Module number 2967




Database revision : gnsdb28.10
Date : Tue Feb 25 17:41:29 2003
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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 mSAP30:Hypothetical ORF,,\n mSGV1:CDC28/cdc2 related protein kinase,CDC28/cdc2 related protein\n kinase,Null mutant is inviable.\n mPDR1:general positive regulator of permeability genes,zinc finger\n transcription factor of the Zn(2)-Cys(6) binuclear cluster \ndomain type,pleiotropic drug resistance, resistant to borrel\nidin, oligomycin, antimycin, cycloheximide, antibiotic, thio\nisoleucine, sulfometuron methyl; accumulation of neutral red\n mYJR083C:Unknown ,, Unknown\n mYKL063C:Unknown ,, Unknown\n mNUP116:Involved in nucleocytoplasmic transport; may be required for\n biogenesis of tRNA,nuclear pore complex subunit,Null mutant\n grows slowly, accumulates unspliced pre-tRNAs, acumulates p\noly(A)+ RNA in the nucleus, and is temperature-sensitive; at\n nonpermissive temperature, null mutants show membrane seals\n covering cytoplasmic face of nuclear pore complexes; synthe\ntically lethal with nsp1, nup100, and nup145\n mURE2:Nitrogen catabolite repression regulator that acts by inhibi\ntion of GLN3 in good nitrogen source. Altered form of Ure2p\n creates [URE3] prion.,glutathione transferase (putative) , \nprion , transcriptional regulator,Null mutant is viable but \nexhibits defects in nitrogen catabolite repression (NCR), an\nd null mutant diploids are defective in pseudohyphal growth \nand display an increased incidence of random bud patterns.\n mVTA1:Unknown ,, Unknown\n mEMP47:47 kDa type I transmembrane protein localized to the Golgi,4\n7 kDa type I transmembrane protein localized to the Golgi,Nu\nll mutant is viable\n mRLF2:Chromatin Assembly Complex, subunit 1: largest (p90) subunit\n of three-subunit protein complex (yeast CAF-I) involved in \nDNA-replication-linked nucleosome assembly. Homol. to p150 s\nubunit human Chromatin Assembly Factor-I (CAF-I),chromatin a\nssembly factor-I (CAF-I) p90 subunit,Null mutant is viable, \nsensitive to UV radiation. Rap1 localization is disrupted an\nd silencing of genes adjacent to telomeric DNA is decreased \nin rfl2 mutants.\n Cond883:5\n mRPB3:45 kDa subunit of RNA polymerase II,RNA polymerase II 45 kDa\n subunit,Null mutant is inviable; rpb3(ts) mutants at restri\nctive temperature exhibit no assembly of RNA polymerase II\n mRPB4:fourth-largest subunit of RNA polymerase II,RNA polymerase I\nI fourth largest subunit,Null mutant is viable, rbp4 mutants\n are heat and cold sensitive, exhibit slow growth at interme\ndiate temperatures\n Cond898:RPN4\n mYPL070W:Unknown ,, Unknown\n mYNR029C:Unknown ,, Unknown\n Cond872:Zero1\n Cond889:4NQO_2\n mTAF10:TFIID subunit (TBP-associated factor) with predicted molecul\nar weight of 23 kD.,TFIID subunit,Null mutant is inviable\n mMSO1:multicopy suppressor of sec1; small hydrophilic protein, enr\niched in microsomal membrane fraction, interacts with Sec1p,\n,Null mutant is viable, exhibits accumulation of secretory v\nesicles in the bud; mso1 null mutants exhibit double mutant \ninviability in combinaiton with sec1, sec2, and sec4 mutants\n COMP.:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mSEY1:Unknown ,, Unknown\n mCSE4:Required for proper kinetochore function; may be involved in\n assembly of a CEN-specific chromatin structure,similar to h\nistone H3 and to human centromere protein CENP-A,Null mutant\n is inviable; cse4-1 mutant causes increased non-disjunction\n of chromosome with mutated CEN and t.s. arrest at G2/M boun\ndary with 2N DNA content\n Cond948:W303_ume6_YPA_\n Cond897:STATMMS\n mRAT1:RNA trafficking protein; transcription activator,5'-3' exori\nbonuclease,Null mutant is inviable.\n mPOB3:binds to catalytic subunit of DNA polymerase alpha (Pol1p),D\nNA polymerase delta binding protein,Null mutant is inviable\n mYOR059C:Unknown ,, Unknown\n Cond888:MNNG_2\n Cond894:G2\n mSCP1:homolog of chicken calponin, thus the name S. cerevisiae Cal\nPonin,calponin homolog,Null mutant is viable and shows no ap\nparent phenotype\n mVID27:Vacuole import and degradation,,Null mutant is viable but ex\nhibits vacuole degradation of cytosolic proteins\n mULP1:Ubl (ubiquitin-like protein) - specific protease 1,Ulp1p-spe\ncific protease,Null mutant is lethal. Temperature-sensitive \nmutants accumulate in G2/M at the restrictive temperature\n mSTH1:helicase related protein, snf2 homolog,helicase related prot\nein , snf2 homolog,conditional mutants arrest at large bud s\ntage with a single nucleus; null is inviable\n mGRS2:Unknown ,, Unknown\n mHRB1:an ORF of unknown function located in a centromeric region d\nuplicated between chromosomes III and XIV,hypothetical RNA-b\ninding protein,\n Cond893:SMMS\n mSPP1:YPL138C,,\n mNAB2:nuclear polyadenylated RNA binding protein,polyadenylated RN\nA binding protein,Null mutant is inviable\n mCET1:Interacts with Ceg1p, the mRNA capping enzyme alpha subunit;\n removes gamma-phosphate from triphosphate-terminated RNA,RN\nA 5'-triphosphatase , mRNA capping enzyme beta subunit (80 k\nDa),Null mutant is inviable\n mYOR262W:Unknown ,, Unknown\n UME6.ume6:The Ume6 regulon coordinates metabolic and meiotic gene expr\nession in yeast. Proc Natl Acad Sci U S A. 2002 Oct 15;99(2\n1):13431-6.\n mNHP10:Non-Histone Protein 10,HMG1-box containing protein,null muta\nnt is viable and has normal growth rate\n mGCR2:activates transcription of glycolytic genes; homologous to G\nCR1; may function in complex with Gcr1p,transcription factor\n,Null mutant is viable and has partial growth defect on gluc\nose-containing media\n Cond895:G2MMS\n Cond878:MNNG\n mHBS1:Protein related to translation elongation factor EF-1alpha a\nnd to Suf12p/Sup2p/Gst1p/Sup35p,,\n mYJR136C:Unknown ,, Unknown\n mSEC12:Required for recruitment of Sar1p and vessicle formation at \nthe endoplasmic reticulum.,guanine nucleotide exchange facto\nr for Sar1p,Null mutant is inviable. Defective in endoplasmi\nc reticulum to Golgi transport.\n mMED4:Member of RNA Polymerase II transcriptional regulation media\ntor,RNA polymerase II holoenzyme/mediator subunit,Null mutan\nt is inviable\n mSPT16:global regulator of transcription,,suppression of Ty inserti\non mutations\n mRUD3:Relieves uso1-1 transport defect; golgin-160 related protein\n,,Null mutant shows severe growth defect or inviability in c\nombination with many ER-to-Golgi transport mutants, such as \nuso1-1, sec34, sec35-1, sec22-3, and bos1-1. Overproduction \nsuppresses mutations in many of the same genes.\n Cond877:MMS\n Cond875:60min\n Cond886:g-ray\n mYPR148C:Unknown ,, Unknown\n mECO1:Establishment of COhesion,,Null mutant is inviable; temperat\nure-sensitive allele prematurely separates sister chromatids\n, and sister chromatid separation occurs in the absence of f\nunctional APC or Esp1p.\n mUBP2:Ubiquitin-specific protease,ubiquitin-specific protease,Null\n mutant is viable. Null yuh1 ubp1 ubp2 ubp3 quadruple mutant\ns are viable and retain the ability to deubiquitinate ubiqui\ntin fusions.\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mMTF1:Mitochondrial RNA polymerase specificity factor,mitochondria\nl RNA polymerase specificity factor,Null mutant is viable, d\nefective in respiration, and lacks mtDNA.\n mYRR1:Yeast Reveromycin-A Resistant,transcription factor,Null muta\nnt is viable, hypersensitive to 4-nitroquinoline oxide (4-NQ\nO); the YRR1-1 allele confers resistance to 4-NQO, reveromyc\nin-A and oligomycin\n mFOL3:FOLinic acid requiring,dihydrofolate synthetase,Null mutant \nis viable; requires folinic acid for growth\n mVPS60:vacuolar protein sorting (putative),,Null mutant is viable b\nut a class E vps mutant (missorts vacuolar hydrolases and ac\ncumulates late endosomal compartment).\n mPAN5:ketopantoate reductase,,\n mTAF6:TATA-binding protein-associated-factor,TATA-binding protein-\nassociated-factor,Null mutant is inviable\n mVPS63:Unknown ,, Unknown\n mSKI6:superkiller; ExtraCellular Mutant; Ribosomal RNA Processing,\nRNAse PH homolog,Null mutant is inviable; mutants show super\nkiller phenotype, improved translation of non-poly(A) mRNA, \nabnormal 60S ribosomal subunits and defective 3' processing \nof 5.8S rRNA; a Tn3 insertion into this gene causes hypersen\nsitivity to the cell surface polymer perturbing agent calcof\nluor white\n mPLP2:Phosducin-like protein,,Null mutant is inviable\n Cond885:20\n mTAF9:TFIID subunit (TBP-associated factor) with predicted molecul\nar weight of 17 kD.,TFIID subunit,Null mutant is inviable\n mCBK1:cell wall biosynthesis kinase,protein kinase,Null mutation i\ns viable; shows alpha factor resistance; in liquid culture l\narge aggregates of cells are formed\n mYKL047W:Unknown ,, Unknown\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 mARC15:Arp complex subunit,,Null mutant is viable, but exhibits sev\nere growth defects\n Cond891:G1MMS\n mPBS2:Involved in osmoregulation, member of the HOG1 mitogen-activ\nated protein kinase (MAPK) cascade,MAP kinase kinase (MEK) ,\n may act as a scaffolding protein for Sho1p, Ste11p, and Hog\n1p , MAP kinase kinase (MEK) , may act as a scaffolding prot\nein for Sho1p, Ste11p, and Hog1p , MAP kinase kinase (MEK) ,\n may act as a scaffolding protein for Sho1p, Ste11p, and Hog\n1p,Null mutant is viable, sensitive to high osmolarity, sens\nitive to the antibiotic polymyxin B; shows marked decreased \ninduction of transcription by osmotic stress that is mediate\nd by stress response elements; a deletion in RGA1 and PBS2 a\nctivates the pheromone-dependent signal transduction pathway\n independently of the G protein\n mYJL184W:Unknown ,, Unknown\n mYKL215C:Unknown ,, Unknown\n mTFG2:transcription initiation factor TFIIF middle subunit,transcr\niption initiation factor TFIIF middle subunit,Null mutant is\n inviable\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 mMTR2:mRNA transport regulator,mRNA transport regulator,Null mutan\nt is inviable; mtr2 mutants exhibit nuclear mRNA accumulatio\nn and nucleolar fragmentation\n mYDR267C:Unknown ,, Unknown\n Cond643:DES459_(mec1-)_+_0.02%_MMS_-_45_min\n mELP4:ELongator Protein 4; 50kD subunit,RNA polymerase II Elongato\nr protein subunit,Null: Slow adaptation to growth on new med\nia; <br> ts- (39 oC); sensitive to 1 M NaCl; insensitive to \npGKL killer toxin\n mSMD1:Homolog of human core snRNP protein D1, involved in snRNA ma\nturation,,Null mutant is inviable\n mLEO1:Product of gene unknown,,Null mutant is viable\n mMON1:Product of gene unknown,,null mutant is sensitive to monensi\nn and brefeldin A\n mSNU114:involved in splicing,U5 snRNP-specific protein related to EF\n-2,Null mutant is inviable; growth inhibitory when over-expr\nessed; required for pre-mRNA splicing in vivo\n Cond884:10\n mCDC36:Required for Start B in mitosis and for meiosis I spindle po\nle body separation,basal transcription inhibitor , transcrip\ntional regulator , basal transcription inhibitor , transcrip\ntional regulator,Null mutant is viable, cdc36 mutant arrests\n in G(sub)1; forms shmoo morphology at restrictive temperatu\nre, arrests at pachytene at the mononucleate stage with dupl\nicated spindle pole bodies and no spindles\n mTAF10 mTAF6 mTAF9 mSPT16 mPOB3 mRPB3 mMED4
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Computational Genomics Lab, Tel-Aviv uniresity