Module number 1092




Database revision : gnsdb28.10
Date : Tue Feb 25 17:44:47 2003
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mTLG2:member of the syntaxin family of t-SNAREs,tSNARE that affect\ns a late Golgi compartment,Null mutant is viable in SEY6210,\n exhibits endocytosis defect and loss of Kex2p\n mPKR1:Pichia farinosa Killer toxin Resistance,,Confers resistance \nto Pichia farinosa killer toxin (SMK toxin) when overexpress\ned\n Jelinski.Jelinski:Regulatory networks revealed by transcriptional profiling of\n damaged Saccharomyces cerevisiae cells: Rpn4 links base exc\nision repair with proteasomes. Mol Cell Biol. 2000 Nov;20(2\n1):8157-67.\n mLYS7:Involved in lysine biosynthesis, oxidative stress protection\n,copper chaperone for superoxide dismutase Sod1p,Null mutant\n is viable, methionine and lysine auxotroph, pH and temperat\nure sensitive; sensitive to superoxide generating drugs and \nlight irradiation, exhibits diminution of calcineurin activi\nty\n Cond895:G2MMS\n Cond878:MNNG\n mSWM1:Spore Wall Maturation 1,,Null mutant completes meiotic nucle\nar division but does not show spore wall maturation\n mHBS1:Protein related to translation elongation factor EF-1alpha a\nnd to Suf12p/Sup2p/Gst1p/Sup35p,,\n mYKR035C:Unknown ,, Unknown\n Cond879:MMC\n mORM2:Unknown ,, Unknown\n mYML117W:Unknown ,, Unknown\n Cond877:MMS\n Cond875:60min\n mPTK2:Putative serine/threonine protein kinase that enhances sperm\nine uptake,,Mutant shows reduced spermine and putrescine upt\nake and is resistant to toxic polyamine analogs and Li+ and \nNa+ ions; ptk1 ptk2 double mutant shows virtaully abolished \nhigh-affinity spermidine transport\n mYKL086W:Unknown ,, Unknown\n Cond886:g-ray\n mKAE1:Unknown ,, Unknown\n mIMP2':Protein involved in nucleo-mitochondrial control of maltose,\n galactose and raffinose utilization,transcription factor,Nu\nll mutant is viable, Inability to grow on maltose, galactose\n and raffinose in respiratory-deficient conditions or in the\n presence of ethidium bromide and erythromycin; leaky phenot\nype on oxidizable carbon sources: sensitivity to heat shock \nand sporulation deficiency\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mAPS2:Related to the sigma subunit of the mammalian plasma membran\ne clathrin-associated protein (AP-2) complex,clathrin associ\nated protein complex small subunit,null mutant is viable; sl\night effect on chc1-ts cell growth\n mYJR111C:Unknown ,, Unknown\n mSYS1:Multicopy suppressor of ypt6 null mutation,,Null mutant is v\niable. sys1 ypt6 double mutant displays enhanced defects in \nvacuolar sorting and cell growth\n Cond892:S\n Cond874:30min\n mSDT1:suppressor of deletion of TFIIS,,null mutant is viable, but \nis sensitive to 6-azauracil\n Cond898:RPN4\n mPHO86:May collaborate with Pho87p and Pho84p in phosphate uptake,i\nnorganic phosphate transporter (putative),Null mutant is via\nble and expresses repressible acid phosphatase in high phosp\nhate medium; pho86 pho87 double mutant and pho86 pho88 doubl\ne mutant constituvely synthesize repressible acid phosphatas\ne and are arsenate-resistant; pho84 pho86 pho87 triple mutan\nt grows more slowly than pho84 mutant\n mRNH70:RNase H(70), a 70 kDa ribonuclease H,ribonuclease H,Null mut\nant is viable.\n mYKL207W:Unknown ,, Unknown\n Cond885:20\n Cond889:4NQO_2\n mGCS1:Zn-finger-containing protein that functions as ADP-ribosylat\nion factor GTPase-activating protein and is involved in regu\nlating vesicle transport,ADP-ribosylation factor GTPase-acti\nvating protein (ARF GAP),Null mutant is cold-sensitive for r\neentry into mitotic cell cycle from stationary phase and sho\nws inefficient secretion of invertase\n mYPK1:76.5 kDa Serine/threonine protein kinase with similarity to \nprotein kinase C, is 90% identical to Ypk2p,76.5 kDa serine/\nthreonine protein kinase , similarity to protein kinase C, i\ns 90% identical to Ypk2p,Null mutant is viable, slow growing\n, ypk1 ypk2 double deletion mutants are defective for vegeta\ntive growth\n mSRP21:part of the signal recognition particle (SRP) ribonucleoprot\nein (RNP) complex that functions in protein targeting to the\n endoplasmic reticulum (ER) membrane,signal recognition part\nicle component,Null mutant is viable, associated with slow c\nell growth and inefficient protein translocation across the \nER membrane\n mTSA1:antioxidant enzyme that provides protection against oxidatio\nn systems capable of generating reactive oxygen and sulfur s\npecies,thioredoxin-peroxidase (TPx); reduces H2O2 and alkyl \nhydroperoxides with the use of hydrogens provided by thiored\noxin, thioredoxin reductase, and NADPH,Null mutant is viable\n, grows slower than wild-type under aerobic conditions\n Cond873:10min\n mAPL2:Beta-adaptin, large subunit of the clathrin-associated prote\nin (AP-1) complex,beta-adaptin , clathrin associated protein\n complex large subunit,null mutant is viable\n mMOD5:transfer RNA isopentenyl transferase,transfer RNA isopenteny\nl transferase,Null mutant is viable but temperature sensitiv\ne and cannot grow on nonfermentable carbon sources.\n mUFE1:t-SNARE that resides on the endoplasmic reticulum and mediat\nes retrograde traffic from the Golgi complex,t-SNARE (ER),Nu\nll mutant is inviable\n mYKL206C:Unknown ,, Unknown\n mYPT32:probably involved in intra-Golgi transport or in the formati\non of transport vesicles at the most distal Golgi compartmen\nt,GTPase , YPT31 homolog , ras homolog,Null mutant is viable\n; ypt31 ypt32 double deletion mutants are inviable\n mIWS1:Interacts with Spt6,,Null: Null Mutant is Lethal.\n mAPL5:Delta-like subunit of the yeast AP-3 complex which functions\n in transport of alkaline phosphatase to the vacuole via the\n alternate pathway, suppressor of loss of casein kinase 1 fu\nnction,clathrin assembly complex AP-3 adaptin component delt\na-like subunit,Null mutant is viable, rescues yck1,yck2 doub\nle mutant\n mRTF1:Directly or indirectly regulates the DNA-binding properties \nof Spt15p, the TATA box-binding protein, and the relative ac\ntivities of different TATA elements,nuclear protein,Null mut\nant is viable and can suppress TATA box-binding protein muta\nnts (SPT15) in an allele-specific fashion\n mIXR1:intrastrand crosslink recognition protein,intrastrand crossl\nink recognition protein,Null mutant is viable; exhibits decr\neased sensitivity to the anticancer drug, cisplatin\n mVPS5:vacuolar Protein Sorting Defective; Golgi retention and vacu\nolar protein sorting,simialr to sorting nexin I,Null mutant \nis viable, missort and secrete soluble vacuolar proteins, co\nntain fragmented vacuoles and mislocalize carboxypepsidase a\nnd Vps10p.\n mHOC1:Homologous to OCH1, an alpha-1,6-mannosyltransferase; Golgi-\nlocalized, type II integral membrane protein,mannosyltransfe\nrase (putative),Null mutant is viable but is hypersensitive \nto calcofluor white and hygromycin B and has lowered restric\ntive temperature in a pkc1-371 background; high copy suppres\nsor of pkc1-371\n Cond888:MNNG_2\n Cond894:G2\n Cond893:SMMS\n mYAF9:Yeast homolog of the human leukemogenic protein AF9; member \nof a large protein complex,,Null mutant is viable\n mLEO1:Product of gene unknown,,Null mutant is viable\n mCCT2:cytoplasmic chaperonin of the Cct ring complex related to Tc\np1p; subunit beta,,Null mutant is inviable; some mutant alle\nles exhibit defects in microtubule and actin assembly.\n mTHI6:thiamin biosynthetic bifunctional enzyme,TMP pyrophosphoryla\nse , hydroxyethylthiazole kinase,\n Cond884:10\n
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Computational Genomics Lab, Tel-Aviv uniresity