\n,DNA polymerase sigma,Null mutant is viable; trf4 trf5 mutan\nts are inviable; trf4 (ts) trf5 double mutant is hypersensit\nive to the anti-microtubule agent thiabendazole at a semi-pe\nrmissive temperature, overexpression of TRF5 complements the\n inviability of top1 trf4 mutants\n mCAF40:Hypothetical ORF,,Null mutant is viable\n mYNL046W: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 mMMP1:S-MethylMethionine Permease,high affinity S-methylmethionine\n permease,Null mutant is viable but is unable to use S-methy\nlmethionine as a sulfur source\n mSGN1:contains one RNA recognition (RRM) domain,,\n mSCW10:Soluble Cell Wall protein,soluble cell wall protein,Null mut\nant is viable.\n
this is an automaticly generated SAMBA report
Computational Genomics Lab, Tel-Aviv uniresity