Module number 1984




Database revision : gnsdb28.10
Date : Tue Feb 25 17:35:21 2003
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PEX.Pex:Transcriptome profiling to identify genes involved in peroxi\nsome assembly and function. J Cell Biol. 2002 Jul 22;158(2)\n:259-71.\n Cond541:fus3D+50nMaF,30min/wtlog10(intensity)\n Meiosis.Series0:The core meiotic transcriptome in budding yeasts. Nat Genet\n. 2000 Dec;26(4):415-23.\n mTIR1:cold-shock induced protein of the Srp1p/Tip1p family of seri\nne-alanine-rich proteins,,\n Cond95:mac1\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 mVCX1:Similar to sodium/calcium exchangers, including bovine Na+/C\na2+,K+ antiporter; putative vacuolar transmembrane protein,v\nacuolar H+/Ca2+ exchanger,Null mutant is viable, sensitive t\no high Ca2+ conditions\n mGGA2:Golgi-localized, gamma-adaptin homology, Arf-binding,ARF-bin\nding protein,\n mFET5:ferrous iron transport,multicopper oxidase , type 1 integral\n membrane protein,overexpression of FET5 suppresses a fet3 n\null mutant.\n Cond188:vma8\n mPDR5:multidrug resistance transporter,multidrug resistance transp\norter,pleiotropic drug resistance\n mPDC5:pyruvate decarboxylase,pyruvate decarboxylase,undetectable p\nyruvate decarboxylase activity in pdc1pdc5 double mutants\n mPTM1:Putative membrane protein,membrane protein (putative),Null m\nutant is viable, no observable phenotype\n mERG3:C-5 sterol desaturase,C-5 sterol desaturase,Null mutant is i\nnviable; suppresses syringomycin resistant mutant\n mYJR116W:Unknown ,, Unknown\n mFIT2:Facilitator of iron transport,Cell wall protein involved in \niron transport,impaired siderophore-iron uptake, activation \nof the major iron -dependent transcription factor, AFT1\n Cond140:rps24a(**9)\n mENO1:enolase I,enolase I,Null mutant is viable\n Cond719:t4-SSD1\n mRHR2:DL-glycerol-3-phosphatase,DL-glycerol-3-phosphatase,\n Cond724:t4+SSD1,H44\n Cond:\n mYBR016W:Unknown ,, Unknown\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 mOLE1:delta-9-fatty acid desaturase,delta-9-fatty acid desaturase,\nThe null mutant is inviable but can be rescued by addition o\nf unsaturarted fatty acids to the growth medium. Some allele\ns are temperature-sensitive for growth and show defective in\ntracellular mitochondrial movement atthe non- permissive tem\nperature.\n mERG25:C-4 sterol methyl oxidase,C-4 sterol methyl oxidase,Null mut\nant is inviable\n COMP.:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\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 mGND1:6-phosphogluconate dehydrogenase, decarboxylating; converts \n6-phosphogluconate + NADP to ribulose-5-phosphate + NADPH + \nCO2,,cannot grow on media containing D-glucono-delta-lactone\n as the sole carbon source\n Cond718:t4+SSD1wt\n mALG1:beta-1,4-mannosyltransferase,beta-1,4-mannosyltransferase,Nu\nll mutant is inviable\n mSHM1:Serine hydroxymethyltransferase, mitochondrial,,Null mutant \nis viable.\n Cond717:t2-SSD1\n mCDC91:member of major facilitator superfamily,,\n Cond720:t0+SSD1,H44\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 mFUN12:Function unknown now,97 kDa protein,Null mutant is inviable\n Cond725:t4-SSD1,M31\n Cond708:t0+SSD1\n COMP.KO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mSFH5:Unknown ,, Unknown\n mSTT3:Required for protein glycosylation,integral ER membrane prot\nein , oligosaccharyltransferase complex subunit (putative),N\null mutant is inviable. sst3 mutants are defective in protei\nn glycosylation, sensitive to hygromycin B, and resistant to\n sodium orthovanadate. Depletion of the STT3 protein results\n in loss of oligosaccharyl transferase activity in vivo and \na deficiency in the assembly of oligosaccharyl transferase c\nomplex.\n mBOP1:bypass of PAM1,,\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 mDPM1:dolichol phosphate mannose synthase,dolichol phosphate manno\nse synthase,Null mutant is inviable\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 SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mADE3:Required for the biosynthesis of purines, thymidylate, methi\nonine, histidine, pantothenic acid and formylmethionyl-tRNA,\nC1-tetrahydrofolate synthase,Null mutant is viable, adenine \nauxotroph, histidine auxotroph\n mMVD1:involved in the polyisoprene biosynthesis pathway,mevalonate\n pyrophosphate decarboxylase,Null mutant is inviable; a sing\nle leucine to proline mutation causes temperature sensitivit\ny.\n mCYS3:cystathionine gamma-lyase,cystathionine gamma-lyase,Null mut\nant is viable, cysteine auxotroph\n mNCP1:NADP-cytochrome P450 reductase,NADP-cytochrome P450 reductas\ne,Null mutant is viable\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 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 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 Cond714:t0+SSD1wt\n mTPD3:protein phosphatase 2A regulatory subunit A,protein phosphat\nase 2A regulatory subunit A,Null mutant is viable, defective\n in cytokinesis at reduced temperatures, defective in transc\nription by RNA polymerase III at elevated temperatures; noco\ndazole sensitive and exhibits phenotypes of previously ident\nified kinetochore/spindle checkpoint mutants\n mSUN4:Protein involved in the aging process,,\n mKRE2:N-glycosylation,alpha-1,2-mannosyltransferase,have altered N\n-linked glycosylation of proteins and grow slowly at 30 degr\nees; unable to grow at 37 degrees\n mIDP1:Mitochondrial form of NADP-specific isocitrate dehydrogenase\n,NADP-dependent isocitrate dehydrogenase,Null mutant is viab\nle\n mHXT2:hexose transporter,high affinity hexose transporter-2,Null m\nutant is viable\n mCAR1:arginase,arginase,Null mutant is viable but defective in arg\ninine catabolism\n mCAR2:ornithine aminotransferase,ornithine aminotransferase,Catabo\nlism of arginine defective\n Cond721:t0-SSD1,M31\n mBAT2:Branched-Chain Amino Acid Transaminase,branched-chain amino \nacid transaminase,Null mutant is viable; ILV auxotrophy in b\nat1 bat2 double mutants\n mKRE9:cell wall beta-glucan assembly,,Null mutant is viable, assoc\niated with growth defects, altered cell wall, aberrant multi\nply budded morphology, mating defects; exhibits double mutan\nt lethality in combination with knh1, kre1, kre6, or kre11 m\nutants; killer toxin resistant; reduction in cell wall (1---\n-6)-beta-glucan\n Cond35:cup5\n Cond938:2h\n mGDI1:Regulates vesicle traffic in secretory pathway by regulating\n dissociation of GDP from Sec4/Ypt/rab family of GTP-binding\n proteins,GDP dissociation inhibitor,Null mutant is inviable\n Cond842:expt5\n Cond710:t2+SSD1\n mCCT6:cytoplasmic chaperonin of the Cct ring complex (previously c\nalled TCP1 or TRiC), distantly related to Tcp1p and to Hsp60\n,,Null mutant is inviable; overexpression suppresses a TOR2 \ndominant nagative allele\n
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Computational Genomics Lab, Tel-Aviv uniresity