Module number 969




Database revision : gnsdb28.10
Date : Tue Feb 25 17:17:42 2003
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mRAD27:DNA repair protein that belongs to the RAD2(pombe)/FEN1 subf\namily,42 kDa 5' to 3' exonuclease required for Okazaki fragm\nent processing,Null mutant is viable, demonstrates temperatu\nre-sensitive growth and sensitivity to UV light and to methy\nlmethane sulfonate\n Cond498:wtħ500nMaF,30minlog10(intensity)\n Cond494:wtħ5nMaF,30minlog10(intensity)\n mHLR1:LRE1 homolog,,Null mutant is viable.\n Cond548:cln3-2\n Cond751: 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 Cond533:fus3D+50nMaF/wt+50nMaF,30minlog10(intensity)\n mHHO1:Histone H1,histone H1,Null mutant is viable; other phenotype\n: Increased basal expression of a CYC1-lacz reporter gene; n\nuclear localization of a Hho1-GFP fusion protein\n mCLB5:role in DNA replication during S phase; additional functiona\nl role in formation of mitotic spindles along with Clb3 and \nClb4,B-type cyclin,Null mutant is viable, but has an extende\nd S phase\n mYBR070C:Unknown ,, Unknown\n Cond579:cdc15_140\n mCLB6:role in DNA replication during S phase,B-type cyclin,Null mu\ntant is viable\n mMNN1:Alpha-1,3-mannosyltransferase,alpha-1,3-mannosyltransferase,\nNull mutant is viable\n mRFA1:Required for DNA-damage repair, full levels of gene conversi\non and sporulation,heterotrimeric RPA (RF-A) single-stranded\n DNA binding protein 69 kDa subunit; binds URS1 and CAR1,Nul\nl mutant is inviable; cells lacking RFA1 accumulate as multi\nply budded cells with a single nucleus suggesting a defect i\nn DNA replication; rfa1 repair defects are suppressed by hig\nh copy RAD52\n mRFA2:Involved in nucleotide excision repair,29% identical to the \nhuman p34 subunit of RF-A , replication factor RF-A subunit \n2,Null mutant is inviable; arrests as budded and multiply bu\ndded cells; rfa2 (ts) cells have a mutator and a hyper-recom\nbination phenotype and are more sensitive to hydroxyurea and\n methyl-methane-sulfonate than wild-type cells\n mRFA3:subunit 3 of replication factor-A,replication factor-A subun\nit 3,Null mutant is inviable and arrests as budded and multi\nply budded cells\n Cell Cycle.ko: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 mYLR049C:Unknown ,, Unknown\n mYKR012C:Unknown ,, Unknown\n mPOL12:Required for DNA synthesis and correct progression through S\n phase; plays an essential role at early stage of chromosoma\nl DNA replication, before the hydroxyurea-sensitive step,DNA\n polymerase alpha-primase complex B subunit,Null mutant is i\nnviable\n mCDC45:Cdc45p assembles into a complex with Cdc46p/Mcm5p,chromosoma\nl DNA replication initiation protein,required for minichromo\nsome maintenance and chromosomal DNA replication\n mYDL163W:Unknown ,, Unknown\n mGAS1:Glycophospholipid-anchored surface protein,cell surface glyc\noprotein 115-120 kDa,Null mutant is slow growing and exhibit\ns cell wall defects.\n mCDC9:essential for mitosis and meiosis, dispensable for intrageni\nc recombination, but required for haploidization and spores,\nDNA ligase,cell division cycle blocked at 36 degrees, increa\nsed sensitivity to ultraviolet radiation and bleomycin; temp\nerature sensitive\n mCTF18:Chromosome transmission,,Null mutant is viable, exhibits inc\nreased level of spontaneous mitotic recombination, slow grow\nth, and cold sensitivity\n Cond562:alpha77\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 Cond480:WT+/-100mM3AT(SetA)(R491)\n mMRC1:Mediator of the Replication Checkpoint; required for full ac\ntivation of Rad53p in response to replication stress.,,Null:\n sensitive to hydroxyurea; replication checkpoint defective;\n slower DNA replication than wild type; partial loss of sile\nncing at telomeres and HM loci; synthetic lethal with rad9 n\null, rad53-21, and mec1-21.\n mCRH1:congo red hypersensitive,cell wall protein,Null mutant is vi\nable and hypersensitive to Congo Red and Calcofluor White\n mYKR077W:Unknown ,, Unknown\n Cond568:alpha119\n mPDS1:May be an anaphase inhibitor that plays a critical role in c\nontrol of anaphase by both the anaphase promoting complex (A\nPC) and DNA-damage checkpoints,42 kDa nuclear protein,Null m\nutant is viable but is temperature-sensitive; shows higher r\nates of chromosome loss at permissive temperature; at restri\nctive temperature, fails to elongate spindles and shows unco\nupling of cell cycle progression from completion of anaphase\n mYMR144W:Unknown ,, Unknown\n mPDS5:Precocious Dissociation of Sister chromatids,,\n mYPL267W:Unknown ,, Unknown\n Cond279:ERG11(tetpromoter)\n Cond553:alpha14\n Cond508:bni1Dħ50nMaF,120minlog10(intensity)\n mYHP1:Hypothetical ORF,,\n mRDH54:genetic interaction with DMC1,helicase (putative) , similar \nto RAD54,Required for meiosis. Early meiotic induction of ge\nne conversion is wild-type in a tid1 deletion but mature cro\nssover products form slowly and cells block with single nucl\nei even though the spindle pole bodies duplicate and separat\ne twice, as if progressing to entry into the second meiotic \ndivision.\n mMSH2:Functions with Pms1p and Pms2/Mlh1p in a complex that intera\ncts with Pms3p/Msh6p to repair single-base and insertion-del\netion mispairs, or Msh3p to repair insertion-deletion mispai\nrs.,mutS homolog,Null mutant is viable. Haploid mutants disp\nlay an 85-fold increased rate of spontaneous mutation to can\navanine resistance. Mutants are defective for gene conversio\nn polarity gradients and high spore viability.\n mMSH6:Required for mismatch repair in mitosis & meiosis, low level\ns of postmeiotic segregation & high spore viability; forms c\nomplex with Msh2p to repair both single-base & insertion-del\netion mispairs; redundant with Msh3p in repair of in-dels,hu\nman GTBP protein homolog,Null mutant is viable, msh3 msh6 do\nuble deletion mutants exhibit microsatellite instability and\n mutability similar to that in a msh2 mutant\n Cond580:cdc15_150\n mHIF1:Hat1 Interacting Factor 1,,Null mutant is viable and does no\nt show any obvious phenotypes\n mPRI2:p58 polypeptide of DNA primase,DNA primase p58 polypeptide,l\nethal\n mYHR149C:Unknown ,, Unknown\n mBBP1:Involved in mitotic cell cycle and meiosis,,Null mutant is i\nnviable; cells depleted of Bbp1p are defective in nuclear se\ngregation, bud formation, cytokinesis and nuclear spindle fo\nrmation; overexpression gives ascus that contains asci inste\nad of spores\n mYBR071W:Unknown ,, Unknown\n mSPC98:Involved in microtubule organization by the SBP,spindle pole\n body component,Null mutant is inviable; overexpression is t\noxic resulting in accumulation of cells with large buds, 2N \nDNA content, defect in microtubule structure. ts-phenotype: \narrest in G2 of cell cycle with large bud, duplicated spindl\ne pole bodies, short spindle and elongated cytoplasmic micro\ntubules\n Cond54:erg3(haploid)\n Cond581:cdc15_160\n Cond558:alpha49\n mSEN34:tRNA splicing endonuclease 34kDa subunit; homologous to the \n42-kDa subunit, SEN2; contains active site for 3' splice sit\ne cleavage,tetrameric tRNA splicing endonuclease 34 kDa subu\nnit,Null mutant is inviable and shows H242A impaired 3'splic\ne site cleavage\n Cond734: mRTT107:Establishes Silent Chromatin,,\n mRTT109:Regulation of mitochondrial network; Killed in Mutagen, sens\nitive to diepoxybutane and/or mitomycin C,,Mutant exhibits a\nbnormal mitochondrial morphology and slight growth defect in\n dextrose; insertion/truncation at amino acid 332 yields sen\nsitivity to diepoxybutane and to mitomycin C\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n Cond746: Cond582:cdc15_170\n mRAD51:Involved in processing ds breaks, synaptonemal complex forma\ntion, meiotic gene conversion and reciprocal recombination.,\nRad51p colocalizes to ~ 65 spots with Dmc1p prior to synapsi\ns (independently of ZIP1 and DMC1), and interacts with Rad52\np and Rad55p; human Rad51p homolog interacts with Brca2 prot\nein which has been implicated in causing breast cancer , Rec\nA homolog,Null mutant is viable; accumulates meiosis-specifi\nc double strand breaks at a recombination hotspot and reduce\ns the formation of physical recombinants and processed doubl\ne strand breaks with long heterogeneous tails; rad51 mutants\n are also defective for X-ray damage repair and gene convers\nions; rad51 rad27 mutants are inviable.\n mPOL30:Accessory factor for DNA polymerase delta, mRNA increases in\n G1, peaks in S in mitosis, & increases prior to DNA synthes\nis in meiosis; required for DNA replication & repair, requir\ned for viability in cdc44, rad50, rad52 or rad57 backgrounds\n,,Null mutant is inviable\n Cond571:cdc15_50\n mRAD53:Required for DNA damage-induced checkpoint arest in G1, S/M,\n and G2/M in mitosis, dispensable for sporulation but requir\ned for wild-type spore viability; Mec1p and Tel1p regulate r\nad53p phosphorylation,protein kinase,Null mutant is inviable\n, radiation sensitive\n mDPB2:DNA polymerase epsilon, subunit B,DNA polymerase epsilon sub\nunit B,Null mutant is inviable; conditional mutant shows def\nects in DNA replication\n mRSR1:Gtp-binding protein of the ras superfamily involved in bud s\nite selection,,random budding pattern\n mPRY2: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 Cond965:ndt80_delete_mid_g/r_ratio_\n Cond737: Cond555:alpha28\n Cond493:wtħ1.5nMaF,30minlog10(intensity)\n mYNR009W:Unknown ,, Unknown\n mMSB2:putative integral membrane protein,integral membrane protein\n (putative),multicopy suppressor of cdc24 ts mutation\n mSVS1:involved in vanadate resistance,,Null mutant is viable, show\ns increased sensitivity to vanadate, but not other metallic \nions or drugs\n Cond570:cdc15_30\n mRNR1:ribonucleotide reductase,ribonucleotide reductase, large (R1\n) subunit,Null mutant is inviable\n Cond503:wtħ50nMaF,60minlog10(intensity)\n Cond511:GAL-STE4,3hrs.gallog10(intensity)\n mRNR3:Ribonucleotide reductase (ribonucleoside-diphosphate reducta\nse) large subunit,ribonucleotide reductase, large (R1) subun\nit,Null mutant is viable\n mESC8:Unknown ,, Unknown\n Cond750: Cond510:fus3Dħ50nMaF,30minlog10(intensity)\n Cond567:alpha112\n Cond547:cln3-1\n mTOS2:Hypothetical ORF,,\n mMCD1:Mitotic Chromosome Determinant; similar to S. pombe RAD21; m\nay function in chromosome morphogenesis from S phase through\n mitosis,,Null mutant is inviable; temperature sensitive mut\nants are defective in mitotic sister chromatid cohesion and \nmitotic chromosome condensation; multicopy suppressor of smc\n1-2 mutation\n mAXL2:involved in polarity establishment/cellular polarization dur\ning budding,,AXL2 can serve as a multicopy suppressor of rho\n3 and is required for the haploid axial budding pattern of S\n. cerevisiae.\n mPOL1:Required for mitotic DNA synthesis, premeiotic DNA synthesis\n, recombination, and full sporulation,DNA polymerase I alpha\n subunit p180,Null mutant is inviable. pol1(ts) mutants show\n blocked cell division at 36 degrees C\n mTOS4:Hypothetical ORF,,\n mPOL2:DNA polymerase II,DNA polymerase II,\n mTOS6:Hypothetical ORF,,\n Cond500:wtħ50nMaF,15minlog10(intensity)\n mOCH1:membrane-bound alpha-1,6-mannosyltransferase,alpha-1,6-manno\nsyltransferase,Null mutant is viable, temperature sensitive,\n lacks mannose outer chains\n mGIN4:Growth inhibitory gene,serine/threonine kinase (putative),Nu\nll mutant is viable, exhibits a mild elongated bud phenotype\n and some cell clumping\n mYIL141W:Unknown ,, Unknown\n mTUB4:spindle pole body component that organizes both cytoplasmic \nand nuclear microtubule arrays,gamma tubulin-like protein , \ninteracts with Spc98p and Spc97p, the Tub4p-Spc98p-Spc97p co\nmplex may be part of the microtubule attachment site at the \nspindle pole body,Null mutant is inviable. Tub4p-depleted ce\nlls arrest during nuclear division; most arrested cells cont\nain a large bud, replicated DNA, and a single nucleus. Immun\nofluorescence and nuclear staining experiments indicate that\n cells depleted of Tub4p contain defects in the organization\n of both cytoplasmic and nuclear microtubule arrays; such ce\nlls exhibit nuclear migration failure, defects in spindle fo\nrmation, and/or aberrantly long cytoplasmic microtubule arra\nys.\n Cond504:wtħ50nMaF,90minlog10(intensity)\n mHPR5:Required for proper timing of committment to meiotic recombi\nnation and the transition from Meiosis I to Meiosis II,DNA h\nelicase,Null mutant is viable, radiation (ultraviolet or ion\nizing sensitive), loss of function results in RAD52-dependen\nt hyperrecombination suggesting recombination suppression oc\ncurs by antagonizing the Rad52 recombinational repair pathwa\ny; wild-type suppresses mitotic recombination; some mutant a\nlleles have lower spore viability which is not rescued by sp\no13, suggesting they affect a late recombination function; h\npr5 mutations are rad6 suppressors\n Cond519:rst1Drst2Dħ50nMaF,30minlog10(intensity)\n Cond586:cdc15_210\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 Cond733: Cond507:bni1Dħ50nMaF,90minlog10(intensity)\n Cond509:kss1Dħ50nMaF,30minlog10(intensity)\n Cond496:wtħ50nMaF,30minlog10(intensity)\n mCLN1:role in cell cycle START,G1 cyclin,Null mutant is viable, ex\nhibits G1 arrest\n mCLN2:role in cell cycle START,G1 cyclin,Null mutant is viable, ex\nhibits G1 arrest; dominant mutation advances the G(sub)1- to\n S- phase transition and impairs ability of cells to arrest \nin G(sub)1 phase in response to external signals\n mSPH1:SPa2-Homolog; protein involved in shmoo formation and requir\ned for bipolar bud site selection (GB:AF008236).,Spa2p homol\nog,Null mutant is viable but results in defects in shmoo for\nmation.\n mPMS1:Required for mismatch repair in mitosis and meiosis, low lev\nels of postmeiotic segregation, and high spore viability, di\nspensable for homeologous recombination,mutL homolog , simil\nar to Mlh1p, associates with Mlh1p, possibly forming a heter\nodimer, Pms1p and Msh1p act in concert to bind to a Msh2p-he\nteroduplex complex containing a G-T mismatch,Null mutant is \nviable; postmeiotic segregation increased\n mYCL022C:Unknown ,, Unknown\n mCTF4:May function in DNA synthesis,DNA polymerase alpha binding p\nrotein,Null mutant is viable but shows increase in the rate \nof mitotic chromosome loss, increased mitotic recombination,\n shift toward cells with G2 DNA content, and large budded ce\nlls with the nucleus in the bud neck; shows synthetic intera\nctions with rad52, pol1, rad9, and esr1\n mYGR151C:Unknown ,, Unknown\n mCSI2:chitin synthase involved,chitin synthase 3 complex structura\nl component (putative),Null mutant is viable but shows deloc\nalized chitin deposition\n Cond495:wtħ15.8nMaF,30minlog10(intensity)\n COMP.CH:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n Cond550:clb2-1\n mHHT1:Histone H3 (HHT1 and HHT2 code for identical proteins),histo\nne H3 (HHT1 and HHT2 code for identical proteins),Null mutan\nt is viable\n mHHT2:Histone H3 (HHT1 and HHT2 code for identical proteins),histo\nne H3 (HHT1 and HHT2 code for identical proteins),\n mYBR089W:Unknown ,, Unknown\n Cond506:bni1Dħ50nMaF,60minlog10(intensity)\n mASF1:anti-silencing protein that causes depression of silent loci\n when overexpressed,,\n mERP3:Emp24p/Erv25p related protein 2,p24 protein involved in memb\nrane trafficking,viable\n mERP5:Emp24p/Erv25p related protein 5,p24 protein involved in memb\nrane trafficking,viable\n Cond502:wtħ50nMaF,45minlog10(intensity)\n COMP.KO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n Cond563:alpha84\n Sporulation.Series0:The transcriptional program of sporulation in budding yeast.\n Science. 1998 Oct 23;282(5389):699-705.\n mCDC21:cell division cycle blocked at 36 degree C,thymidylate synth\nase,defective in continued replication during S phase of the\n cell cycle; temperature-sensitive thymidylate auxotroph\n mSMC3:involved in sister chromatid cohesion,SMC chromosomal ATPase\n family member,Null mutant is inviable\n Cond501:wt+/-50nMaF,30minlog10(intensity)\n mKCC4:involved in septin organization,S. pombe Nim1 homolog , prot\nein kinase,Null mutant is viable\n mHTA1:Histone H2A (HTA1 and HTA2 code for nearly identical protein\ns),histone H2A (HTA1 and HTA2 code for nearly identical prot\neins),Null mutant is viable\n mHTA2:Histone H2A (HTA1 and HTA2 code for nearly identical protein\ns),histone H2A (HTA1 and HTA2 code for nearly identical prot\neins),Null mutant is viable. Deletion of the HTA2-HTB2 (TRT2\n) locus has no reported observable phenotypes, presumably be\ncause HTA1-HTB1 (TRT1) expression is upregulated and can com\npensate in the absence of TRT2. Overexpression of TRT2 can s\nuppress Ty insertion mutations\n Cond554:alpha21\n mHCM1:Dosage-dependent suppressor of cmd1-1 mutation; shows homolo\ngy to fork head family of DNA-binding proteins,,Null mutant \nis viable; exacerbates temperature-sensitivity of a cmd1-1 (\ncalmodulin) mutant\n Cond738:90\n Cond575:cdc15_100\n mHHF1:Histone H4 (HHF1 and HHF2 code for identical proteins),histo\nne H4 (HHF1 and HHF2 code for identical proteins),\n mHHF2:Histone H4 (HHF1 and HHF2 code for identical proteins),histo\nne H4 (HHF1 and HHF2 code for identical proteins),\n Cond294:Itraconazole\n Cond574:cdc15_90\n mDUN1:DNA damage response,protein kinase,Null mutant is viable, de\nfective in DNA damage repair and in DNA damage-resposive ind\nuction of RNR genes, and sensitive to DNA damaging agents\n Cond747: mSPT21:involved in trascriptional regulation of Ty1 LTRs,non-specif\nic DNA binding protein,Null mutant is viable, spt21 mutation\ns suppress Ty insertion mutations\n Cond497:wtħ158nMaF,30minlog10(intensity)\n mHSL1:Negative regulator of swe1 kinase (which regulates cdc28),pr\notein kinase (putative) , similar to S. pombe cdr1/nim1,Nul\nl mutant is viable; synthetically lethal with histone H3 mut\nations; G2 delay\n Cond560:alpha63\n Cond576:cdc15_110\n Cond736: Cell Cycle.cdc15: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 COMP.TE:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n Cond559:alpha56\n mSRL1:Suppressor of rad53 lethality,,\n mSWE1:protein kinase homolog,protein kinase homolog,Null mutant is\n viable\n fkh1,2sf.Series0:Two yeast forkhead genes regulate the cell cycle and pseudoh\nyphal growth. Nature. 2000 Jul 6;406(6791):90-4.\n mHTB1:Histone H2B (HTB1 and HTB2 code for nearly identical protein\ns),histone H2B (HTB1 and HTB2 code for nearly identical prot\neins),Null mutant is viable\n Cond551:alpha0\n Cond549:clb2-2\n mHTB2:Histone H2B (HTB1 and HTB2 code for nearly identical protein\ns),histone H2B (HTB1 and HTB2 code for nearly identical prot\neins),Null mutant is viable. Deletion of the HTA2-HTB2 (TRT2\n) locus has no reported observable phenotypes, presumably be\ncause HTA1-HTB1 (TRT1) expression is upregulated and can com\npensate in the absence of TRT2\n mYOX1:Homeodomain protein that binds leu-tRNA gene,homeobox-domain\n containing protein,Null mutant is viable\n
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Computational Genomics Lab, Tel-Aviv uniresity