Module number 1266




Database revision : gnsdb28.10
Date : Tue Feb 25 17:03:26 2003
How to read this figure?



mHAP2:Global regulator of respiratory genes,transcriptional activa\ntor protein of CYC1 (component of HAP2/HAP3 heteromer),\n mFAT2:Fatty acid transporter, very similar to FAT1,,\n Cond912:(99i1)_S150-2B_YPGL_NormInt\n mPMR1:Ca++-Pump, ATPase,Ca2+ ATPase,pmr1 null mutants suppress ypt\n1-1\n mMPD2:protein disulfide isomerase related protein,protein disulfid\ne isomerase related protein,Null mutant is viable; overprodu\nction of Mpd2p suppresses lethality and carboxypeptidase Y m\naturation defect caused by pdi1 deletion -- this suppression\n depends on the CXXC sequence of Mpd2p\n Meiosis.Series0:The core meiotic transcriptome in budding yeasts.  Nat Genet\n. 2000 Dec;26(4):415-23.\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 mYSC84:SH3 domain in C-terminus,,Null mutant is viable\n mCRZ1:calcineurin responsive zinc-finger,transcription factor (put\native),Null mutant is viable\n mRAD6:Involved in DNA repair and sporulation. Rad6p interacts with\n Ubr1 and Rad18p. mRNA is induced early in meiosis and peaks\n at meiosis I.,ubiquitin-conjugating enzyme,Radiation sensit\nive. Defective for postreplication repair, repression of ret\nrotransposition, meiotic gene conversion and sporulation. Mu\ntations in srs2 suppress rad6 radiation-sensitivity but not \nthe sporulation defect. rad6 forms recombination intermediat\nes.\n mYBR139W:Unknown ,, Unknown\n mDAL81:Positive regulator of multiple nitrogen catabolic genes,tran\nscriptional activator for allantoin and GABA catabolic genes\n, contains a Zn[2]-Cys[6] fungal-type binuclear cluster doma\nin in the N-terminal region,Null mutant is viable, unable to\n degrade allantoin\n mYPL150W:Unknown ,, Unknown\n mYCK1:membrane-bound casein kinase I homolog,casein kinase I homol\nog,Null mutant is viable; yck1 yck2 double deletion mutants \nare inviable; yck1 point mutants suppress defective Snf1p ki\nnase activity in snf4 strains\n Cond916:(99i5)__HBY4_YPGL+G_NormInt\n mYFL067W:Unknown ,, Unknown\n mPRE10:proteasome component YC1 (protease yscE subunit 1),proteasom\ne component YC1 (protease yscE subunit 1),Null mutant is inv\niable\n mSWC1:Unknown ,, Unknown\n mCYR1:Required for START A of cell cycle, and glucose and nitrogen\n repression of sporulation,adenylate cyclase,Null mutant is \ninviable. cyr1 transiently arrests in G1 and sporulates prec\nociously. N-terminal domain is dispensable for mitotic G1 ar\nrest after nitrogen starvation, but required for sporulation\n. When altered, cAMP levels remain high and cells continue t\no bud with abnormal spindles\n mARP3:actin-related gene,,Null mutant is inviable\n Cond935:10h\n Cond915:(99i4)_HBY4_YPGL_NormInt\n mOPI1:Negative regulator of phospholipid biosynthesis,,The null mu\ntant is viable but constitutively accumulates INO1 mRNA.\n mYLR104W:Unknown ,, Unknown\n mYGR031W:Unknown ,, Unknown\n mYDL237W:Unknown ,, Unknown\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 mYGR017W:Unknown ,, Unknown\n mRCK2:Serine/threonine protein kinase,,Null mutant is viable\n mSRC1:Spliced mRNA and Cell cycle regulated gene,,Null mutant is v\niable and shows normal growth in standard media; expression \nis induced at G2/M transition.\n mYKL105C:Unknown ,, Unknown\n mMDV1:Involved in mitochondrial division,,Null mutant is viable, m\nitochondrial fission blocked, mitochondrial membranes form n\nets\n COMP.KO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mRTT103:Regulator of Ty1 Transposition,,Gene disruption causes Ty1 h\nypertransposition phenotype\n mCMP2:calmodulin binding protein homologous to mammalian calcineur\nin,calcineurin subunit A,Null mutant is viable (no obvious p\nhenotype)\n Cond256:ymr141c\n mTPK1:putative catalytic subunit of cAMP-dependent protein kinase,\ncAMP-dependent protein kinase catalytic subunit (putative),m\nulticopy suppression of ras mutant\n Cond52:erd1\n mTPK2:Involved in nutrient control of cell growth and division,cAM\nP-dependent protein kinase catalytic subunit,Null mutant hap\nloids are defective for invasive growth; diploid homozygous \nnull mutants are defective for pseudohyphal growth.\n mYEL006W:Unknown ,, Unknown\n mTPK3:Involved in nutrient control of cell growth and division,cAM\nP-dependent protein kinase catalytic subunit,Null mutant is \nviable, tpk1 tpk2 tpk3 triple mutant is inviable\n mVPS21:Rab5-like GTPase involved in vacuolar protein sorting and en\ndocytosis post vesicle internalization; geranylgeranylated; \ngeranylgeranylation required for membrane association,small \nGTP-binding protein,Null mutant is viable, temperature-sensi\ntive, missorts multiple vacuolar proteins, accumulate 40-50 \nnm vesicles, and contain a large vacuole\n mYLR218C:Unknown ,, Unknown\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mYLR177W:Unknown ,, Unknown\n mPGD1:Probable transcription factor, polyglutamine domain protein,\n,Suppresses hyper-deletion phenotype of hpr1 null mutant; re\nduces frequency of deletions in rad52-1 mutant\n mVTC4:Phosphate metabolism; transcription is regulated by PHO syst\nem,polyphosphate synthetase (putative),Null mutant has been \nshown to be either inviable, or viable while exhibiting no p\nolyphosphate accumulation\n mENB1:Siderophore transporter for enterobactin; AFT1 regulon,enter\nobactin transporter,Null mutants are viable but are unable t\no take up and utilize iron from enterobactin\n mBCY1:Involved in heat shock resistance, glycogen accumulation, an\nd sporulation,cAMP-dependent protein kinase regulatory subun\nit,Null mutant is viable; sra1 mutants are associated with r\neduction of glycogen accumulation, temperature sensitivity, \nreduced growth rate on maltose and sucrose, inability to gro\nw on galactose and nonfermentable carbon sources and nitroge\nn starvation intolerance. Cells lacking Sra1p are constituti\nve for cAPK activity resulting in meiotic arrest prior to pr\nemeiotic DNA synthesis\n mITR1:member of sugar transporter superfamily,myo-inositol transpo\nrter,Null mutant is viable\n mYOR060C:Unknown ,, Unknown\n mMNT3:MaNnosylTransferase; involved in adding the 4th and 5th mann\nose residues of O-linked glycans,alpha-1,3-mannosyltransfera\nse,\n mGSY2:Highly similar to GSY1. GSY2 is the predominantly expressed \nglycogen synthase. Activity is probably regulated by cAMP-de\npendent and SNF1 protein kinases and type 1 phosphatase,glyc\nogen synthase (UDP-glucose-starch glucosyltransferase),Null \nmutant is viable. Mutant lacking both GSY1 and GSY2 is viabl\ne but lacks glycogen synthase activity and glycogen depositi\non\n mYGL051W:Unknown ,, Unknown\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 mEFR4:PHO _E_ighty _F_ive _R_equiring,,Transposon insertion allele\n is synthetically lethal with pho85-delta\n mSIS2:Involved in cell cycle control and ion homeostasis,,Null mut\nant is viable, displays salt sensitivity\n mKTR3:Putative alpha-1,2-mannosyltransferase,alpha-1,2-mannosyltra\nnsferase (putative),\n mWTM2:WD repeat containing transcriptional modulator 2,transcripti\nonal modulator,Null mutant is viable\n mYPT53:Involved in vacuolar protein sorting and endocytosis,GTP-bin\nding protein , rab family,Null mutant is viable\n mADE16:AICAR transformylase/IMP cyclohydrolase,5-aminoimidazole-4-c\narboxamide ribonucleotide (AICAR) transformylase/IMP cyclohy\ndrolase,Null mutant is viable; ade16 ade17 double mutant req\nuires adenine\n mYGL161C:Unknown ,, Unknown\n mTBS1:Probable Zn-finger protein,,\n mFAA2:acyl-CoA synthetase (long-chain fatty acid CoA ligase) (fatt\ny acid activator 2), activates endogenous but not imported f\natty acids and provides substrates for N-myristoylation,acyl\n-CoA synthetase (fatty acid activator 2),Not essential for v\negetative growth when fatty acid synthase (fas) is active\n mTGL1:triglyceride lipase-cholesterol esterase,cholesterol esteras\ne , triglyceride lipase,\n Cond11:arg5,6\n mCDC34:ubiquitin-conjugating enzyme, E2,ubiquitin-conjugating enzym\ne,Null mutant is inviable\n mYSP3:subtilisin-like protease III,subtilisin-like protease III,\n mTPD3 mYCK1 mBCY1 mTPK3 mYPT53 mVPS21 mTPK2 mTPK1

this is an automaticly generated SAMBA report
Computational Genomics Lab, Tel-Aviv uniresity