Module number 436




Database revision : gnsdb28.10
Date : Tue Feb 25 17:34:30 2003
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mARE1:Acyl-CoA cholesterol acyltransferase (sterol-ester synthetas\ne),acyl-CoA cholesterol acyltransferase (sterol-ester synthe\ntase),Null mutant is viable, slightly reduces in vivo and in\n vitro ergosterol esterification. Deletion of both ARE1 and \nARE2 completely eliminates of in vivo and in vitro ergostero\nl esterification\n mCDC39:Required for Start B in mitosis and spindle pole body separa\ntion at meiosis I,basal transcription inhibitor , transcript\nional regulator , basal transcription inhibitor , transcript\nional regulator , basal transcription inhibitor , transcript\nional regulator,Null mutant is inviable; arrests in G(sub)1 \nat pachytene at the mononucleate stage with duplicated, unse\nparated spindle pole bodies and no spindles; temperature sen\nsitive mutation which causes increased basal transcription o\nf many genes\n Cond476:GCN4C/GCN4(R4760/R6257)\n mARG1:arginosuccinate synthetase,arginosuccinate synthetase,Argini\nne requiring\n mMET17:O-Acetylhomoserine-O-Acetylserine Sulfhydralase,O-acetylhomo\nserine (thiol)-lyase,Null mutant is viable, methionine auxot\nroph, becomes darkly pigmented in the presence of Pb2+ ions;\n resistant to methylmercury and exhibits increased levels of\n H2S\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 Cond45:ecm1(**3)\n mYCR100C:Unknown ,, Unknown\n mYJL119C:Unknown ,, Unknown\n mCIT2:non-mitochondrial citrate synthase,citrate synthase,Null mut\nant is viable; disruption of both CIT1 and CIT2 result in gl\nutamate auxotrophy and poor growth on rich medium containing\n lactate.\n mYIH1:piecemeal microautophagy of the nucleus (PMN),,Null mutant i\ns viable and exhibits no growth defects; derepression of PMN\n in rich medium.\n mYCP4:Protein with similarity to S. pombe brefeldin A resistance p\nrotein obr1 and E. coli WrbA protein which stimulates bindin\ng of Trp repressor to DNA,,\n COMP.KO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mAAD3:high degree of similarity with the AAD of P. chrysosporium,a\nryl-alcohol dehydrogenase (putative),\n mTRX3:mitochondrial thioredoxin,thioredoxin,Null mutant is viable,\n normal sensitivity to hydrogen peroxide\n mILV6:acetolactate synthase regulatory subunit,,\n mCVT17:Cytoplasm to vacuole targeting mutant,lipase (putative),cvt1\n7 is defective in lysis of autophagic vesicles after deliver\ny to the vacuole. Null mutant is viable but starvation-sensi\ntive, accumulates subvacuolar vesicles, defective in maturat\nion of aminopeptidase I and in autophagy.\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mPGS1:17 kDa phosphatidylglycerolphosphate synthase,17 kDa phospha\ntidylglycerolphosphate synthase,Null mutant is viable but is\n synthetically lethal with cho1 and mitochondrial petite mut\nations; nonviable at higher temperatures; cannot utilize gly\ncerol and ethanol on synthetic media; cannot survive ethidiu\nm bromide mutagenesis; contains low levels of cardiolipin, p\nhosphatidyglycerol and phosphatidylcholine but increased lev\nels of phosphatidylinositol\n mRAD18:Zn finger protein, putative ATPase,ATPase (putative) , zinc \nfinger protein,radiation sensitive\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 mCTF13:58 kd component (Cbf3c) of the multisubunit 'Cbf3' kinetocho\nre protein complex, which binds to the CDE III element of ce\nntromeres,,Null mutant is inviable\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 mRBK1:ribokinase,ribokinase,\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 Cond409:diauxic_shift_timecourse_15.5_h\n mYPR123C:Unknown ,, Unknown\n mCSR1:chs5 spa2 rescue; isolated as a multicopy suppressor of the \nlethality of chs5 spa2 double mutant at 37 degrees.,,Null mu\ntant is viable\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 Cond195:yap3\n mTHR1:homoserine kinase,homoserine kinase,Null mutant is viable, t\nhreonine auxotroph\n Mating.Mating:Signaling and circuitry of multiple MAPK pathways revealed b\ny a matrix of global gene expression profiles.  Science. 200\n0 Feb 4;287(5454):873-80\n mYCR095C:Unknown ,, Unknown\n mTHR4:threonine synthase,threonine synthase,threonine requiring\n Cond966:swi1,_YPD_(a)\n Cond539:fus3Dtec1D/wtlog10(intensity)\n mYCR023C:Unknown ,, Unknown\n Cond274:yor080w(**3)\n mYCR050C:Unknown ,, Unknown\n mCTR86:CTR86 shares a terminator region with THR4. CTR86 contains a\nGCN4 responsive site suggesting it may also be involved in a\nmino acid biosynthesis.,,\n mYCR082W:Unknown ,, Unknown\n mMAK31:Like Sm protein; member of the Sm protein family, though sli\nghtly divergent because Mak31/Lsm9p does not contain a glyci\nne or cysteine at amino acid 107.,,Mutant exhibits defects i\nn the structural stability of L-A family of dsRNA-containing\n viral particles.\n mYCL033C:Unknown ,, Unknown\n mRDS1:Unknown ,, Unknown\n mMAK32:Protein necessary for structural stability of L-A double-str\nanded RNA-containing particles,,\n mYCR043C:Unknown ,, Unknown\n mYIR042C:Unknown ,, Unknown\n mCSM1:Hypothetical ORF,,missegregates chromosomes in meiosis\n mSSK22:functionally redundant with, and homologous to, SSK2,,\n Stress.dshift:Genomic expression programs in the response of yeast cells t\no environmental changes.  Mol Biol Cell. 2000 Dec;11(12):424\n1-57\n

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Computational Genomics Lab, Tel-Aviv uniresity