Module number 721




Database revision : gnsdb28.10
Date : Tue Feb 25 17:02:18 2003
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Cond158:sir2\n Cond281:HMG2(tetpromoter)\n Cond292:Glucosamine\n Cond221:yer083c\n Cond136:rpl27a(**4)\n mPLB2:Phospholipase B 2,lysophospholipase , phospholipase B,overex\npression confers resistance to lysophosphatidylcholine\n mRPI1:inhibitor of ras,ras inhibitor,Null mutant is viable but sho\nws heat-shock sensitivity\n mEPT1:sn-1,2-diacylglycerol ethanolamine- and cholinephosphotranfe\nrase,sn-1,2-diacylglycerol ethanolamine- and cholinephosphot\nranferase,Null mutant is viable\n Pho85.pho85:Chemical inhibition of the Pho85 cyclin-dependent kinase rev\neals a role in the environmental stress response.  Proc Natl\n Acad Sci U S A. 2001 Oct 23;98(22):12578-83.\n Cond29:clb2\n Cond130:rml2(**13)\n mYLR132C:Unknown ,, Unknown\n Cond13:ase1(**12)\n mYEL073C:Unknown ,, Unknown\n mCLB1:Involved in mitotic induction,B-type cyclin,Null mutant is v\niable (lethal in combination with clb2 mutation)\n Cond224:CMD1(tetpromoter)\n mCLB6:role in DNA replication during S phase,B-type cyclin,Null mu\ntant is viable\n Stress.HypoOsmot:Genomic expression programs in the response of yeast cells t\no environmental changes.  Mol Biol Cell. 2000 Dec;11(12):424\n1-57\n mMNN1:Alpha-1,3-mannosyltransferase,alpha-1,3-mannosyltransferase,\nNull mutant is viable\n Cond31:cmk2\n mCKI1:choline kinase,choline kinase,Null mutant is viable\n Cond244:ymr010w\n GCN4.gcn4:Transcriptional profiling shows that Gcn4p is a master regul\nator of gene expression during amino acid starvation in yeas\nt.  Mol Cell Biol. 2001 Jul;21(13):4347-68.\n Cond384:Hypo-osmotic_shock_-_5_min\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 Cond53:erg2\n Cond286:YEF3(tetpromoter)\n mGAS3:Unknown ,, Unknown\n mYGR052W:Unknown ,, Unknown\n mINO1:involved in the rate limiting step of inositol biosynthesis,\nL-myo-inositol-1-phosphate synthase,Null mutant is viable, i\nnositol auxotroph\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 mACC1:acetyl-CoA carboxylase,acetyl CoA carboxylase,acc1 spores fa\nil to enter vegetative growth\n Cond184:ubr1\n Cond6:anp1\n Cond298:Terbinafine\n COMP.CH:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n Cond85:imp2\n Cond983:WT_vs_pho85D\n mCDS1:CDP-diacylglycerol synthase, CTP-phosphatidic acid cytidylyl\ntransferase, CDP-diglyceride synthetase,phosphatidate cytidy\nlyltransferase,Null mutant is inviable\n Cond229:yhr011w(**14)\n mWSC4:cell wall integrity and stress response component 4,contains\n novel cysteine motif , integral membrane protein (putative)\n , similar to SLG1 (WSC1), WSC2 and WSC3,\n Cond216:yer044c(haploid)\n Cond86:imp2'(**12)\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 Cond479:WT+/-100mM3AT(SetD)(R491)\n Cond176:swi5\n mCHO1:phosphatidylserine synthase,phosphatidylserine synthase,The \nnull mutant is viable but grows slowly on minimal medium. Th\ne growth rate of the null mutant on minimal medium can be in\ncreased by supplementing the medium with choline or other ph\nospholipid precursors.\n Cond226:yhl029c\n Cond194:yap1\n mCHO2:First step in the methylation pathway for phosphatidylcholin\ne biosynthesis,phosphatidyl-ethanolamine N-methyltransferase\n,Null mutant is viable and accumulates phosphatidylethanolam\nine and has reduced levels of phosphatidylcholine\n Cond287:2-deoxy-D-glucose\n Cond478:WT+/-10mM3AT(R491)\n SwiSnf.swisnf:Whole-genome expression analysis of snf/swi mutants of Sacch\naromyces cerevisiae.  Proc Natl Acad Sci U S A. 2000 Mar 28;\n97(7):3364-9.\n Cond54:erg3(haploid)\n COMP.KO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n Cond24:cem1\n mALD6:Utilizes NADP+ as the preferred coenzyme. Activated by Mg2+.\n,aldehyde dehydrogenase,Null mutant is viable, grows at appr\noximately one-third the rate of wild-type, unable to grow on\n ethanol as a carbon source\n Cond68:gas1\n Cond171:ste24(haploid)\n Cond116:pex12\n Cond175:swi4\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n Cond250:ymr031w-a\n Cond284:PMA1(tetpromoter)\n Cond153:sgs1\n Stress.tempgrow:Genomic expression programs in the response of yeast cells t\no environmental changes.  Mol Biol Cell. 2000 Dec;11(12):424\n1-57\n mITR1:member of sugar transporter superfamily,myo-inositol transpo\nrter,Null mutant is viable\n Cond283:KAR2(tetpromoter)\n mCHA1:catabolism of hydroxy amino acids,catabolic serine (threonin\ne) dehydratase,Null mutant is viable and cannot grow on medi\na with L-serine or L-threonine as sole nitrogen source\n mZRT1:High-affinity zinc transport protein,,disruption viable\n Cond475:0.5x/1xAA(MildLeu,HisStarvation)(R176)\n Cond294:Itraconazole\n mZRT2:Low-affinity zinc transport protein,low affinity zinc transp\nort protein,Null mutant is viable; ZRT2 overexpression incre\nases rate of zinc uptake\n Cond295:Lovastatin\n Cond265:ymr293c\n Cond461:21_deg_growth_ct-1\n Cond299:Tunicamycin\n Cond970:swi1,_minimal_(c)\n COMP.TE:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mFAA1:cellular lipid metabolism and protein N-myristolation,long c\nhain fatty acyl:CoA synthetase,Null mutant is viable as long\n as fatty acid synthase (fas) complex is active\n Cond11:arg5,6\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

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Computational Genomics Lab, Tel-Aviv uniresity