Module number 760




Database revision : gnsdb28.10
Date : Tue Feb 25 17:07:18 2003
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mNUP53:Component of karyopherin docking complex of the nuclear pore\n complex,karyopherin docking complex component of the nuclea\nr pore complex,Null mutant is viable but disrupts Kap121 loc\nalization to the nuclear envelope.\n mDGA1:DiacylGlycerol Acyltransferase,Acyl-CoA : diacylglycerol acy\nltransferase,\n Cond717:t2-SSD1\n mBRR6:Unknown ,, Unknown\n Cond871:yhe710-ss\n Cond720:t0+SSD1,H44\n Cond716:t2+SSD1wt\n mUFD1:Ubiquitin fusion degradation protein,,Homozygous ufd1-1 muta\nnt diploids exhibit sporulation defects.\n Cond708:t0+SSD1\n Cond725:t4-SSD1,M31\n Cond711:t2+Vec\n Cond869:yhe711-30\n mYCR061W:Unknown ,, Unknown\n Cond870:yhe710-30\n mYGR093W:Unknown ,, Unknown\n mTAD1:Deaminates adenosine-37 to inosine in eukaryotic tRNA-Ala.,t\nRNA-specific adenosine deaminase subunit,Null mutant is viab\nle\n mNUP170:Component of yeast nuclear pore complex; may play a role in \nlocalizing specific nucleoporins to nuclear pore complex; Hi\ngh identity with Sc nucleoporin NUP157 & to mammalian nucleo\nporin Nup155p. Complemented with Nup155p,nuclear pore comple\nx subunit,Null mutant is viable; synthetically lethal with n\nup157, nup188, and pom152; changing NUP170 expression causes\n morphological abnormalities in nuclear envelope\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n Cond865:p40-ss\n mAHA1:Unknown ,, Unknown\n mYGR012W:Unknown ,, Unknown\n mFAB1:May regulate vacuole homeostasis; mutation causes pleiotropi\nc effects on nuclear migration and orientation and separatio\nn of mitotic chromosomes,1-phosphatidylinositol-3-phosphate \n5-kinase,Null mutant is temperature-sensitive, forms aploid \nand binucleate cells and has defects in vacuolar function an\nd morphology\n mYHR192W:Unknown ,, Unknown\n Cond867:ts19-30\n mCSL4:Represses the replication of double-stranded RNA viruses, pr\notecting the host from the otherwise lethal effects of the v\nirus,,Null mutant is inviable, csl4-1 exhibits double mutant\n inviability in combination with cbf1(cep1) deletion mutants\n Cond723:t2-SSD1,M31\n Cond864:ph2-ss\n Cond863:ms221-ss\n mYGL211W:Unknown ,, Unknown\n Cond724:t4+SSD1,H44\n mYGL198W:Unknown ,, Unknown\n mUBC9:ubiquitin-conjugating enzyme,ubiquitin-conjugating enzyme,Nu\nll mutant is inviable\n Cond713:t4+Vec\n mMRP1:shows allele-specific genetic interactions with pet122 and p\net123,37 kDa mitochondrial ribosomal protein,defective mitoc\nhondrial protein synthesis; absence of a and b type cytochro\nmes; reduced levels of mitochondrial 15 S rRNA; defective pr\nocessing of apocytochrome b intron; convert to rho- and rho0\n at high frequency\n COMP.:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mCUP2:Upregulates metallothionein (CUP1) expression in response to\n Cu2+,transcriptional activator,Null mutant is sensitive to \nCu2+\n mYLR243W:Unknown ,, Unknown\n Cond868:ts19-ss\n mCKB2:Casein kinase II, beta' subunit,Casein kinase II beta' subun\nit,Null mutant is viable\n mYDR466W:Unknown ,, Unknown\n Cond866:jk9-30\n Cond862:pm71-ss\n TorRama.Series0:Partitioning the transcriptional program induced by rapamyci\nn among the effectors of the Tor proteins. Curr Biol. 2000 D\nec 14-28;10(24):1574-81\n mYGL010W:Unknown ,, Unknown\n Cond709:t0+Vec\n mRRN3:Required for transcription of rDNA by RNA Polymerase I,DNA i\nndependent RNA polymerase I transcription factor,Null mutant\n is inviable\n mCDC50:cell division cycle mutant,,Null mutant is cold-sensitive an\nd sensitive to MMS and HU\n mCCT4:cytoplasmic chaperonin subunit required for actin cytoskelet\non assembly or function,,Null mutant is inviable; cct4 mutan\nt exhibit allele-specific non-complementing interactions wit\nh different act1 mutations; anc2-1 mutants contain abnormal \nand disorganized actin structures, are defective in cellular\n morphogenesis, and are hypersensitive to the microtubule in\nhibitor benomyl. Overexpression of wild-type Anc2p ameliorat\nes defects in actin organization and cell growth caused by a\nctin overproduction.\n
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Computational Genomics Lab, Tel-Aviv uniresity