Module number 914




Database revision : gnsdb28.10
Date : Tue Feb 25 17:09:53 2003
How to read this figure?



Cond217:yer050c\n Cond3:aep2\n mYOL083W:Unknown ,, Unknown\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 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 mPMC1:May be involved in depleting cytosol of Ca2+ ions,Ca2+ ATPas\ne (putative),Null mutant is viable but fails to grow in high\n Ca2+ medium; this death in high calcium is suppressed by mu\ntations in calcineurin (CNA1, CNA2, CNB1) and calmodulin (CM\nD1); pmc1 vcx1 double mutant is even more sensitive to Ca2+\n mYLR171W:Unknown ,, Unknown\n Cond130:rml2(**13)\n mMDM35:Unknown ,, Unknown\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 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 mYBL006C:Unknown ,, Unknown\n mMRPL32:Mitochondrial ribosomal protein MRPL32 (YmL32),ribosomal pro\ntein (YmL32),\n mMRPL33:essential for mitochondrial function,ribosomal protein (YmL3\n3) (E. coli L30),Null mutant is viable\n mSCO2:Originally identified as a multicopy suppressor of a respira\ntory defective mutant; homolog of Sco1p,,\n mYNL200C:Unknown ,, Unknown\n mMRPL37:Probable mitochondrial protein L37,ribosomal protein L37 (pu\ntative),\n Cond4:afg3(haploid)\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 mPDR8:Unknown ,, Unknown\n mFTR1:Plasma membrane iron permease,iron permease,Lacks high affin\nity iron uptake\n mEMP46:Unknown ,, Unknown\n mMRPL39:Mitochondrial ribosomal protein MRPL39 (YmL39),ribosomal pro\ntein (YmL39),\n mSNQ2:ABC transporter,ABC transporter,null mutant is viable; overe\nxpression confers multi-drug resistance\n mFRE3:similar to FRE2,,\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 mYMD8:similar to vanadate resistance protein Gog5,,\n mRSM10:mitochondrial ribosome small subunit component,mitochondrial\n ribosome small subunit component,\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 mYPL150W:Unknown ,, Unknown\n mYPL013C:Unknown ,, Unknown\n mJIP3:Unknown ,, Unknown\n mUBC8:Ubiquitin-conjugating enzyme that is able to ubiquitinate hi\nstones in vitro,ubiquitin-conjugating enzyme , ubiquitin-pro\ntein ligase,Null mutant is viable\n mNCE102: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 mYKL136W:Unknown ,, Unknown\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 mMSS1:May play a part in mitochondrial translation,GTPase (putativ\ne),respiratory deficient in presence of pr454 mutation in mi\ntochondrial 15S rRNA; block in splicing of mitochondrial int\nrons\n mYGR035C:Unknown ,, Unknown\n mBGL2:Cell wall endo-beta-1,3-glucanase,cell wall endo-beta-1,3-gl\nucanase,Null mutant is viable\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 mYDL110C:Unknown ,, Unknown\n COMP.CH:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mMBA1:involved in assembly of mitochondrial respiratory complexes,\n,Null mutant is viable, conditionally defective in the assem\nbly of mitochondrial respiratory complexes\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 mYLR169W:Unknown ,, Unknown\n Cond61:fks1(haploid)\n mYMR029C:Unknown ,, Unknown\n Cond287:2-deoxy-D-glucose\n mCOX14:mitochondrial membrane protein,mitochondrial membrane protei\nn,Nuclear respiration deficient, lack cytochromes a and a3 a\nnd detectable cytochrome oxidase activity\n mYGL069C:Unknown ,, Unknown\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 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 Cond278:CDC42(tetpromoter)\n mDIN7:DNA-damage inducible gene,,\n mYMR102C: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 mYPR100W:Unknown ,, Unknown\n COMP.KO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mRTT103:Regulator of Ty1 Transposition,,Gene disruption causes Ty1 h\nypertransposition phenotype\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 Cond256:ymr141c\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 mAPS1:Involved in a subset of clathrin functions at the Golgi,clat\nhrin associated protein complex small subunit,Null mutant is\n viable; aps1 mutants demonstrate synthetic effects with chc\n1 alleles\n mYLR177W:Unknown ,, Unknown\n mYLR218C:Unknown ,, Unknown\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mYNL122C:Unknown ,, Unknown\n mYGR021W:Unknown ,, Unknown\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 mOST6:Putative new 37kDa subunit of N-oligosaccharyltransferase co\nmplex,N-oligosaccharyltransferase complex 37kDa subunit (put\native),\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 mYMR157C:Unknown ,, Unknown\n Cond103:msu1\n Cond265:ymr293c\n mCTS1:Endochitinase,endochitinase,Null mutant is viable; exhibits \na defect in cell separation\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 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 COMP.TE:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mYBR062C: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 mYBR262C:Unknown ,, Unknown\n mCCC2 mATX1

this is an automaticly generated SAMBA report
Computational Genomics Lab, Tel-Aviv uniresity