Module number 660




Database revision : gnsdb28.10
Date : Tue Feb 25 17:03:20 2003
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mYDL180W:Unknown ,, Unknown\n mCPR5:Cyclophilin D, Peptidyl-prolyl cis-trans isomerase D,cycloph\nilin D , peptidyl-prolyl cis-trans isomerase (PPIase),Null m\nutant is viable\n mDOS2:Product of gene unknown,,\n mYDR327W:Unknown ,, Unknown\n mNHP10:Non-Histone Protein 10,HMG1-box containing protein,null muta\nnt is viable and has normal growth rate\n mPPZ2:serine-threonine phosphatase Z,,Null mutant is viable but sh\nows increase in cell size and cell lysis (remediated by 1 M \nsorbitol); ppz1 ppz2 double mutant shows increased expressio\nn of ENA1, resistance to sodium and lithium, and sensitivity\n to 5 mM caffeine (which is suppressed by 1 M sorbitol)\n mTRP1:Note that the sequence of TRP1 from strain S228C, which is t\nhe sequence stored in SGD, contains an ochre mutation at cod\non 67.,N-(5'-phosphoribosyl)-anthranilate isomerase,tryptoph\nan requiring\n mENT1:epsin N-terminal homology-containing protein,,Null mutant is\n viable, synthetically lethal with ent2 (YLR206w). ent1/2 do\nuble mutants have endocytosis and actin cytoskeleton defects\n.\n mKRS1:lysyl-tRNA synthetase,lysine-tRNA ligase,Null mutant is invi\nable; mutants can show resistance to 5-methyltryptophan, 5-f\nluorotryptophan and canavanine; constitutive derepression an\nd slow growth; posttranscriptional increase in histidine bio\nsynthetic enzyme activity\n mSWM1:Spore Wall Maturation 1,,Null mutant completes meiotic nucle\nar division but does not show spore wall maturation\n mSSD1:Product of gene unknown,,Suppressor of regulatory subunit of\n protein kinase\n mYDL186W:Unknown ,, Unknown\n mYDR287W:Unknown ,, Unknown\n mSIT4:SIT4 suppress mutations in DBF2,type 2A-related protein phos\nphatase,sit1-sit4 or sit2-sit4 double mutants are lethal\n mRTT103:Regulator of Ty1 Transposition,,Gene disruption causes Ty1 h\nypertransposition phenotype\n mHNT1:Hint homolog, member of the histidine triad superfamily of n\nucleotide-binding proteins,,\n Cell Cycle.alpha:Comprehensive identification of cell cycle-regulated genes o\nf the yeast Saccharomyces cerevisiae by microarray hybridiza\ntion. Mol Biol Cell. 1998 Dec;9(12):3273-97.\n GCR1.gcr1:Understanding the growth phenotype of the yeast gcr1 mutant \nin terms of global genomic expression patterns. J Bacteriol\n. 2000 Sep;182(17):4970-8.\n Cond679:DES460(wt)_vs._DES459(mec1)_genomic_DNA_comparison\n mYDR186C:Unknown ,, Unknown\n mYDR455C:Unknown ,, Unknown\n Cond561:alpha70\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mYHR126C:Unknown ,, Unknown\n mYDR119W:Unknown ,, Unknown\n Cond680:DES460(wt)_vs._DES459(mec1)_genomic_DNA_comparison_,\n2\n mSFA1:Long-chain alcohol dehydrogenase (glutathione-dependent form\naldehyde dehydrogenase),glutathione-dependent formaldehyde d\nehydrogenase , long-chain alcohol dehydrogenase,Null mutant \nis viable; sensitive to formaldehyde\n mGLO2:Cytoplasmic glyoxylase-II,glyoxylase-II,Null mutant is viabl\ne but shows increased sensitivity to methylglyoxal\n mARG82:Regulator of arginine-responsive genes with ARG80 and ARG81,\ndual specificity inositol 1,4,5-trisphosphate 6-kinase/inosi\ntol 1,4,5,6-tetrakisphosphate 3-kinase (IP3 6-/IP4 3-kinase)\n,Null mutant is viable but requires arginine at 23C; growth \ndefect at 30C; inviable at 37C; null is defective in sporula\ntion, mating, amino acid metabolism (fails to grow on medium\n in which arginine or ornithine is the sole nitrogen source)\n; null mutants accumulate IP3, I(4,5)P2 and have drastically\n reduced levels of IP4, IP5 and IP6.\n mYDR116C:Unknown ,, Unknown\n mZIP1:Synaptonemal complex protein, component of the central eleme\nnt,,Null mutant is viable and shows defects in meiosis\n mYDR291W:Unknown ,, Unknown\n mCRD1:Cardiolipin synthase,cardiolipin synthase,Null mutant is via\nble, exhibits growth defects in galactose and glycerol/ethan\nol media\n COMP.:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mINO2:Transcription factor required for derepression of inositol-c\nholine-regulated genes involved in phospholipid synthesis,he\nlix-loop-helix protein,The null mutant is viable but auxotro\nphic for inositol and choline. The null mutant can also disp\nlay aberant cell shape and defects in nuclear segregation. H\nomozygous mutant ino2 delta-1 diploids fail to sporulate. Ot\nher mutant alleles show pleiotropic defects in phospholipid \nmetabolism.\n mMDH3:malate dehydrogenase,malate dehydrogenase,Null mutant is via\nble, does not grow on oleate and grows slowly on acetate\n Cond677:DES459_(mec1)_-_log_phase_(IR_time_=_0_sample)\n mSWR1:Sick With Rat8 ts,RNA helicase (putative) , deah box protein\n,Null mutant is viable and shows no growth defects; swr1 rat\n8-2 double mutant has a slow growth phenotype; SWR1 is a par\ntial High copy suppressor of pse1-1 kap123\n Cond681:DES460_genomic_DNA_vs._MHY26_(dun1)_genomic_DNA\n mPEP7:vacuolar segregation protein required for vacuole inheritanc\ne and vacuole protein sorting,three zinc fingers; cysteine r\nich regions of amino acids are essential for function,Null m\nutant is viable but grows more slowly and is temperature-sen\nsitive; defective in vacuole segregation; mislocalizes carbo\nxypeptidase Y and other vacuolar proteins; shows loss of vac\nuolar acidity and defects in vacuolar morphology\n mYDL012C:Unknown ,, Unknown\n mTCP1:chaperonin subunit alpha,chaperonin subunit alpha,Null mutan\nt is inviable\n mCDC13:is required for the G2/M transition in mitosis, dispensable \nfor premeiotic DNA synthesis but required for synaptonemal c\nomplexes, recombination, meiosis I, meiosis II, and spores,s\ningle-stranded TG1-3 telomere G-tails binding protein,Null m\nutant is inviable. cdc13 mutants arrest just before mitotic \ndivision in G(sub)2. The cdc13 G2 meiotic arrest is dependen\nt upon the RAD9 checkpoint function.\n mPPH21:serine-threonine protein phosphatase 2A,,Null mutant is viab\nle, pph21 pph22 mutants produce very small spores in some st\nrain backgrounds and are inviable in others, pph21 pph22 pph\n3 mutants are inviable\n mMSW1:mitochondrial tryptophanyl-tRNA synthetase,tryptophan-tRNA l\nigase,Null mutant is viable, respiratory deficient, defectiv\ne in mitochondrial protein synthesis\n Cond915:(99i4)_HBY4_YPGL_NormInt\n mRPT2:Probable 26S protease subunit and member of CDC48/PAS1/SEC18\n family of ATPases,,Null mutant is inviable\n
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Computational Genomics Lab, Tel-Aviv uniresity