Module number 2493




Database revision : gnsdb28.10
Date : Tue Feb 25 17:25:54 2003
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mISC1:Hypothetical ORF,ISC1 encodes phospholipase C type enzyme wh\nich hydrolyzes inositolphosphosphingolipids (IPC, MIPC, M(IP\n)2C) as well as sphingomyelin.,Null mutant is viable and con\ntains more inositolphosphosphingolipids.\n mPUB1:poly(A)+ RNA-binding protein,poly(A) binding protein,Null mu\ntant is viable\n mNEO1:ATPase that leads to neomycin-resistant protein when overexp\nressed,P-type ATPase,Null mutant is inviable. When overexpre\nssed, Neo1 confers neomycin resistance.\n mNOP2:May participate in nucleolar function during the transition \nfrom stationary phase to rapid growth,90 kDa protein homolog\nous to a human proliferation-associated nucleolar protein, p\n120,Null mutant is inviable; overexpression leads to changes\n in nucleolar morphology\n mSKN1:Involved in (1->6)-beta-glucan biosynthesis,highly homologou\ns to Kre6p , type II membrane protein (putative),Null mutant\n is viable; exhibits no alterations in killer sensitivity, g\nrowth, or (1->6)-beta-glucan levels; skn1 kre6 double deleti\non mutants show a dramatic reduction in both (1-->6)-beta-gl\nucan levels and growth rate compared with either single disr\nuptant\n mDIA1:may be involved in invasive growth, pseudohyphal growth,,Nul\nl mutant is viable and causes invasive growth in haploids an\nd pseudohyphal growth in diploids\n mYKL146W:Unknown ,, Unknown\n Cond711:t2+Vec\n Cond751: 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 mRAS1:ras proto-oncogene homolog,ras homolog,\n mEGT2:cell-cycle regulation protein, may be involved in the correc\nt timing of cell separation after cytokinesis,,\n mPDR5:multidrug resistance transporter,multidrug resistance transp\norter,pleiotropic drug resistance\n mTUB2:beta subunit of tubulin monomer; involved in chromosome segr\negation and nuclear migration,beta-tubulin,null is inviable;\n conditional mutants show block of mitotic nuclear migration\n and chromosome segregation and defects in spindle and/or cy\ntoplasmic microtubules at non-permissive conditions; some mu\ntants are benomyl-hypersensitive\n mUTR2:Product of gene unknown,,\n mNEW1:This gene encodes a protein with an Q/N-rich amino terminal \ndomain that acts as a prion, termed [NU]+.,,Null mutant is v\niable\n mHRP1:Putative polyadenylated-RNA-binding protein located in nucle\nus; similar to vertebrate hnRNP A/B protein family,,Null mut\nant is inviable; mutants can suppress temperature-sensitive \nalleles of npl3 (but not npl3 null mutants)\n mYGL245W:Unknown ,, Unknown\n mHIP1:histidine permease,histidine permease,requires supplementati\non with large amounts of histidine for growth\n mASP1:Asparaginase I, intracellular isozyme,asparaginase I , intra\ncellular isozyme,Aspartic acid requiring\n Cond719:t4-SSD1\n mRSP5:involved in ubiquitin-mediated protein degradation,,Null mut\nant is inviable; an rsp5 mutation was isolated as a suppress\nor of mutations in SPT3; certain rsp5 mutants also exhibit h\nypersensitivity to stresses such as cadmium and canavanine, \nand sporulation defects\n Cond724:t4+SSD1,H44\n mDNF2:Drs2 Neo1 Family,Potential aminophospholipid translocase,via\nble\n mNMD3:putative Upf1p-interacting protein,factor required for a lat\ne assembly step of the 60S subunit,Null mutant is inviable, \nat nonpermissive temperature, nmd3 ts mutants exhibit decrea\nsed levels of 60S subunits resulting in formation of half-me\nr polysomes; nmd3 xrn1(kem1) double mutants are inviable\n mHSP150:Heat shock protein, secretory glycoprotein,heat shock protei\nn , secretory glycoprotein , heat shock protein , secretory \nglycoprotein , heat shock protein , secretory glycoprotein,N\null mutant is viable\n Cond713:t4+Vec\n mALR1:aluminium resistance ,ion transporter (putative),Null mutant\n is inviable; overexpression increases resistance to aluminu\nm and gallium toxicity\n COMP.:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mRPA14:14 kDa subunit of RNA polymerase I,RNA polymerase I subunit,\nNull mutant is viable but is temperature sensitive\n mDAN3:delayed anaerobic gene,putative cell wall protein,unknown\n Cond718:t4+SSD1wt\n mYOR385W:Unknown ,, Unknown\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 mRPN3:proteasome subunit,26S proteasome regulatory module componen\nt , similar to human p58 subunit,Null mutant is inviable. RP\nN3 is a high copy suppressor of the nin1-1 temperature sensi\ntive phenotype\n Cond709:t0+Vec\n mYMR010W:Unknown ,, Unknown\n mHRR25:Similar to YCK1 and YCK2, two other casein kinase I isoforms\n; found primarily in nucleus; may be involved in DNA-damage \nrepair,casein kinase I isoform,Null mutant is viable but sho\nws slow growth; hrr25-1 mutation results in sensitivity to c\nontinuous expression of HO endonuclease, to methylmethanesul\nfonate, and to x-irradiation; homozygous hrr25-1 mutants are\n unable to sporulate\n mENP2:Unknown ,, Unknown\n mCDC19:Required for START A in the cell cycle and sporulation,pyruv\nate kinase,Null mutant is inviable. cdc19 mutants are pyruva\nte kinase deficient and show cell division cycle blocked at \n36 degrees C\n Cond717:t2-SSD1\n mYOL092W:Unknown ,, Unknown\n mYEL074W:Unknown ,, Unknown\n mCST13:Chromosome STability,,Null mutant is viable, but grows slowl\ny and shows increased sensitivity to copper ions\n Cond716:t2+SSD1wt\n mPDA1:alpha subunit of pyruvate dehydrogenase (E1 alpha),pyruvate \ndehydrogenase alpha subunit (E1 alpha),Null mutant is viable\n, exhibits reduced growth on glucose and increased formation\n of petites\n Cond725:t4-SSD1,M31\n mPMT1:Transfers mannose residues from dolichyl phosphate-D-mannose\n to specific serine/threonine residues of proteins in the se\ncretory pathway; acts in complex with Pmt2p,dolichyl phospha\nte-D-mannose:protein O-D-mannosyltransferase,Null mutant is \nviable but shows decrease by 40-50% of in vivo protein O-man\nnosylation; pmt1 pmt2 double mutant shows severe growth defe\nct but residual O-mannosylation activity; the pmt1 pmt2 pmt3\n pmt4 quadruple mutant is inviable\n Cond708:t0+SSD1\n mGPI12:N-acetylglucosaminylphosphatidylinositol de-N-acetylase,N-ac\netylglucosaminylphosphatidylinositol de-N-acetylase,Null mut\nation is inviable\n mPAU6:member of the seripauperin protein/gene family,,\n mBOP1:bypass of PAM1,,\n mIMD3:Hypothetical ORF,IMP dehydrogenase homolog,\n mYNL321W:Unknown ,, Unknown\n mDBP2:ATP-dependent RNA helicase of DEAD box family,ATP dependent \nRNA helicase , dead box protein,Null mutant is inviable\n mYHM2:Yeast suppressor gene of HM mutant (abf2),DNA binding protei\nn , mtDNA stabilizing protein, mitochondrial inner membrane \nprotein with low homology to RIM2,Null mutant is viable but \nshows slow growth in the presence of non-fermentable carbon \nsources; mutant shows mitochondrial genome unstability\n mYBR246W:Unknown ,, Unknown\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 mYHR181W: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 mSWD2:YKL018W,,\n mMRH1:Membrane protein related to Hsp30p; Localized by immunofluor\nescence to membranes, mainly the plasma membr. punctuate imm\nunofluorescence pattern observed in buds. The nuclear envelo\npe, but not vacuole or mitochondrial membranes also stained,\n,Null mutant is viable\n mLYP1:lysine permease,lysine permease,\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n Cond712:t4+SSD1\n mIRA2:Negatively regulates cAPK by antagonizing CDC25,GTPase activ\nating protein , highly homologous to Ira1p , neurofibromin h\nomolog , GTPase activating protein , highly homologous to Ir\na1p , neurofibromin homolog,Null mutant is viable, exhibits \nincreased sensitivity to heat shock and nitrogen starvation,\n sporulation defects, and suppression of the lethality of a \ncdc25 mutants\n mSUP35:altered form creates [PSI] prion,translation termination fac\ntor eRF3,accumulation of large budded cells and substantial \narrest of DNA synthesis at the nonpermissive temperature (ar\nrests at G(sub)1/S transition); omnipotent suppressor of non\nsense mutations\n mTPO1:Polyamine transport protein,,\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 mYIL056W:Unknown ,, Unknown\n mSPB1:Suppressor of PaB1 mutant; involved in 60S ribosomal subunit\n biogenesis,methyltransferase (putative),Null mutant is invi\nable. The spb1-1 mutant is an extragenic suppressor of a pab\n1 null mutation.\n mCYS4:Cystathionine beta-synthase,cystathionine beta-synthase,Null\n mutant is viable, exhibits vacuolar acidification defects; \ncys2 and cys4 mutations are linked together and co-operative\nly confer cysteine dependence\n mCDC60:cytosolic leucyl tRNA synthetase,leucine--tRNA ligase,arrest\n at START point of cell cycle upon shift to restrictive temp\nerature\n mYBR293W:Unknown ,, Unknown\n mYNL190W:Unknown ,, Unknown\n Cond723:t2-SSD1,M31\n mSED1:putative cell surface glycoprotein,cell surface glycoprotein\n (putative),Null mutant is viable; during stationary phase, \nnull mutants exhibit increased sensitivity to Zymolyase.\n mAFG1:ATPase family gene,ATPase family,\n mDED1:ATP-dependent RNA helicase of DEAD box family; suppressor of\n a pre-mRNA splicing mutation, prp8-1,,Null mutant is inviab\nle\n mZRT3:Hypothetical ORF,,\n mEPS1:Hypothetical ORF,,\n mIMP4:Interacts With Mpp10. Imp4p is a specific component of the U\n3 snoRNP and is required for pre-18S rRNA processing.,,Null \nmutant is inviable\n mTEF4:Translation elongation factor EF-1gamma,translation elongati\non factor EF-1gamma,\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 mYRF1-4:Y'-helicase protein 1,Y'-helicase protein 1,\n Cond710:t2+SSD1\n mUTP22:Unknown ,, Unknown\n mAPE3:Aminopeptidase yscIII,aminopeptidase yscIII,Null mutant is v\niable but exhibited reduced vacuolar aminopeptidase activiti\nes and could not hydrolyze Lys-Ala-MCA to Lys and Ala-MCA.\n fkh1,2sf.Series0:Two yeast forkhead genes regulate the cell cycle and pseudoh\nyphal growth. Nature. 2000 Jul 6;406(6791):90-4.\n mCYS4 mHRR25 mNMD3 mNOP2
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Computational Genomics Lab, Tel-Aviv uniresity