Module number 1169




Database revision : gnsdb28.10
Date : Tue Feb 25 17:45:38 2003
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mYGR269W:Unknown ,, Unknown\n mYNL319W:Unknown ,, Unknown\n mVPS71:Unknown ,, Unknown\n mYGR273C:Unknown ,, Unknown\n mMET32:Involved in methionine metabolism,highly homologous to Met31\np , transcriptional regulator of sulfur amino acid metabolis\nm , zinc finger protein,the met31 met32 double mutant is a m\nethionine auxotroph\n mBRE2:Product of gene unknown,,null mutant is sensitive to brefeld\nin A\n mPAD1:Phenylacrylic acid decarboxylase,phenylacrylic acid decarbox\nylase,Null mutant is viable but is cinnamic acid-sensitive\n mHFM1:C4 zinc finger DNA-binding protein of low sequence specifici\nty in vitro; Probable 119 kD DNA/RNA helicase family member,\nC4 zinc finger DNA-binding protein of low sequence specifici\nty in vitro; Probable 119 kDa DNA/RNA helicase family member\n,Null mutant is viable\n mSWM1:Spore Wall Maturation 1,,Null mutant completes meiotic nucle\nar division but does not show spore wall maturation\n mYDR438W:Unknown ,, Unknown\n Meiosis.Series0:The core meiotic transcriptome in budding yeasts. Nat Genet\n. 2000 Dec;26(4):415-23.\n mYDR326C:Unknown ,, Unknown\n mRAS1:ras proto-oncogene homolog,ras homolog,\n mDIT1:Disp. for spores & spore viability - required for dityrosine\n accumul. in the outer spore wall (s.w.), s.w. maturation & \nresist. to ether & lytic enzymes. Spore-autonomous function \nin heterozygotes. mRNA is trans. mid/late in s.w. formation,\nfirst enzyme in dityrosine synthesis in the outer layer of t\nhe spore wall pathway, converting L-tyrosine to N-formyl-L-t\nyrosine,lack outermost layer of spore wall\n mSMA1:Spore Membrane Assembly,,undergoes meiotic nuclear divisions\n but does not form spores\n mDIT2:Disp. for spores & spore viab. - required for dityrosine bio\nsynth. & dityrosine accumul. in outer spore wall (s.w.); s.w\n. matur. & resist. to ether & lytic enz. mRNA trans. mid/lat\ne during s.w. formation,catalyzes oxidation of N-formyl tyro\nsine to N,N-bisformyl dityrosine in vitro , cytochrome P450 \n56,lack outermost layer of spore wall\n mKAR3:kinesin-like nuclear fusion protein,kinesin-like nuclear fus\nion protein,Null mutant is viable, kar3 mutations prevent ka\nryogamy (nuclear fusion)\n mCLB3:Involved in mitotic induction and perhaps in DNA replication\n and spindle assembly,B-type cyclin,Null mutant is viable\n mSMA2:SPOrulation deficient,,Undergoes both meiotic nuclear divisi\nons without chromosome missegregation but fails to form spor\nes , undergoes meiotic nuclear divisions but does not form s\npores\n mFYV8:Function required for Yeast Viability on toxin exposure,,Nul\nl phenotype is K1 killer toxin hypersensitive\n mYBR063C:Unknown ,, Unknown\n mYKL121W:Unknown ,, Unknown\n mYLR030W:Unknown ,, Unknown\n mRNH70:RNase H(70), a 70 kDa ribonuclease H,ribonuclease H,Null mut\nant is viable.\n Cond940:6h\n mEKI1:Ethanolamine Kinase 1,ethanolamine kinase,Null mutant is via\nble\n mSGF29:SaGa associated Factor 29kDa,Probable 29kKDa Subunit of SAGA\n histone acetyltransferase complex,\n mYBL010C:Unknown ,, Unknown\n mISW2:has strong homology to Drosophila ISWI,ATPase component of a\n two subunit chromatin remodeling complex,Null mutant is via\nble, isw1 isw2 chd1 triple deletion mutants are syntheticall\ny temperature and formamide sensitive\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 Cond934:8h\n mYOR175C:Unknown ,, Unknown\n mMEK1:Disp. for chr. pairing & chr. condensation seen by in situ h\nybrid. Required for full double strand breaks, normal length\n synaptonemal complexes, meiotic recomb. & spore viability. \nmek1 is rescued by spo13 & in early recomb. function,meiosis\n-specific serine/threonine protein kinase,Null mutant is via\nble, however diploids homozygous for a mek1 null mutation pr\noduce only low percentages of viable spores, reduced spore v\niability is rescued by spo13 mutations\n Cond961:t7_g/r_ratio\n mHUL4:ubiquitin-protein ligase (E3),ubiquitin ligase (E3),Null mut\nant is viable\n mCCC1:Functions in the homeostasis of both calcium and manganese i\nons,transmembrane Ca2+ transporter (putative),Wild-type comp\nlements csg1 (calcium sensitive-group) mutants when overexpr\nessed\n mCDC16:a component of anaphase-promoting complex required for the G\n2/M transition in mitosis and degradation of mitotic cyclins\n, required for sporulation,metal-binding nucleic acid-bindin\ng protein, interacts with Cdc23p and Cdc27p to catalyze the \nconjugation of ubiquitin to cyclin B (putative),Null mutant \nis inviable. cdc16 mutants are unable to progress through th\ne G(sub)2/M transition, cell division cycle blocked at 36 de\ngrees C\n Cond935:10h\n mALG9:catalyzes the transfer of mannose from Dol-P-Man to lipid-li\nnked oligosaccharides,mannosyltransferase,accumulation of li\npid-linked Man6GlcNAc2; hypoglycosylation of secreted protei\nns\n mAPC5:subunit of the Anaphase Promoting Complex; all known APC sub\nunits co-immunoprecipitate with epitope-tagged Apc5,anaphase\n promoting complex (APC) subunit,Null mutant is inviable at \n25 C\n mYKR100C:Unknown ,, Unknown\n mYOR073W:Unknown ,, Unknown\n mAPC9:subunit of the Anaphase Promoting Complex,anaphase promoting\n complex (APC) subunit,Null mutant is viable at 37 C but sho\nw delay in entry into anaphase at 37 C\n mCRP1:Hypothetical ORF,Cruciform DNA binding protein,Null mutant i\ns viable and shows no growth defects\n mIRS4:Increased rDNA silencing,,Null mutant is viable and shows in\ncreased rDNA silencing\n mYKR089C:Unknown ,, Unknown\n mYDR117C:Unknown ,, Unknown\n Cond936:12h\n mNMT1:N-myristoyl transferase,N-myristoyl transferase,Null mutant \nis inviable\n mGAT4:very short and so far mRNA can't be detected,very short and \nso far mRNA can't be detected,being investigated\n mSIR1:repressor of silent mating loci,silent mating loci repressor\n,\n mDIN7:DNA-damage inducible gene,,\n mGDS1:involved in nuclear control of mitochondria,,Null mutant is \nviable, shows partial impairment of growth on medium contain\ning glycerol as the carbon source. Overexpxression suppresse\ns NAM9-1 glycerol deficient phenotype\n Sporulation.Series0:The transcriptional program of sporulation in budding yeast.\n Science. 1998 Oct 23;282(5389):699-705.\n Cond963:t11.5_g/r_ratio\n mKEL2:protein containing kelch repeats, similar to YHR158c and YPL\n263c,,The null mutant is viable.\n mAOR1:actin overexpression resistant,,Sensitive to NaCl and NaF at\n >35 deg. C.\n mIDS2:IME2-Dependent Signalling,,Null mutations reduce or abolish \nthe ability of IME2p to activate expression of early, middle\n, and late meiotic genes. Recessive and null ids2 mutants pr\nevent toxicity of Ime2p expression in rad52 haploids, but do\n not affect Ime2p polypeptide accumulation.\n mSEO1:Suppressor of Sulfoxyde Ethionine resistance,permease (putat\nive),\n mSWD1:YAR003W,,\n mCNB1:Type 2B protein phosphatase; regulatory B subunit of calcine\nurin,calcineurin regulatory B subunit , type 2B protein phos\nphatase , calcineurin regulatory B subunit , type 2B protein\n phosphatase,Null mutant is viable, Li+ and Na+ sensitive, c\nnb1 fks1 and cnb1 vma3 double mutants are inviable\n mYOR365C:Unknown ,, Unknown\n mYMR313C:Unknown ,, Unknown\n mVAM7:Regulator of vacuolar morphogenesis,heptad repeat motif , hy\ndrophilic protein,Null mutant is viable, exhibits prominent \nlarge vacuoles\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mCDC23:Required for mitosis and RNA synthesis,,unable to complete G\n(sub)2/M transition\n mYPT1:involved in the secretion pathway at the ER-to-Golgi step; r\nequired for sporulation,GTP-binding protein , ras homolog , \nsimilar to mammalian Rab1A protein,Null mutant is inviable, \nat non-permissive temp, ts and cs mutants accumulate ER memb\nranes and small vesicles, fail to process invertase and othe\nr secreted proteins, and show cytoskeletal defects; ypt1 cau\nses lethality during nitrogen starvation\n mCDC26:component of anaphase-promoting complex; required for ubiqui\ntination of Clb2p and Clb3p, is a nuclear protein, and is in\nduced by heat shock,,thermosensitive cell growth (lethal at \nhigh temperature)\n mYHL012W:Unknown ,, Unknown\n mSSP2:Sporulation Specific,,Null mutant is viable, fails to sporul\nate\n mMNE1:similar to Lucilia illustris mitochondria cytochrome oxidase\n,,\n mKIP1:Mitotic spindle assembly,kinesin related protein,Null mutant\n is viable; kip1 cin8 double deletion mutants are inviable\n mSMK1:involved in sporulation,MAP kinase,smk1 asci are defective i\nn organizing spore wall assembly and display enhanced sensit\nivity to enzymatic digestion, heat shock, and ether\n mYPT10:similar to Rab proteins and other small GTP-binding proteins\n,,\n mAUT1:Protein involved in autophagocytosis during starvation,,Null\n mutant is viable, defective in starvation-induced bulk flow\n transport of cytoplasmic proteins to the vacuole, exhibits \ndecreased survival rates during starvation, defective in pro\ntein degradation in the vacuoles induced by nitrogen starvat\nion, homozygous diploids fail to sporulate\n mYJR119C:Unknown ,, Unknown\n mDRS2:P-type ATPase, potential aminophospholipid translocase,P-typ\ne ATPase, potential aminophospholipid translocase , cation t\nransport (E1-E2) ATPase family member , P-type ATPase, poten\ntial aminophospholipid translocase , cation transport (E1-E2\n) ATPase family member,Null mutant is viable but cold sensit\nive with perturbed late Golgi function; drs2 arf1 double mut\nants are inviable.\n mRIF1:RAP1-interacting factor, involved in establishment of repres\nsed chromatin,RAP1-interacting factor,defective in telomeric\n silencing and telomere length regulation\n mPCT1:phosphorylcholine transferase; or cholinephosphate cytidylyl\ntransferase,cholinephosphate cytidylyltransferase , phosphor\nylcholine transferase,Null mutant is viable\n mHOT1:high osmolarity induced transcription,nuclear protein,osmost\nress hypersensitivity\n Cond960:t5_g/r_ratio\n mYND1:Yeast Nucleoside Diphosphatase,apyrase (NDPase/NTPase),Null \nmutant is viable but vanadate-resistant and hygromycin-sensi\ntive. The double mutant ynd1 gda1 exhibits slow growth and s\nubstantial defects in protein glycosylation and cell morphol\nogy.\n mVPS9:Required for Golgi to vacuole trafficking, shares similarity\n to mammalian ras inhibitors,,Null mutant is viable, exhibit\ns severe vacuolar protein sorting defects and is temperature\n sensitive\n mHXT12:High-affinity hexose transporter,hexose permease,\n Cond964:ndt80_delete_early_g/r_ratio\n mTRS33:Trapp subunit of 33 kDa,,Null mutant is viable\n mYKR007W:Unknown ,, Unknown\n Cond962:t9_g/r_ratio\n mYFL040W:Unknown ,, Unknown\n mSWM1 mCDC23 mCDC26 mCDC16 mAPC9 mAPC5
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Computational Genomics Lab, Tel-Aviv uniresity