Module number 2748




Database revision : gnsdb28.10
Date : Tue Feb 25 17:30:15 2003
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Cond458:YP_raffinose_vs_reference_pool_car-2\n mTIM17:Mitochondrial inner membrane protein involved in protein imp\nort,16.5 kDa inner membrane protein required for import of m\nitochondrial precursor proteins,Null mutant is inviable\n mYNL010W:Unknown ,, Unknown\n Jelinski.Jelinski:Regulatory networks revealed by transcriptional profiling of\n damaged Saccharomyces cerevisiae cells: Rpn4 links base exc\nision repair with proteasomes. Mol Cell Biol. 2000 Nov;20(2\n1):8157-67.\n mTIM18:mitochondrial inner membrane translocase,translocase,Null mu\ntant is viable\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 mFPR1:FK506 binding protein; proline rotamase; rapamycin-binding p\nrotein,peptidyl-prolyl cis-trans isomerase (PPIase),Null mut\nant is viable but exhibits slow growth. Null mutant also exi\nbits partial resistance to FK506 and complete resistance to \nrapamycin.\n mDFG10:Protein required for filamentous growth, cell polarity, and \ncellular elongation,,Null mutant is viable and defective in \nfilamentous growth\n mTIR2:cold-shock induced protein of the Srp1p/Tip1p family of seri\nne-alanine-rich proteins,,Null mutant is viable.\n mURA5:Fifth step in pyrimidine biosynthesis pathway,orotate phosph\noribosyltransferase 1,Null mutant is viable\n mTIR3:TIP1-related,cell wall mannoprotein,inviable under unaerobic\n conditions\n mTIR4:Hypothetical ORF,cell wall mannoprotein,inviable under anaer\nobic conditions\n mFET4:Putative transmembrane low-affinity Fe(II) transporter,low a\nffinity Fe2+ transport protein,Mutant lacks low affinity Fe(\nII) transport but has more active high affinity Fe(II) trans\nport activity\n mYDR492W:Unknown ,, Unknown\n mYHR133C:Unknown ,, Unknown\n mENO1:enolase I,enolase I,Null mutant is viable\n Cond883:5\n mCYB5:cytochrome b5,cytochrome b5,Null mutant is viable, cyb5 muta\ntions suppress ketoconazole hypersensitivity of a P450 reduc\ntase deficient strain\n Stress.Carbon:Genomic expression programs in the response of yeast cells t\no environmental changes. Mol Biol Cell. 2000 Dec;11(12):424\n1-57\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 mARD2:Unknown ,, Unknown\n mHNM1:choline transport protein; may also control uptake of nitrog\nen mustard,transporter (permease) for choline and nitrogen m\nustard; share homology with UGA4,Null mutant is viable, but \nhyper-resistant to nitrogen mustard; ctr1,cho1 double null i\ns inviable\n mZRC1:Zinc- and cadmium-resistance protein,,Null mutant is viable \nand sensitive to zinc\n mRPS12:Homology to rat S12,ribosomal protein S12,\n mRSM19:mitochondrial ribosome small subunit component,mitochondrial\n ribosome small subunit component,\n Cond:\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 mGAS5:Unknown ,, Unknown\n mYNR021W:Unknown ,, Unknown\n mSSC1:Nuclear-encoded mitochondrial protein; member of the heat sh\nock protein 70 (HSP70) family; most similar to E. coli DnaK \nprotein; acts as a chaperone for protein import across the i\nnner membrane,SceI endonuclease subunit , mitochondrial matr\nix protein involved in protein import , SceI endonuclease su\nbunit , mitochondrial matrix protein involved in protein imp\nort,Null mutant is inviable; some alleles demonstrate effect\ns in sporulation and germination\n mCIS3:cik1 suppressor,similar to Hsp150p and Pir1p, Pir2p, and Pir\n3p,Null mutant is viable; CIS3 is a high copy suppressor of \ncik1 deletion mutants\n mYIL059C:Unknown ,, 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 Cond888:MNNG_2\n mSAR1:Secretion-Associated, Ras-related. Component of COPII coat o\nf vesicles; required for ER to Golgi protein transport,ARF f\namily , GTP-binding protein,Null mutant is inviable. When ov\nerexpressed, wild-type SAR1 suppresses a sec12 mutation.\n mMRPL44:Mitochondrial ribosomal protein MRPL44 (YmL44),ribosomal pro\ntein (YmL44),\n mYPR147C:Unknown ,, Unknown\n mYIL088C:Unknown ,, Unknown\n mYPL246C:Unknown ,, Unknown\n mCYC1:iso-1-cytochrome c,iso-1-cytochrome c,Cytochrome c deficienc\ny\n mTAT2:Tryptophan permease, high affinity,tryptophan permease, high\n affinity,suppressor of chromosome segregation mutation\n mSNC2:mediate the targeting and transport of secretory proteins,ve\nsicle-associated membrane protein (synaptobrevin) homolog,Nu\nll mutant is viable, snc1 snc2 double mutants are deficient \nin normal bulk secretion, accumulate large numbers of post-G\nolgi vesicles, and display a variety of conditional lethal p\nhenotypes\n mSMF1:Isolated as high copy suppressor of a cdc1 mutation & involv\ned in high affinity Mn2+ uptake. SMF1 was isolated as a high\n copy suppressor of a ts mutation in the PEP (mito. matrix p\nrotease) gene & may influence PEP-dependent protein import,p\nlasma membrane/mitochondrial membrane protein,Null mutant is\n viable, exhibits reduced Mn2+ uptake; shows double mutant s\nickness with smf2 null\n mRTN1:Unknown ,, Unknown\n mADH4:Alcohol dehydrogenase type IV,alcohol dehydrogenase isoenzym\ne IV,Null mutant is viable\n mYPL144W:Unknown ,, Unknown\n mYOL092W:Unknown ,, Unknown\n mCAM1:Calcium and phospholipid binding protein homologous to trans\nlation elongation factor 1-gamma (EF-1gamma),calcium and pho\nspholipid binding protein homologous to translation elongati\non factor 1-gamma (EF-1gamma),Null mutant is viable under no\nrmal growth conditions\n mSPE3:biosynthesis of spermidine,putrescine aminopropyltransferase\n (spermidine synthase),Null mutant is viable, has no spermid\nine synthase activity, requires spermine or spermidine for g\nrowth\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 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 mYHR214W:Unknown ,, Unknown\n mEMP24:type I transmembrane protein, component of COPII-coated, ER-\nderived transport vesicles,type I transmembrane protein,Null\n mutant is viable\n mSCM4:Protein that suppresses ts allele of CDC4 when overexpressed\n,,viable, suppressor of cdc4ts allele\n mPAU7:similar to Pau3, member of Pau1 family,,\n mIMD3:Hypothetical ORF,IMP dehydrogenase homolog,\n mERV14:ER-derived vesicles,14 kDa protein found on ER-derived vesic\nles,Null mutant is viable but exhibits defects in sporulatio\nn (diploids) and bud site selection (haploids). Null mutants\n also retain the bud site selection marker, Axl2p, in the ER\n and exhibit slow recovery from selective to rich media.\n mYOL101C:Unknown ,, Unknown\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\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 mFAS1:pentafunctional enzyme consisting of the following domains :\n acetyl transferase, enoyl reductase, dehydratase and malony\nl/palmityl transferase,acetyl transferase , dehydratase , en\noyl reductase , malonyl/palmityl transferase , pentafunction\nal enzyme,Null mutant is viable\n mOST6:Putative new 37kDa subunit of N-oligosaccharyltransferase co\nmplex,N-oligosaccharyltransferase complex 37kDa subunit (put\native),\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 mYHR113W:Unknown ,, Unknown\n mPRY3: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 Cond891:G1MMS\n mYGL080W:Unknown ,, Unknown\n mYGR106C: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 mACT1:Involved in cell polarization, endocytosis and other cytoske\nletal functions,actin,Null mutant is inviable; ts mutants sh\now osmosensitivity and defects in actin organization at non-\npermissive temp.; overproduction is lethal\n mYOR394W:Unknown ,, Unknown\n mTIF2:translation initiation factor eIF4A,translation initiation f\nactor eIF4A subunit,viable, tif1tif2 double mutant is lethal\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 mERV25:COPII coat component of certain ER-derived vesicles,vesicle \ncoat component,Null mutant is viable, displays a selective d\nefect in transport of secretory proteins from the ER to Golg\ni complex.\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 mTIF6:similar to human translation initiation factor 6 (eIF6); how\never, TIF6 does not act as a true translation initiation fac\ntor.The protein may be involved in the biogenesis and or sta\nbility of the 60S ribosomal subunits,,Null mutant is inviabl\ne; cells are depleted of 60S ribosomal subunits, translation\n initiation is inhibited, and cells arrest in G1\n mERV29:ER Vesicle protein of 29 kDa (apparent MW),ER-Golgi transpor\nt vesicle protein,Null mutant is viable.\n mYPR004C:Unknown ,, Unknown\n mRPL1A:Homology to rat L10a, eubacterial L1, and archaebacterial L1\n; identical to S. cerevisiae L1B (Ssm2p),ribosomal protein L\n1A, forms part of the 60S ribosomal subunit,Null mutant is v\niable; shows double mutant lethality with rpl1b (ssm2b) null\n mutants\n mATP2:F(1)F(0)-ATPase complex beta subunit, mitochondrial,F(1)F(0)\n-ATPase complex beta subunit,Mutant displays a growth defect\n on glycerol\n mYDR133C:Unknown ,, Unknown\n mRPE1:D-ribulose-5-Phosphate 3-epimerase,D-ribulose-5-Phosphate 3-\nepimerase,Null mutants are viable but show no ribulose-5-pho\nsphate epimerase activity, cannot grow on D-xylulose, and ar\ne sensitive to hydrogren peroxide\n mYPR098C:Unknown ,, Unknown\n mERG13:involved in mevalonate synthesis,3-hydroxy-3-methylglutaryl \ncoenzyme A synthase,\n mMRPS18:Unknown ,, Unknown\n mRAS1:ras proto-oncogene homolog,ras homolog,\n mERG1:Squalene monooxygenase,squalene monooxygenase,Null mutant is\n inviable when cells are grown under aerobic conditions; erg\n1 null mutants are viable under anaerobic conditions during \nwhich ergosterol is taken up by the cells\n mERG2:sterol biosynthesis,C-8 sterol isomerase,Null mutant is viab\nle\n mYJR116W:Unknown ,, Unknown\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 mERG6:ergosterol synthesis,,The null mutant is viable, cannot meth\nylate ergosterol precursors at C-24, and lacks ergosterol. T\nhe null mutant shows defective conjugation, diminished capac\nity for transformation, and defective tryptophan uptake. The\n null mutant is hypersensitive to cycloheximide, Li+, and Na\n+, sensitive to anthracyclines, dactinomycin, and bretfeldin\n A, and resistant to nystatin.\n mSYS1:Multicopy suppressor of ypt6 null mutation,,Null mutant is v\niable. sys1 ypt6 double mutant displays enhanced defects in \nvacuolar sorting and cell growth\n mPRS5:Phosphoribosylpyrophosphate synthetase (ribose-phosphate pyr\nophosphokinase),phosphoribosylpyrophosphate synthetase (ribo\nse-phosphate pyrophosphokinase),Null mutant is viable but re\nduces the cellular 5-phosphoribosyl-1(alpha)-pyrophosphate s\nynthetase activity by 84%. prs5 mutations are synthetically \nlethal with mutations in prs1 or prs3.\n mSIM1:(putative) invovled in control of DNA replication,,Null muta\nnt is viable; mutant allows an extra round of DNA replicatio\nn without mitosis\n mYIP3:Interacts with YPT proteins,,\n mYDR134C:Unknown ,, Unknown\n mSCW4:Soluble Cell Wall protein,soluble cell wall protein,Null mut\nant is viable.\n mLEE1:Product of gene unknown,,\n Cond889:4NQO_2\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 mYPR063C:Unknown ,, Unknown\n mYIL157C:Unknown ,, Unknown\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 mMIR1:Product of gene unknown,,Null mutant is viable on glucose co\nntaining media, but is unable to grow on a non-fermentable c\narbon source, shows reduced levels of mitochondrial proteins\n mBGL2:Cell wall endo-beta-1,3-glucanase,cell wall endo-beta-1,3-gl\nucanase,Null mutant is viable\n mYMR221C:Unknown ,, Unknown\n mCAF20:binds to eIF4E, the mRNA cap-binding protein, and represses \ncap-dependent translation initiation by interfering with the\n interaction of eIF4E and eIF4G,20 kDa subunit , mRNA cap bi\nnding protein eIF-4F , 20 kDa subunit , mRNA cap binding pro\ntein eIF-4F,Null mutant is viable and grows faster; deletion\n of CAF20 partially suppresses mutations in translation init\niation factors; overexpression of CAF20 causes slower growth\n and enhances translation mutation phenotypes\n mTOM20:Translocase of Outer Mitochondrial membrane,20 kDa mitochond\nrial outer membrane protein import receptor,Null mutant is v\niable but respiration deficient; defective in import of mito\nchondrial preproteins\n mERV41:ER vesicle protein,,Null mutant is viable.\n Cond893:SMMS\n mTOM6:involved in supporting the cooperativity between receptors a\nnd the general insertion pore and facilitating the release o\nf preproteins from import components,associates with TOM40 ,\n protein translocation complex component , associates with T\nOM40 , protein translocation complex component,Null mutant i\ns viable, associated with a delay of import of preproteins, \nstabilization of preprotein binding to receptors and the gen\neral insertion pore, and destabilization of the interaction \nbetween receptors and the general insertion pore; tom6 tom40\n double mutants are inviable.\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 mTOM7:Involved in mitochondrial protein import,translocase of the \nouter mitochondrial membrane,Null mutant is viable\n mCPR3:cyclophilin-3 (cyclosporin-sensitive proline rotamase-3),cyc\nlophilin , peptidyl-prolyl cis-trans isomerase (PPIase),Null\n mutant is viable, unable to grow on L-lactate at 37 degrees\n C\n mPFY1:profilin (actin-binding protein),profilin,Null mutant is eit\nher inviable or viable (but temperature sensitive) under cer\ntain conditions, temperature sensitive null mutants exhibit \ndelocalized chitin deposition and arrest as large, unbudded \ncells with multiple nuclei and delocalized actin\n mERP4:Emp24p/Erv25p related protein 4,p24 protein involved in memb\nrane trafficking,viable\n mNDE1: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 mCHS7:The seventh gene identified that is involved in chitin synth\nesis; involved in Chs3p export from the ER,,Null mutant is v\niable but exhibit reduced chitin synthesis due to a severe r\neduction of Chitin Synthase III activity.\n COMP.KO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mYIL121W:Unknown ,, Unknown\n Cond877:MMS\n mYIL041W:Unknown ,, Unknown\n mYNL321W:Unknown ,, Unknown\n Cond886:g-ray\n mDPM1:dolichol phosphate mannose synthase,dolichol phosphate manno\nse synthase,Null mutant is inviable\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 mYPR021C:Unknown ,, Unknown\n mFSH2:Unknown ,, Unknown\n mVMA4:vacuolar ATPase V1 domain subunit E (27 kDa),E subunit of V1\n sector , vacuolar ATPase V1 domain subunit E (27 kDa) , vac\nuolar H(+) ATPase 27 kDa subunit,Null mutant is viable, slow\n growing, cold-sensitive, thermo-sensitive, and exhibits poo\nr growth on glycerol; fails to grow on media supplemented wi\nth 100 mM CaCl2 or ZnCl2\n mITR2:member of sugar transporter superfamily,myo-inositol transpo\nrter,Null mutant is viable\n mYPL098C:Unknown ,, Unknown\n Cond885:20\n mYMR157C:Unknown ,, Unknown\n mMRP2:14 kDa mitochondrial ribosomal protein; homologous to E. col\ni S14 protein,14 kDa mitochondrial ribosomal protein , simil\nar to E. coli S14 protein,defective mitochondrial protein sy\nnthesis; absence of a and b type cytochromes; reduced levels\n of mitochondrial 15 S rRNA; defective processing of apocyto\nchrome b intron; convert to rho- and rho0 at high frequency\n mIMP1:Inner membrane protease (mitochondrial protein),inner membra\nne protease,petite; unable to grow on non-fermentable carbon\n sources\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 mTEF4:Translation elongation factor EF-1gamma,translation elongati\non factor EF-1gamma,\n mEGD1:beta subunit of the nascent-polypeptide-associated complex (\nNAC); homologous to human BTF3b; GAL4 enhancer protein,pol I\nI transcribed genes regulator,Null mutant is viable; reduced\n induction of galactose-regulated genes upon shift from gluc\nose to galactose\n mYOP1:Ypt Interacting Protein,,\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 mHMG1:3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase is\nozyme,3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reduct\nase isozyme,Null mutant is viable, sensitive to compactin, a\n competitive inhibitor of HMG-CoA reductase; hmg1 hmg2 doubl\ne deletion mutants are inviable\n mTOM40:Translocase of Outer Mitochondrial membrane,forms the outer \nmembrane import channel , mitochondrial outer membrane prote\nin , forms the outer membrane import channel , mitochondrial\n outer membrane protein,Null mutant is inviable; cells accum\nulate uncleaved mitochondrial precursor proteins\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 mARC1:associated with tRNA and amino acyl-tRNA synthetases; has af\nfinity for quadruplex nucleic acids,,Null mutant is viable, \nleads to slow growth and reduced MetRS activity; arc1- mutan\nts are synthetic lethals and are complemented by the genes f\nor methionyl-tRNA and glutamyl-tRNA synthetase.\n mYGR182C:Unknown ,, Unknown\n Cond884:10\n mPSD1:converts phosphatidylserine to phosphatidylethanolamine,phos\nphatidylserine decarboxylase,Null mutant is viable, shows li\nttle change in growth properties or phospholipid composition\n, but shows loss of detectable decarboxylase activity; psd1 \npsd2 double mutant is auxotrophic for ethanolamine and shows\n severe defect in conversion of phosphatidylserine to phosph\natidylethanolamine\n mACT1 mPFY1 mEMP24 mSAR1 mTOM20 mTOM7 mTOM40 mTIM17 mSSC1
this is an automaticly generated SAMBA report
Computational Genomics Lab, Tel-Aviv uniresity