Module number 3208




Database revision : gnsdb28.10
Date : Tue Feb 25 17:12:39 2003
How to read this figure?


mMRPL4:essential for mitochondrial function and for proper cell gro\nwth under non-respiratory conditions,ribosomal protein 60S L\n4,Null mutant is viable, fails to grow on nonfermentable car\nbon sources, has growth defects on fermentable carbon source\ns\n mYKR040C:Unknown ,, Unknown\n mYKL097C:Unknown ,, Unknown\n mYGL007W:Unknown ,, Unknown\n mYBR077C:Unknown ,, Unknown\n mYPL025C:Unknown ,, Unknown\n mYHR149C:Unknown ,, Unknown\n mYFR017C:Unknown ,, Unknown\n mYHR150W:Unknown ,, Unknown\n mYKL084W:Unknown ,, Unknown\n mYER079W:Unknown ,, Unknown\n mUIP5:Unknown ,, Unknown\n mCLB2:Involved in mitotic induction,B-type cyclin,Null mutant is v\niable (lethal in combination with clb1 mutation)\n mYDR526C:Unknown ,, Unknown\n mELO1:elongation enzyme 1, required for the elongation of the satu\nrated fatty acid tetradecanoic acid (14:0) to that of hexade\ncanoic acid (16:0),,Null mutant is viable, but shows no grow\nth on media supplemented with less than 16-C saturated fatty\n acid in a fatty acid synthase minus background\n mGDH3:Involved in glutamate biosynthesis,NADP-linked glutamate deh\nydrogenase,Null mutant is viable\n mYER078C:Unknown ,, Unknown\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mGIC1:Gtpase-interacting component 1,,Null mutant is viable; gic1 \ngic2 double null is temperature sensitive at 33 degrees C\n mYHR151C:Unknown ,, Unknown\n mSPO12:Thought to be a positive regulator of exit from M-phase in m\nitosis and meiosis; interacts with Dbf2p and Dbf20p protein \nkinases,20 kDa protein with negatively charged C-terminus re\nquired for function , positive regulator of exit from M-phas\ne in mitosis and meiosis (putative),sporulation defective; l\noss of function in mitosis results in delay in G2; loss of f\nunction in meiosis results in a prolonged pachytene stage an\nd presence of synaptonemal complexes, a single meiosis II-li\nke equational division at the time of meiosis II, and dyad a\nsci containing two diploid spores. Gain of function in mitos\nis suppresses M-phase anaphase arrest caused by overexpressi\non of CLB2 deg- and mutants (e.g. dbf2-ts). mRNA is cell cyc\nle regulated (with DBF2 ) in mitosis and increases 5-10x in \nmeiosis.\n mTSL1:123 kD regulatory subunit of trehalose-6-phosphate synthase/\nphosphatase complex; homologous to TPS3 gene product,similar\n to TPS3 gene product , trehalose-6-phosphate synthase/phosp\nhatase complex 123 kDa regulatory subunit,Null mutant is via\nble\n mECM33:ExtraCellular Mutant,,A Tn3 insertion into this gene causes \nhypersensitivity to the cell surface polymer perturbing agen\nt calcofluor white.\n mCDC6:Protein involved in initiation of DNA replication,pre-initia\ntion complex component,arrest at initiation of S phase\n mNCA3:With NCA2, regulates proper expression of subunits 6 (Atp6p)\n and 8 (Atp8p ) of the Fo-F1 ATP synthase,,Null mutant is vi\nable\n mYHL012W:Unknown ,, Unknown\n mLSM3:Like Sm-D2 protein,contains Sm-like domain; coprecipitates w\nith U4, U5 and U6 snRNAs , snRNP protein (putative) , contai\nns Sm-like domain; coprecipitates with U4, U5 and U6 snRNAs \n, snRNP protein (putative),Null mutant is inviable\n mYGR125W:Unknown ,, Unknown\n mTOS11:Hypothetical ORF,,\n mEXG1:Exo-1,3-beta-glucanase,exo-1,3-beta-glucanase,Null mutant is\n viable, displays modest increase in killer toxin sensitivit\ny and beta 1,6-glucan levels\n mCLN1:role in cell cycle START,G1 cyclin,Null mutant is viable, ex\nhibits G1 arrest\n mNDD1:Nuclear Division Defective 1,,Null mutant is inviable and ar\nrests prior to nuclear division but after DNA replication; c\nells are large budded with short mitotic spindles.\n mYKR043C:Unknown ,, Unknown\n mPPN1:Phosphate metabolism; transcription is regulated by PHO syst\nem,vacuolar polyphosphatase,Null mutant is viable and shows \naccumulation of long chain polyphosphate\n mNCE4:negative regulator of cts1 expression,,Null mutant is viable\n and suppresses the failure of an ace2 null to activate CTS1\n; also grows slowly at 37 C\n mCIS3:cik1 suppressor,similar to Hsp150p and Pir1p, Pir2p, and Pir\n3p,Null mutant is viable; CIS3 is a high copy suppressor of \ncik1 deletion mutants\n 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 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 mCWP2:major constituent of the cell wall containing GPI-anchor, pl\nays a role in stabilizing the cell wall, low pH resistance p\nrotein,cell wall mannoprotein,Null mutant is viable, display\ns increased sensitivity to Congo red, calcofluor white, and \nZymolyase\n mYMR144W:Unknown ,, Unknown\n mYOR246C:Unknown ,, Unknown\n mYHL013C:Unknown ,, Unknown\n mBAT2:Branched-Chain Amino Acid Transaminase,branched-chain amino \nacid transaminase,Null mutant is viable; ILV auxotrophy in b\nat1 bat2 double mutants\n mYNR018W:Unknown ,, Unknown\n mRNR1:ribonucleotide reductase,ribonucleotide reductase, large (R1\n) subunit,Null mutant is inviable\n mCUE4:Unknown ,, Unknown\n mYER189W:Unknown ,, Unknown\n mYML102C-A:Unknown ,, Unknown\n mSNA2:Unknown ,, Unknown\n mSRL1:Suppressor of rad53 lethality,,\n mYML053C:Unknown ,, Unknown\n mYHP1:Hypothetical ORF,,\n mRAX2:Involved in the maintenance of bipolar pattern,,Null mutant \nis defective in bipolar pattern\n mYOR315W:Unknown ,, Unknown\n mNUD1:Spindle pole body protein,,Null mutant is inviable\n mUTH1:Youth, involved in determining yeast longevity,,extension of\n yeast lifespan\n mFKS3:Protein with similarity to Gls1p and Gls2p (GB:Z49212),,\n
this is an automaticly generated SAMBA report
Computational Genomics Lab, Tel-Aviv uniresity