Module number 1382




Database revision : gnsdb28.10
Date : Tue Feb 25 17:11:23 2003
How to read this figure?



mRPT4:Proteasome Cap Subunit,26S proteasome cap subunit component \n, ATPase , 26S proteasome cap subunit component , ATPase , 2\n6S proteasome cap subunit component , ATPase,Null mutant is \ninviable; ts mutant strain arrests as large-budded cells aft\ner 1, 2, 3 divisions with a G2 content of DNA and a monopola\nr spindle; unduplicated spindle pole body is enlarged as in \nother monopolar mutants; they also fail to arrest at G1 when\n starved for a single amino acid (but do arrest at G1 when d\neprived of all nitrogen), are resistant to cyclohexamide, an\nd are hypersensitive to amino acid analogs, hygromycin B and\n 3-aminotriazole\n mVPS70:Unknown ,, Unknown\n mCAK1:binds and phosphorylates Cdc28p,cyclin-dependent kinase-acti\nvating kinase,Null mutant is inviable; temperature-sensitive\n mutant confers a G2 delay accompanied by low Cdc28p protein\n kinase activity\n mRPT6:member of the 26 S proteasome,ATPase,Null mutant is inviable\n 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 Meiosis.Series0:The core meiotic transcriptome in budding yeasts.  Nat Genet\n. 2000 Dec;26(4):415-23.\n mGOD1:Unknown ,, Unknown\n mNSP1:Nucleoskeletal protein found in nuclear pores and spindle po\nle body,nuclear pore complex subunit,Null mutant is inviable\n.\n mTRS120:targeting complex (TRAPP) component involved in ER to Golgi \nmembrane traffic,,Null mutant is inviable\n Cond892:S\n Cond883:5\n mCDC4:Init. of DNA synthesis & spindle pole body separation; dispe\nnsable for both mitotic and meiotic spindle pole body dupl.;\n essential for mitotic but not premeiotic DNA synth.; wt lev\nels of synaptonemal complexes and intragenic recombination,u\nbiquitin ligase subunit,Null mutant is inviable. cdc4 mutant\ns arrest in meiosis at the mononucleate stage with duplicate\nd spindle pole bodies.\n mYTA12:Mitochondrial ATPase (similar to E. coli FtsH protein) that \nresides in the innner mitochondrial membrane,ATPase , CDC48/\nPAS1/SEC18 (AAA) family,Null mutant is viable, petite grossl\ny deficient in mitochondrial respiratory and ATPase complexe\ns, yet synthesizes all proteins encoded by mitochondrial DNA\n Cond890:G1\n Cond872:Zero1\n Cond940:6h\n Cond889:4NQO_2\n mYMR115W:Unknown ,, Unknown\n mRTF1:Directly or indirectly regulates the DNA-binding properties \nof Spt15p, the TATA box-binding protein, and the relative ac\ntivities of different TATA elements,nuclear protein,Null mut\nant is viable and can suppress TATA box-binding protein muta\nnts (SPT15) in an allele-specific fashion\n Cond897:STATMMS\n mSTE23:involved in a-factor processing,,effects a-factor secretion \nand mating by a cells\n mMDJ1:involved in protection against heat-induced protein aggregat\nion but not necessary for protein import into the mitochondr\nion,DnaJ homolog , involved in mitochondrial biogenesis and \nprotein folding,Null mutant is viable, displays a petite phe\nnotype, loss of mitochondrial DNA, and inviability at 37 deg\nrees C\n mYOR015W:Unknown ,, Unknown\n Cond894:G2\n mRPN1:Subunit of 26S Proteasome (PA700 subunit),26S proteasome PA7\n00 subunit,Null mutant is inviable; hrd2-1 mutation slows de\ngradation of Hmg2p. hrd2-1 strains are sensitive to canavani\nne and show a global accumulation of ubiquitin-conjugated pr\noteins, but are not temperature-sensitive\n Cond934:8h\n mABF1:transcriptional activator and ARS1 binding protein,ARS1 bind\ning protein , transcriptional activator , ARS1 binding prote\nin , transcriptional activator , ARS1 binding protein , tran\nscriptional activator,Null mutant is inviable\n mRPN12:Part of 26S proteasome complex that may activate Cdc28p,32-3\n4 kDa protein,Null mutant is inviable; nin1-1 mutant is temp\nerature-sensitive mutant that shows i) higher rates of recom\nbination and chromosome and plasmid loss; ii) greater sensit\nivity to UV irradiation; iii) at restrictive temperature, ar\nrest in G2, failure to activate histone H1 kinase, and accum\nulation of polyubiquinated proteins\n Cond893:SMMS\n mMAS1:mitochondrial processing protease subunit,mitochondrial proc\nessing protease subunit,Null mutant is inviable; Elevated mi\ntotic recombination and chromosomal missegregation when over\nproduced\n Cond59:erp4\n mAIP1:Protein localizes to actin cortical patches. Probable bindin\ng site on actin lies on front surface of subdomain 3 and 4.,\nactin cortical patch component,Null mutant is viable\n mPRE5:alpha-type of subunit of 20S proteasome,20S proteasome alpha\n-type subunit,Null mutant is inviable\n mSIN3:DNA binding protein involved in transcriptional regulation,D\nNA binding protein , involved in transcriptional regulation \n, DNA binding protein , involved in transcriptional regulati\non , DNA binding protein , involved in transcriptional regul\nation , DNA binding protein , involved in transcriptional re\ngulation , DNA binding protein , involved in transcriptional\n regulation , DNA binding protein , involved in transcriptio\nnal regulation,inviable, reduced potassium dependency\n Cond895:G2MMS\n Cond879:MMC\n COMP.KO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n Cond877:MMS\n Cond875:60min\n mQNS1:Hypothetical ORF,,\n Cond886:g-ray\n mNUP2:Localizes to discrete spots in the nuclear envelope; probabl\ny functions in transport through nuclear pore,nuclear pore c\nomplex subunit,Null mutant is viable; some combinations of a\nlleles of nup1, nsp1 and nup2 are synthetically lethal\n mYKL195W:Unknown ,, Unknown\n mIMH1:Product of gene unknown,,Null mutant is viable; imh1 ypt6 do\nuble disruption causes growth inhibition\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mUBA1:ubiquitin activating enzyme, similar to Uba2p,ubiquitin acti\nvating enzyme, similar to Uba2p,Null mutant is inviable\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 mDOP1:homolog of Emericella nidulans developmental regulatory gene\n, dopey (dopA).,,essential gene\n mFAD1:Flavin adenine dinucleotide (FAD) synthetase, which performs\n second step in synthesis of FAD from riboflavin,FAD synthet\nase,Null mutant is inviable\n mYLR290C:Unknown ,, Unknown\n mTAF6:TATA-binding protein-associated-factor,TATA-binding protein-\nassociated-factor,Null mutant is inviable\n Cond876:zero2\n Cond885:20\n mMAI1:Unknown ,, Unknown\n mTFC3:transcription factor tau (TFIIIC) subunit 138,138 kDa , tran\nscription factor tau (TFIIIC) subunit , 138 kDa , transcript\nion factor tau (TFIIIC) subunit,Null mutant is inviable\n Cond891:G1MMS\n Cond881:4NQO\n mYGL226W:Unknown ,, Unknown\n mYPT52:rab5-like GTPase involved in vacuolar protein sorting and en\ndocytosis,,Null mutant is viable; ypt51 ypt52 double deletio\nn exacerbates the temperature sensitivity and vacuolar prote\nin sorting defects of ypt51 deletion\n mMVP1:Protein required for sorting proteins to the vacuole,,MVP1 w\nas identified as a multicopy suppressor of dominant-negative\n vps1 mutations, as well as an extragenic suppressor of a te\nmperature-sensitive pma1 mutation (sop gene)\n mHLJ1:Homologous to E coli dnaJ protein,,\n mBNA6:Unknown ,, Unknown\n Cond938:2h\n mUGT51:Udp-glycosyltransferase,UDP-glucose:sterol glucosyltransfera\nse,Null mutant is viable and unable to synthesize sterol glu\ncoside\n mVPS30:Required for sorting and delivery of soluble hydrolases to t\nhe vacuole.,,Vacuolar hydrolases sorting receptor Vps10p is \nmislocalized in vps30 mutants.\n mPHB2:Possible role in aging,mammalian BAP37 and S. cerevisiae Phb\n1p homolog , prohibitin homolog,Null mutant is viable, exhib\nits a slightly decreased lifes span; phb1 phb2 double deleti\non mutants exhibit a more decreased replicative lifespan and\n a defect in mitochondrial membrane potential\n Cond884:10\n mRPT6 mRPT4

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