Module number 689




Database revision : gnsdb28.10
Date : Tue Feb 25 17:05:52 2003
How to read this figure?


mREV1:Protein required for mutagenesis by physical and chemical ag\nents,deoxycytidyl transferase,Null mutant is viable, exhibts\n decreased revertibility\n Cond698:gal3-gal\n Cond700:gal5-gal\n mYBR051W:Unknown ,, Unknown\n mSLK19:synthetic lethal KAR3,leucine zipper (putative),Null mutant \nexibits long astral microtubules, short spindles, bypass mei\nosis I, partial mitotic arrest; synthetic lethal with kar3*,\n loss of both produces mitotic arrest\n mSIT1:Siderophore Iron Transport,ferrioxamine B permease,Viable. C\nells deleted from the gene are unable to take up ferrioxamin\ne B\n COMP.KO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n gala.+gal:Integrated genomic and proteomic analyses of a systematicall\ny perturbed metabolic network. Science. 2001 May 4;292(5518\n):929-34.\n mALD4:Glucose repressed. Utilizes NADP+ or NAD+ as a coenzyme equa\nlly well. (sold by SIGMA under the catalogue number A5550, a\nccording to A. Blomberg).,aldehyde dehydrogenase,\n Cond62:fpr1\n mKAP120:karyopherin,karyopherin,\n Cond185:ubr2\n gala.-gal:Integrated genomic and proteomic analyses of a systematicall\ny perturbed metabolic network. Science. 2001 May 4;292(5518\n):929-34.\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mDLD1:mitochondrial enzyme D-lactate ferricytochrome c oxidoreduct\nase,D-lactate ferricytochrome c oxidoreductase,Null mutant i\ns viable and cannot grow on media containing lactate as the \nsole carbon source\n mZDS2:multicopy suppressor of a sin4 defect,,Null mutant is viable\n; zds1 zds2 double deletion causes slow growth and defects i\nn bud morphology and cell cycle progression\n mFIT2:Facilitator of iron transport,Cell wall protein involved in \niron transport,impaired siderophore-iron uptake, activation \nof the major iron -dependent transcription factor, AFT1\n mTOP2:dispensable for premeiotic DNA synthesis and recombination, \nbut required for meiosis I,topoisomerase II,Null mutant is i\nnviable; top2 mutants arrest at the mononucleate stage, Rec-\n mutants suppress the meiosis I block, suggesting TOP2 resol\nves recombinant chromosomes\n Stress.Carbon:Genomic expression programs in the response of yeast cells t\no environmental changes. Mol Biol Cell. 2000 Dec;11(12):424\n1-57\n Cond687:gal1+gal\n mRAD50:coiled-coil protein, contains a purine-binding domain, two h\neptad repeats and a hydrophobic tail,Mre11-Rad50-Xrs2 protei\nn complex member involved in joining double-stranded breaks \nand DNA recombination,Null mutant is viable but defective fo\nr X-ray damage repair, sporulation, chromosome pairing, form\nation and processing of DS breaks, gene conversion and recip\nrocal recombination in non-rDNA, tripartite synaptonemal com\nplexes and heteroduplex DNA. Exhibits blocked meiotic recomb\nination and formation of synaptonemal complex at early stage\ns. rad50-1 or null is rescued by spo13 and rescues rad52 spo\n13.\n Cond706:gal2gal80-gal\n mYPL216W:Unknown ,, Unknown\n Cond702:gal7-gal\n Cond696:gal1-gal\n mISF1:May regulate NAM7 function, possibly at level of mRNA turnov\ner,,Null mutant is viable; overexpression suppresses defects\n in hap2, hap3, and hap3 mutants; isf1 mbr1 double mutant ha\ns synthetic phenotypes\n mYIL057C:Unknown ,, Unknown\n Cond690:gal4+gal\n Cond705:gal1gal10+gal\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 Cond701:gal6-gal\n Cond449:glucose_vs._reference_pool_car-1\n Cond693:gal7+gal\n mYNL018C:Unknown ,, Unknown\n
this is an automaticly generated SAMBA report
Computational Genomics Lab, Tel-Aviv uniresity