Module number 3273




Database revision : gnsdb28.10
Date : Tue Feb 25 17:23:12 2003
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mYDR049W:Unknown ,, Unknown\n mAGE1:ADP-ribosylation factor (ARF) GTPase activating protein (GAP\n) effector,ARF GAP with effector function(s),Null mutant is \nviable\n mHSE1:Unknown ,, Unknown\n mVPS71: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 mSAP30:Hypothetical ORF,,\n mSET5:,,\n mYKL037W:Unknown ,, Unknown\n mSIP3:Interacts with SNF1 protein kinase,transcriptional activator\n (putative),Null mutant is viable; does not confer snf1 phen\notypes\n mYDR326C:Unknown ,, Unknown\n mELM1:cell morphology,protein kinase,formation of expanded, branch\ned chains of elongated cells; grow invasively under the surf\nace of agar medium\n mBEM3:Gtpase-activating protein activity toward the essential bud-\nsite assembly GTPase Cdc42,rho GTPase activating protein (GA\nP),Null mutant is viable.\n mYGL231C:Unknown ,, Unknown\n mDFG16:Involved in cell wall maintenance, filamentous growth,,Null \nmutant is viable, a Tn3 insertion into this gene causes hype\nrsensitivity to the cell surface polymer perturbing agent ca\nlcofluor white.\n mMNN2:Probable type II membrane protein involved in mannan synthes\nis,golgi alpha-1,2-mannosyltransferase (putative),Null mutan\nt is viable. Mannan lacks the main alpha-1,2-linked branches\n mKAR9:cortical protein required for cytoplasmic microtubule orient\nation; localizes to the tip of shmoo projections and to the \ntip of budding cells in a cell-cycle dependent manner,,Null \nmutant is viable; cytoplasmic microtubule orientation defect\ns, nuclear migration defects, benomyl sensitive\n mMNN5:mannan synthesis,golgi alpha-1,2-mannosyltransferase (putati\nve),Null mutant is viable but defective in addition of the a\nlpha-1,3-linked mannose branch to the mannan structure found\n on N-linked glycans.\n mLSM1:Like Sm protein; the finding that Lsm1 contains the Sm conse\nnsus motifs and most closely resembles Sm-B has been controv\nersial (Fromont-Racine et al, 1997 Nature Genetics 16:277-28\n2, and Bertrand Seraphin, personal communication).,,Null mut\nant is viable but grows slowly at 23deg and 30deg, and is re\nquired for growth at 37deg; absence of LSM1p leads to the ac\ncumulation of deadenylated capped mRNAs and also suppresses \na PAB1 deletion.\n mRCY1:Unknown ,, Unknown\n mYOR051C:Unknown ,, Unknown\n mYNR029C:Unknown ,, Unknown\n mDCW1:Unknown ,, Unknown\n mGPM2:Similar to GPM1 (phosphoglycerate mutase); converts 3-phosph\noglycerate to 2-phosphoglycerate in glycolysis,,Null mutant \nis viable, gpm2 gpm3 double deletion mutants exhibit no synt\nhetic phenotypes\n mNPR2:Putative post-transcriptional regulator of nitrogen permease\ns,,Changes in urea and proline transport capacities\n mHOC1:Homologous to OCH1, an alpha-1,6-mannosyltransferase; Golgi-\nlocalized, type II integral membrane protein,mannosyltransfe\nrase (putative),Null mutant is viable but is hypersensitive \nto calcofluor white and hygromycin B and has lowered restric\ntive temperature in a pkc1-371 background; high copy suppres\nsor of pkc1-371\n mYDR203W:Unknown ,, Unknown\n mGAL1:Haploid specific protein localized in the Golgi and plasma m\nembrane,galactokinase,Null mutant is viable and cannot utili\nze galactose.\n mALG5:UDP-glucose:dolichyl-phosphate glucosyltransferase,UDP-gluco\nse:dolichyl-phosphate glucosyltransferase,underglycosylation\n of carboxypeptidase Y\n mYHR155W:Unknown ,, Unknown\n mALG6:Required for glucosylation in the N-linked glycosylation pat\nhway,glucosyltransferase,Null mutant is viable and defective\n in protein glycosylation.\n mYKL075C:Unknown ,, Unknown\n mVPS13:vacuolar Protein Sorting,,Null mutant is viable but exhibits\n defects in vacuolar protein sorting.\n mSAC7:Suppressor of actin mutation,GTPase activating protein (GAP)\n for RHO1,null mutant is viable, has growth and actin assemb\nly defects at low temperatures, displays allele-specific sup\npression and double mutant lethality with actin mutations, s\nuprresses tor mutations\n mALG8:adds glucose to the dolichol-linked oligosaccharide precurso\nr prior to transfer to protein,glycosyl transferase,Null mut\nant is viable, secretes under-glycosylated proteins\n mYHP1:Hypothetical ORF,,\n mWSC2:cell wall integrity and stress response component 2,contains\n novel cysteine motif , integral membrane protein (putative)\n , similar to SLG1 (WSC1), WSC3 and WSC4,Null mutant is viab\nle and shows no phenotypes; slg1 (wsc1)-null wsc2-null doubl\ne mutant shows a lysis defect on YPD at room temperature and\n heat shock sensitivity; overexpression of WSC genes suppres\nses heat shock sensitivity of hyperactivated ras mutant; hea\nt shock sensitivity of wsc mutant strain is suppressed by de\nletion of ras2\n mCDC50:cell division cycle mutant,,Null mutant is cold-sensitive an\nd sensitive to MMS and HU\n mRPL18B:Homology to rat ribosomal protein L18,ribosomal protein L18B\n (rp28B),\n mCNE1:Functions in endoplasmic reticulum protein quality control,c\nalnexin and calreticulin homolog,Null mutant is viable, incr\nease of cell-surface expression of ste2-3p, increase in secr\netion of heterologously expressed mammalian alpha 1-antitryp\nsin\n mSRN2:Suppressor of rna1-1 mutation,,Null mutant is viable\n mYER119C-A:Unknown ,, Unknown\n mIRS4:Increased rDNA silencing,,Null mutant is viable and shows in\ncreased rDNA silencing\n mYBL083C:Unknown ,, Unknown\n mBSD2:metal homeostasis protein; putative membrane protein,,Null m\nutant is viable; suppressor of oxygen toxicity in sod1 mutan\nts, increased sensitivity to copper and cadmium toxicity, el\nevation in copper ion accumulation\n mMED1:Subunit 1 of the Mediator complex essential for transcriptio\nnal regulation,essential for transcriptional regulation , me\ndiator complex subunit 1,Defects in both repression and indu\nction of GAL genes; supresses loss of the Snf1 kinase\n mYGR206W:Unknown ,, Unknown\n mYKR035C:Unknown ,, Unknown\n mYBR108W:Unknown ,, Unknown\n mYMR102C:Unknown ,, Unknown\n mYJL162C:Unknown ,, Unknown\n mCYK3:involved in CYtoKinesis,,Null mutant is viable, exhibits slo\nw growth, mild cytokinesis defects, and aberrant mother-bud \nneck morphology. cyk3/hof1 and cyk3/myo1 double mutants are\n inviable\n mMRS2:mitochondrial magnesium ion transporter similar to bacterial\n CorA, essential for splicing of group II introns,magnesium \nion transporter,Null mutant is viable; has a pet- phenotype,\n associated with a block in mitochondrial RNA splicing of al\nl mitochondrial group II introns\n mYKL033W-A:Unknown ,, Unknown\n mFZF1:involved in sulfite resistance,contains five zinc fingers , \ntranscription factor (putative) , contains five zinc fingers\n , transcription factor (putative),Null mutant is viable, su\nlfite sensitive. FZF1 is a high copy suppressor of grr1 muta\nnts\n mYDR357C:Unknown ,, Unknown\n mVPS20:vaculolar protein sorting (putative),,Null mutant is viable \nbut is a class E vps mutant (missorts vacuolar hydrolases an\nd accumulates late endosomal compartment).\n mVPS21:Rab5-like GTPase involved in vacuolar protein sorting and en\ndocytosis post vesicle internalization; geranylgeranylated; \ngeranylgeranylation required for membrane association,small \nGTP-binding protein,Null mutant is viable, temperature-sensi\ntive, missorts multiple vacuolar proteins, accumulate 40-50 \nnm vesicles, and contain a large vacuole\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mSCP160:May be required during cell division for faithful partitioni\nng of the ER-nuclear envelope membranes, involved in control\n of mitotic chromsome transmission,,Null mutant is viable, b\nut exhibits decreased viability, abnormal morphology, and in\ncreased DNA content.\n mBRO1:BCK1-like resistance to osmotic shock,,Temperature-sensitive\n growth defect, sensitive to caffeine and respond abnormally\n to nutrient limitation at the permissive temperature\n mVPS24:involved in secretion,,Null mutant missorts vacuolar hydrola\nses and accumulates a late endosomal compartment; Class E vp\ns mutant\n mVPS25:vacuolar protein sorting (putative),,Null mutant is viable b\nut a class E vps mutant (missorts vacuolar hydrolases and ac\ncumulates late endosomal compartment vacuolar hydrolases and\n accumulates a late endosomal compartment).\n mKRE11:Involved in biosynthetic pathway for cell wall beta-glucans,\n,Null mutant is viable; killer toxin resistant; reduced leve\nls of 1,6-beta-glucan in cell wall\n mVAB2:Vac8p binding protein of 31 kDa,,\n mGIT1:permease involved in the uptake of glycerophosphoinositol (G\nroPIns),permease involved in the uptake of glycerophosphoino\nsitol (GroPIns),Null mutant is viable, exhibits decreased Gr\noPIns transport\n mVPS27:hydrophilic protein; has cysteine rich putative zinc finger \nesential for function,cysteine rich putative zinc finger ess\nential for function , hydrophilic protein , cysteine rich pu\ntative zinc finger essential for function , hydrophilic prot\nein , cysteine rich putative zinc finger essential for funct\nion , hydrophilic protein , cysteine rich putative zinc fing\ner essential for function , hydrophilic protein , cysteine r\nich putative zinc finger essential for function , hydrophili\nc protein , cysteine rich putative zinc finger essential for\n function , hydrophilic protein,required for membrane traffi\nc to the vacuole\n mYOS9:Unknown ,, Unknown\n mVPS28:soluble, hydrophilic protein involved in transport of precur\nsors for soluble vauolar hydrolases from the late endosome t\no the vacuole,,Null mutant is viable, shows moderate defects\n in both biosynthetic traffic and endocytic traffic destined\n for the vacuole\n mYKL061W:Unknown ,, Unknown\n mPOL32:Polymerase-associated gene,55 kDa , DNA polymerase delta sub\nunit,Null mutant is viable but is cold-sensitive, hydroxyure\na-sensitive, defective for induced mutagenesis, synthetic le\nthal with pol3, pol30 and pol31\n mYKL207W:Unknown ,, Unknown\n mSPF1:Sensitivity to a killer toxin (SMK toxin) produced by Pichia\n farinosa,P-type ATPase,The null mutant is viable and resist\nant to the SMK toxin, but grows slowly and has glycosylation\n defects.\n mYCL005W:Unknown ,, Unknown\n mEPS1:Hypothetical ORF,,\n mYPR061C:Unknown ,, Unknown\n mSTB3:binds Sin3p in two-hybrid assay,,Null mutant is viable\n mVPS4:Defective in vacuolar protein sorting; homologous to mouse S\nKD1 and to human hVPS4,AAA ATPase,Null mutant is viable, exh\nibits protein sorting and morphological defects\n mYPR170C:Unknown ,, Unknown\n mVPS5:vacuolar Protein Sorting Defective; Golgi retention and vacu\nolar protein sorting,simialr to sorting nexin I,Null mutant \nis viable, missort and secrete soluble vacuolar proteins, co\nntain fragmented vacuoles and mislocalize carboxypepsidase a\nnd Vps10p.\n mYDR466W:Unknown ,, Unknown\n mSTP22:Ste pseudorevertant; required for vacuolar targeting of temp\nerature-sensitive plasma membrane proteins; homologous to th\ne mouse and human Tsg101 tumor susceptibility gene; mutants \nexhibit a Class E Vps phenotype.,,\n mVPS8:involved in vacuolar protein sorting; required for localizat\nion and trafficking of the CPY sorting receptor,membrane-ass\nociated hydrophilic protein which contains a C-terminal cyst\neine-rich region that conforms to the H2 variant of the RING\n finger Zn2+ binding motif,Null mutant is viable, missorts a\nnd secretes vacuolar hydrolases, overexpression of VPS21 par\ntially suppresses vps8 null\n mRIM13:calpain-like protease involved in proteolytic processing of \nRim1p,cysteine protease , similar to E. nidulans palB,Mutant\n shows reduced expression of IME1, defect in Rim1p C-termina\nl proteolytic processing, reduced sporulation, slow growth a\nt 17 degrees, smooth colony morphology and slow growth in al\nkaline medium (pH8.0).\n mFIS1:Involved in mitochondrial division,outer mitochondrial membr\nane protein required to localize Dnm1p and Mdv1p during mito\nchondrial division,Null mutant is viable, mitochondrial fiss\nion blocked, mitochondrial membranes form nets\n mMAK31:Like Sm protein; member of the Sm protein family, though sli\nghtly divergent because Mak31/Lsm9p does not contain a glyci\nne or cysteine at amino acid 107.,,Mutant exhibits defects i\nn the structural stability of L-A family of dsRNA-containing\n viral particles.\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 mDCR2:Unknown ,, Unknown\n mSNT1:,,\n mLCB3:Protein involved in incorporation of exogenous long chain ba\nses in sphingolipids,plasma membrane transporter (putative),\nNull mutant is viable, has reduced rate of exogenous long ch\nain base incorporation into sphingolipids, increased resista\nnce to growth inhibition by long chain bases\n mGTS1:Protein homologous to Drosophila clock protein,glycine-threo\nnine-serine repeat protein,Null mutant is viable; shows redu\nced lag phase\n mNBP2:interacts with Nap1, which is involved in histone assembly,,\n mYNL043C:Unknown ,, Unknown\n mKRE20:Killer toxin REsistant,,Null mutant is viable but exhibits K\n1 killer toxin resistance.\n mMYO5:contains proline-rich tail homology 2 (TH2) and SH3 domains,\nmyosin I,Null mutant is viable; myo3 myo5 double deletion mu\ntants exhibit loss of actin polarity, growth arrest at 37 de\ngrees or high osmotic strength, accumulation of intracellula\nr membranes, and loss of polarized cell surface growth; myo3\n myo5 double mutants have longer doubling times and thicker \ncell walls\n mVPS36:Defective in vacuolar protein sorting,,\n mVPS38:involved in vacuolar protein targeting,,\n mVTH1:vps ten homolog,potential membrane glycoprotein (putative) ,\n strong similarity to Vth2 and Pep1/Vps10,Null mutant is via\nble; overexpression partially suppresses the sorting defect \nof a pep1 null mutant.\n mYUR1:Probable glycosyltransferase of KRE2/KTR1/YUR1 family; locat\ned in the Golgi,mannosyltransferase,Null mutant is viable\n mPSH1:Unknown ,, Unknown\n mYAP3:bZIP protein; transcription factor,,\n mPRK1:p53 regulatory kinase,serine/threonine kinase (putative),Nul\nl mutant is viable. Strains that overexpress Prk1 are inviab\nle.\n mHOM6:catalyzes third step in common pathway for methionine and th\nreonine biosynthesis,L-homoserine:NADP oxidoreductase , homo\nserine dehydrogenase,Homoserine requiring\n mDIP5:dicarboxylic amino acid permease,dicarboxylic amino acid per\nmease,Null mutant is viable, exhibits loss of L-aspartate an\nd L-glutamate uptake\n mYNR068C:Unknown ,, Unknown\n mYGL045W:Unknown ,, Unknown\n mRPL20A:Homology to rat L18a,ribosomal protein L20A (L18A),\n mYBL006C:Unknown ,, Unknown\n mBBC1:shows synthetic fitness defect with bni1 mutants and associa\ntes with the Bee1p-Vrp1p-Myo3/5p complex,,\n mMDM39:Unknown ,, Unknown\n mYGR164W:Unknown ,, Unknown\n mRIM20:Unknown ,, Unknown\n mVTA1:Unknown ,, Unknown\n mRIM21:Unknown ,, Unknown\n mMAL11:Part of MAL1 complex locus; encodes funct. maltose permease \nin all strains, exhibits sign. seq. variability; shows homol\n. to functional maltose permease from S. carlsbergenesis; me\nmber of the 12 tm domain superfamily of sugar transporters,a\nlpha-glucoside transporter , hexose transporter , maltose pe\nrmease,Mutant is defective in maltose fermentation.\n mCWH43:,,\n mYGL242C:Unknown ,, Unknown\n mYDR105C:Unknown ,, Unknown\n mYPL176C:Unknown ,, Unknown\n mYCK2:membrane-bound casein kinase I homolog,casein kinase I homol\nog,Null mutant is viable; yck1 yck2 double deletion mutant i\ns inviable\n mSMI1:Protein involved in (1,3)-beta-glucan synthesis, possibly th\nrough regulation of cell wall glucan and chitin synthesis; c\nhromatin binding protein,57 kDa nuclear protein,Null mutant \nis viable, shows osmotic sensitivity, sensitivity to cercosp\noramide, resistance to zymolase; temperature sensitive mutan\nt arrests at S phase with small buds\n mKIN3:protein kinase,protein kinase,Null mutant is viable\n mEND3:Required for endocytosis and organization of the cytoskeleto\nn,,Null mutant is viable and defective in endocytosis\n mSNF7:Involved in derepression of SUC2 in response to glucose limi\ntation,,Null mutant is viable. Similar to disruption SNF8, S\nNF7 disruption causes a fewfold decrease in invertase derepr\nession, a growth defect on raffinose, temperature-sensitive \ngrowth on glucose, and a sporulation defect in homozygous di\nploids. Genetic interactions suggest SNF7 is different from \nSNF2, SNF5 and SNF6, members of the SNF/SWI chromatin remode\nling complex\n mSNF8:appears to be functionally related to SNF7,,Null mutant is v\niable, sporulation defective, grows poorly on raffinose as a\n carbon source, shows a five-fold decrease in invertase dere\npression\n mYBL086C:Unknown ,, Unknown\n mTHR1:homoserine kinase,homoserine kinase,Null mutant is viable, t\nhreonine auxotroph\n mAAT2:aspartate aminotransferase, cytosolic,aspartate aminotransfe\nrase,\n mYOR164C:Unknown ,, Unknown\n mYGL046W:Unknown ,, Unknown\n mCCW12:Hypothetical ORF,cell wall mannoprotein,Null mutant is viabl\ne and shows decrease in mating efficiency and defect in aggl\nutination\n mYIL077C:Unknown ,, Unknown\n mSWR1:Sick With Rat8 ts,RNA helicase (putative) , deah box protein\n,Null mutant is viable and shows no growth defects; swr1 rat\n8-2 double mutant has a slow growth phenotype; SWR1 is a par\ntial High copy suppressor of pse1-1 kap123\n mYLR126C:Unknown ,, Unknown\n mCDC10:cell division cycle blocked at 36 degree C,septin,abnormal c\nell-wall deposition and bud growth, inability to complete cy\ntokinesis, failure to form the ring of 10nm filaments in the\n neck region of budding cells\n mSWC1:Unknown ,, Unknown\n mARP1:actin-related protein of the dynactin complex,,Null mutant i\ns viable, but both null mutations and overexpression lead to\n defects in spindle orientation and nuclear migration\n mYLR111W:Unknown ,, Unknown\n mARP6:actin-related protein,,\n mOPI3:Second and third steps of methylation pathway for phosphatid\nylcholine biosynthesis,methylene-fatty-acyl-phospholipid syn\nthase (unsaturated phospholipid N-methyltransferase),Null mu\ntant is viable, temperature sensitive in the presence of mon\nomethylethanolamine, exhibits an inositol secretion phenotyp\ne\n mYOR091W:Unknown ,, Unknown\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 mSIN4:involved in positive and negative regualtion of transcriptio\nn, possibly via changes in chromatin structure,RNA polymeras\ne II holoenzyme/mediator subunit,Null mutant is viable, temp\nerature sensitive, displays defects in both positive and neg\native regulation of transcription, suppresses Ty insertion m\nutations (Spt-), exhibits decreased superhelical density of \ncircular DNA molecules, exhibits expression from promoters l\nacking UAS elements; associated with a defect in RME1-depend\nent repression and a methionine or cysteine requirement, exh\nibits flocculant/lacy colony morphology, suppressor of snf/s\nwi mutations\n mWHI2:Protein involved in growth regulation,,Null mutant is viable\n mYER084W:Unknown ,, Unknown\n mSGT2:small glutamine-rich tetratricopeptide repeat containing pro\ntein,,\n mPSY1:Unknown ,, Unknown\n mYNR040W:Unknown ,, Unknown\n mPSY3:Unknown ,, Unknown\n mCHS5:Involved in chitin synthase III activity, also required for \nhomozygosis in the first stages of mating,,Null mutant is vi\nable, cells exhibit a strong mating defect; sensitive to Cal\ncofluor, reduced amount of chitin in the cell wall\n mMRPL13:mitochondrial ribosomal protein YmL13,ribosomal protein (YmL\n13),Null mutant is viable, grows poorly on non-fermentable c\narbon sources\n mYIL041W:Unknown ,, Unknown\n mAOR1:actin overexpression resistant,,Sensitive to NaCl and NaF at\n >35 deg. C.\n mYNR005C:Unknown ,, Unknown\n mMNL1:mannosidase like,,\n mRPL15B:Homology to rat L15,ribosomal protein L15B (YL10) (L13B) (rp\n15R),\n mYJR111C:Unknown ,, Unknown\n mBUD14:Hypothetical ORF,,Null mutant is viable; random budding in d\niploid null mutants\n mTRM1:N2,N2-dimethylguanosine-specific tRNA methyltransferase,N2,N\n2-dimethylguanosine-specific tRNA methyltransferase,An uncha\nracterized allele affects a specific base modification of bo\nth cytoplasmic and mitochondrial tRNA.\n mVPS60:vacuolar protein sorting (putative),,Null mutant is viable b\nut a class E vps mutant (missorts vacuolar hydrolases and ac\ncumulates late endosomal compartment).\n mCAJ1:Homologous to E. coli DnaJ; contains leucine zipper-like mot\nif,,\n mYJL064W:Unknown ,, Unknown\n mITC1:Imitation switch Two Complex 1,,Null mutant is viable, but s\nhows abnormal morphology and reduced mating efficiency when \nthe disruption is in a MATalpha background. \n mRIM9:Regulator of Rim1p, required for IME1 expression,,Null mutan\nt is viable but displays reduced sporulation (due to defect \nin proteolytic processing of Rim1p) and smooth colony morpho\nlogy; haploid grows slowly at low temperature and is defecti\nve in invasive growth; RIM1, 8,9 and 13 act in a single path\nway (RIM1 pathway) functioning in parallel to MCK1 by epista\nsis analysis\n mSCJ1:dnaJ homolog,DnaJ homolog,Null mutant is viable but exhibits\n defects in protein sorting and sensitivity to tunicamycin.\n mYLR374C:Unknown ,, Unknown\n mDUN1:DNA damage response,protein kinase,Null mutant is viable, de\nfective in DNA damage repair and in DNA damage-resposive ind\nuction of RNR genes, and sensitive to DNA damaging agents\n mCOG7:Unknown ,, Unknown\n mKRE1:cell wall beta-glucan assembly,,Null mutant is viable, exhib\nits reduction in cell wall (1--6)-beta-glucan\n mCOG8:Unknown ,, Unknown\n mPHO13:p-nitrophenyl phosphatase,p-nitrophenyl phosphatase,Null mut\nant is viable\n mEGD1:beta subunit of the nascent-polypeptide-associated complex (\nNAC); homologous to human BTF3b; GAL4 enhancer protein,pol I\nI transcribed genes regulator,Null mutant is viable; reduced\n induction of galactose-regulated genes upon shift from gluc\nose to galactose\n mDID2:Doa4-independent degradation; Rad52 Inhibitor (Fifty Two Inh\nibitor),class E vacuolar-protein sorting and endocytosis fac\ntor,Overexpression causes growth inhibition and G2 arrest in\n rad52 and cdc9 mutants; null mutants are canavanine-hyperse\nnsitive, temperature sensitive, and suppress defects associa\nted with loss of DOA4\n mCUE1:Cue1p assembles with Ubc7p. Cue1p recruits Ubc7p to the cyto\nsolic surface of the endoplasmic reticulum. Assembly with Cu\ne1p is a prerequisite for the function of Ubc7p,Ubc7p bindin\ng and recruitment protein,Null mutant is viable and shows st\nabilization of ER degradation substrates\n mGEF1:Integral membrane protein highly homologous to voltage-gated\n chloride channels from humans, mice and fish,transport prot\nein involved in intracellular iron metabolism (putative),Nul\nl mutant is viable; cells grow slowly on rich media containi\nng carbon sources utilized by respiration; fail to grow on g\nlucose when iron concentrations are low in the media\n mRAV2:Regulator of (H+)-ATPase in Vacuolar membrane,,\n mPAK1:high copy suppressor of temperature sensitive cdc17 (DNA pol\nymerase alpha) mutations,,Null mutant is viable\n mCAF40:Hypothetical ORF,,Null mutant is viable\n mYDL133W:Unknown ,, Unknown\n mRER1:Protein involved in retention of membrane proteins, includin\ng Sec12p, in the ER; localized to Golgi, where it may functi\non in returning membrane proteins to the ER,,Null mutant is \nviable and shows mislocalization of transmembrane proteins t\nhat are normally retained in the early secretory compartment\ns\n mRIM101:Rim101p is similar to the Aspergillus Phenotype-response reg\nulator PacC and the Yarrowia proteinase YlRim1010p; transcri\nptional activator required for entry into meiosis,,Poor grow\nth at low temperature, altered colony morphology, inefficien\nt sporulation due to reduced expression of the meiotic activ\nator IME1, and defective invasive growth\n mARR4:Unknown ,, Unknown\n mARR4 mMDM39 mSTB3 mSIN3 mHSE1 mYNR005C mVPS27 mYJL064W mYNR029C mVPS24 mSNF7 mVPS4 mVPS36 mSNF8
this is an automaticly generated SAMBA report
Computational Genomics Lab, Tel-Aviv uniresity