Module number 2974




Database revision : gnsdb28.10
Date : Tue Feb 25 17:44:06 2003
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mSPR3:a sporulation-specific homologue of the yeast CDC3/10/11/12 \nfamily of bud neck microfilament genes; regulated by ABFI,,N\null mutant is viable\n mYLR012C:Unknown ,, Unknown\n mPBP2:Overexpression confers resistance to the antimalarial drug m\nefloquine,,Null mutant is viable\n mUBC11:homolog of ubiquitin carrier protein E2-C,,Null mutant is vi\nable\n mSWM1:Spore Wall Maturation 1,,Null mutant completes meiotic nucle\nar division but does not show spore wall maturation\n mQRI1:UDP-N-acetylglucosamine pyrophosphorylase,UDP-N-acetylglucos\namine pyrophosphorylase,\n mYDR326C:Unknown ,, Unknown\n mDTR1:dityrosine transporter MFS-MDR,dityrosine transporter MFS-MD\nR,Null mutant is viable; bisformyl dityrosine accumulates in\n cytoplasm of spores; spore wall dityrosine is significantly\n reduced\n mDIT1:Disp. for spores & spore viability - required for dityrosine\n accumul. in the outer spore wall (s.w.), s.w. maturation & \nresist. to ether & lytic enzymes. Spore-autonomous function \nin heterozygotes. mRNA is trans. mid/late in s.w. formation,\nfirst enzyme in dityrosine synthesis in the outer layer of t\nhe spore wall pathway, converting L-tyrosine to N-formyl-L-t\nyrosine,lack outermost layer of spore wall\n mFET5:ferrous iron transport,multicopper oxidase , type 1 integral\n membrane protein,overexpression of FET5 suppresses a fet3 n\null mutant.\n mCLB1:Involved in mitotic induction,B-type cyclin,Null mutant is v\niable (lethal in combination with clb2 mutation)\n mDIT2:Disp. for spores & spore viab. - required for dityrosine bio\nsynth. & dityrosine accumul. in outer spore wall (s.w.); s.w\n. matur. & resist. to ether & lytic enz. mRNA trans. mid/lat\ne during s.w. formation,catalyzes oxidation of N-formyl tyro\nsine to N,N-bisformyl dityrosine in vitro , cytochrome P450 \n56,lack outermost layer of spore wall\n mKAR3:kinesin-like nuclear fusion protein,kinesin-like nuclear fus\nion protein,Null mutant is viable, kar3 mutations prevent ka\nryogamy (nuclear fusion)\n mCLB3:Involved in mitotic induction and perhaps in DNA replication\n and spindle assembly,B-type cyclin,Null mutant is viable\n mYML119W:Unknown ,, Unknown\n mCLB4:Involved in mitotic induction,B-type cyclin,Null mutant is v\niable\n mMPH3:Unknown ,, Unknown\n mCLB5:role in DNA replication during S phase; additional functiona\nl role in formation of mitotic spindles along with Clb3 and \nClb4,B-type cyclin,Null mutant is viable, but has an extende\nd S phase\n mCLB6:role in DNA replication during S phase,B-type cyclin,Null mu\ntant is viable\n mCIK1:In vegetative growth, CIK1 is important for proper organizia\ntion of microtubule arrays and establishment of a spindle; C\nIK1 is also essential for karyogamy; expression regulated by\n KAR4 and mating,spindle pole body associated protein,Null m\nutant is viable but is defective in both karyogamy and chrom\nosome maintenance and does not show proper localization of K\nar3p to microtubule-associated structures\n mPOX1:fatty-acyl coenzyme A oxidase,fatty-acyl coenzyme A oxidase,\nNull mutant is viable, exhibits diminished ability to use ol\neic acid as a carbon source\n mYLR049C:Unknown ,, Unknown\n mUBC1:ubiquitin-conjugating enzyme,ubiquitin-conjugating enzyme,Nu\nll mutant is viable but exhibit moderately slow growth.\n mYJL037W:Unknown ,, Unknown\n mSPS1:dispensable for mitosis, involved in middle/late stage of me\niosis, required for spore wall formation,,Null mutant is via\nble\n mDOC1:Doc1p and Cdc26p are associated with the anaphase-promoting \ncomplex and are involved in the degradation of Clb2p,,Null m\nutant is viable, grows slowly and forms colonies in which mo\nst of the cells have large buds and cannot grow at 37 degree\ns C; doc1-1 is temperature sensitive and shows a Clb2p degra\ndation defect\n mYKR005C:Unknown ,, Unknown\n mSPS2:Middle/late gene of meiosis,,Null mutant is viable\n mSPS4:sporulation-specific protein,,normal sporulation\n Cond:\n mEKI1:Ethanolamine Kinase 1,ethanolamine kinase,Null mutant is via\nble\n mYNR014W:Unknown ,, Unknown\n mISW2:has strong homology to Drosophila ISWI,ATPase component of a\n two subunit chromatin remodeling complex,Null mutant is via\nble, isw1 isw2 chd1 triple deletion mutants are syntheticall\ny temperature and formamide sensitive\n mYJL038C:Unknown ,, Unknown\n mNDT80:Meiosis-specific gene; mRNA is sporulation specific; require\nd for exit from pachytene and for full meiotic recombination\n,DNA binding transcription factor that activates middle spor\nulation genes,Null mutant is viable, arrests in pachytene st\nage of meiosis at the mononucleate stage with duplicated spi\nndle pole bodies and no spindles, is not rescued by spo11 or\n rad50; no mitotic phenotype detected, dispensable for doubl\ne-stranded breaks\n mSPR28:Septin-related protein expressed during sporulation,,Null mu\ntant is viable\n mCWP1:cell wall protein, involved in O and N glycosylation, accept\nor of B1-6 glucan.,cell wall mannoprotein,Null mutant is via\nble, has increased sensitivities to calcoflour white and con\ngo red\n mYMR188C:Unknown ,, Unknown\n mSUT1:Involved in sterol uptake,,Null mutant is viable\n mTID3:Product of gene unknown,,Null mutant is inviable\n mBNR1:Bni1p-related protein, helps regulate reorganization of the \nactin cytoskeleton, potential target of Rho4p,,Null mutant i\ns viable; bni1 bnr1 double mutant exhibits severe temperatur\ne sensitive growth\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 mAPC1:anaphase-promoting complex component,ubiquitin ligase subuni\nt,\n mAPC2:subunit of the Anaphase Promoting Complex; all known APC sub\nunit co-immunoprecipitate with epitope-tagged Apc2. Apc2 sho\nws similarity to cullins.,anaphase promoting complex (APC) s\nubunit,Null mutant is inviable at 25 deg. C; ts mutants arre\nst in metaphase due to defect in the degradation of Pds1; ex\ntracts from G1-arrested apc2 mutants are defective in the ub\niquitination of mitotic cyclins\n mAPC4:subunit of the Anaphase Promoting Complex; all known APC sub\nunits co-immunoprecipitate with epitope-tagged Apc4p,anaphas\ne promoting complex (APC) subunit,Null mutant is inviable at\n 25 C\n mGAL7:galactose-1-phosphate uridyl transferase,galactose-1-phospha\nte uridyl transferase,Null mutant is viable and cannot utili\nze galactose.\n mAPC5:subunit of the Anaphase Promoting Complex; all known APC sub\nunits co-immunoprecipitate with epitope-tagged Apc5,anaphase\n promoting complex (APC) subunit,Null mutant is inviable at \n25 C\n mTEP1:Similar to human tumor suppressor gene known as TEP1, MMAC1 \nand PTEN1,tyrosine phosphatase (putative),\n mAPC9:subunit of the Anaphase Promoting Complex,anaphase promoting\n complex (APC) subunit,Null mutant is viable at 37 C but sho\nw delay in entry into anaphase at 37 C\n mYOR073W:Unknown ,, Unknown\n mSGA1:intracellular sporulation-specific glucoamylase involved in \nglycogen degradation. Induced during starvation of a/a late \nin sporulation, but dispensable for sporulation,glucoamylase\n,suppression of growth arrest of cdc25\n mYDR117C:Unknown ,, Unknown\n mDCI1:Delta(3,5)-delta(2,4)-dienoyl-CoA isomerase,delta(3,5)-delta\n(2,4)-dienoyl-CoA isomerase,\n mGDS1:involved in nuclear control of mitochondria,,Null mutant is \nviable, shows partial impairment of growth on medium contain\ning glycerol as the carbon source. Overexpxression suppresse\ns NAM9-1 glycerol deficient phenotype\n mYLL047W:Unknown ,, Unknown\n Cond963:t11.5_g/r_ratio\n mYAL018C:Unknown ,, Unknown\n mYDL114W:Unknown ,, Unknown\n mCBC2:cap binding complex,nuclear cap binding complex subunit,muta\nnts exhibit promiscuous 3'-end formation; sae-1 mutation cau\nses temporary cell cycle arrest in meiotic prophase\n mYOR365C:Unknown ,, Unknown\n mYMR313C:Unknown ,, Unknown\n mECM11:ExtraCellular Mutant,,A Tn3 insertion into this gene causes \nhypersensitivity to the cell surface polymer perturbing agen\nt calcofluor white.\n mTYS1:tyrosyl-tRNA synthetase, cytoplasmic,tyrosine-tRNA ligase,Nu\nll mutant is inviable.\n mSPC29:Nuclear import protein,spindle pole body associated protein,\nNull mutant is inviable\n mZIP1:Synaptonemal complex protein, component of the central eleme\nnt,,Null mutant is viable and shows defects in meiosis\n mZIP2:Required for 'ZIPpering' up meiotic chromosomes during chrom\nosome synapsis,,Null mutant is viable but is defective in ch\nromosome synapsis, but not chromosome pairing, and causes me\niosis I non-disjunction and reduced homologous recombination\n mHYM1:The homolog in Aspergillus nidulans, hymA, is involved in de\nvelopment, see Karos, M. and Fischer, R. (1996). hymA (hypha\n-like metulae), a new developmental mutant of Aspergillus ni\ndulans. Microbiol. 142:3211-3218.,,Null mutant is inviable\n mYSW1:Spore-specific protein,,\n mSPS18:sporulation-specific protein,transcription factor,suppressio\nn of X-ray sensitivity of rad55\n mAUT7:Forms a protein complex with Aut2p to mediate attachment of \nautophagosomes to microtubules. Defective in maturation of t\nhe vacuolar protein, aminopeptidase I,similar to LC3, a micr\notubule-associated protein from rat,Null mutant is viable bu\nt lacks autophagocytosis and is unable to sporulate. AUT7 is\n a suppressor of mutant phenotypes of aut2-1 cells. Uptake o\nf precursor Aminopeptidase I into the vacuole depends on Aut\n2p and Aut7p.\n mMIP6:RNA-binding protein, interacts with MEX67,,\n mCCP1:Cytochrome-c peroxidase,cytochrome c peroxidase,\n Cond960:t5_g/r_ratio\n mNDJ1:Involved in meiotic chromosome segregation; may stabilize ho\nmologus DNA interactions at telomeres and is required for a \ntelomere activity in distributive segregation; is associated\n with telomeres,,Null allele exhibits errors in meiotic chro\nmosome segregation about 10-fold higher than the wild-type e\nrror rate. Spore viability of homozygous diploids with the n\null allele is approximately 50% of wild-type. Mutant also sh\nows delayed meiotic chromosome synapsis, disrupted crossover\n interference and increased frequency of nonexchange chromos\nomes leading to meiosis I nondisjunction and disruption of d\nistributive disjunction\n Cond964:ndt80_delete_early_g/r_ratio\n mYLL012W:Unknown ,, Unknown\n mYCR045C:Unknown ,, Unknown\n mECM23:ExtraCellular Mutant; similar to SRD1,,A Tn3 insertion into \nthis gene causes hypersensitivity to the cell surface polyme\nr perturbing agent calcofluor white.\n mADY2:Accumulation of DYads,,Null mutant is viable; forms predomin\nantly asci containing 2 spores (dyads) whensporulated; requi\nred for long-term growth on YPD at 37 degrees C.\n mADY3:Protein involved in Accumulation of DYads,,forms largely asc\ni that contain 2 spores (dyads) when sporulated\n mADY4:Hypothetical ORF,,largely forms asci that contain 2 spores (\ndyads) when sporulated\n mYGR273C:Unknown ,, Unknown\n mCRR1:CRH-Related,,\n mYKR015C:Unknown ,, Unknown\n mYHR150W:Unknown ,, Unknown\n mRPM2:involved in processing of mitochondrial precursor tRNAs and \nprotein import,mitochondrial RNase P subunit,Null mutant is \nviable, respiratory deficient, accumulate mitochondrial tRNA\n precursors with 5' extensions\n mSMA1:Spore Membrane Assembly,,undergoes meiotic nuclear divisions\n but does not form spores\n mYOL015W:Unknown ,, Unknown\n mSMA2:SPOrulation deficient,,Undergoes both meiotic nuclear divisi\nons without chromosome missegregation but fails to form spor\nes , undergoes meiotic nuclear divisions but does not form s\npores\n mYPR077C:Unknown ,, Unknown\n mYGR266W:Unknown ,, Unknown\n mYLR030W:Unknown ,, Unknown\n mYBR168W:Unknown ,, Unknown\n mSPC42:involved in SPB duplication, may facilitate attachment of th\ne SPB to the nuclear membrane,spindle pole body component,Nu\nll mutant is inviable; temperature sensitive mutations show \nSBP duplication\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 mYNL080C:Unknown ,, Unknown\n mPNP1:purine nucleoside phosphorylase, specifically metabolizes in\nosine and guanosine nucleosides,purine nucleoside phosphoryl\nase,null mutants excrete inosine and guanosine into the grow\nth medium\n mHEM4:catalyzes the fourth step in the heme biosynthesis pathway,u\nroporphyrinogen III synthase,respiratory deficiency, accumul\nation of porphyrins, and heme auxotrophy\n mYPR027C:Unknown ,, Unknown\n mGFA1:catalyzes first step in hexosamine pathway required for bios\nynthesis of cell wall precursors,glucoseamine-6-phosphate sy\nnthase , glutamine_fructose-6-phosphate amidotransferase,Nul\nl mutant is viable, glucosamine auxotroph\n mYFR012W:Unknown ,, Unknown\n mYLR445W:Unknown ,, Unknown\n mCCC1:Functions in the homeostasis of both calcium and manganese i\nons,transmembrane Ca2+ transporter (putative),Wild-type comp\nlements csg1 (calcium sensitive-group) mutants when overexpr\nessed\n mHUL4:ubiquitin-protein ligase (E3),ubiquitin ligase (E3),Null mut\nant is viable\n mCDC14:Required for mitosis and sporulation,soluble tyrosine-specif\nic protein phosphatase,Null mutant is inviable; ts mutant ar\nrests at late anaphase with phenotypes similar to cdc5 mutan\nts\n mCDC16:a component of anaphase-promoting complex required for the G\n2/M transition in mitosis and degradation of mitotic cyclins\n, required for sporulation,metal-binding nucleic acid-bindin\ng protein, interacts with Cdc23p and Cdc27p to catalyze the \nconjugation of ubiquitin to cyclin B (putative),Null mutant \nis inviable. cdc16 mutants are unable to progress through th\ne G(sub)2/M transition, cell division cycle blocked at 36 de\ngrees C\n mYPR078C:Unknown ,, Unknown\n mAPG1:Required for autophagy,protein kinase,Defective in autophagy\n; loses viability more rapidly than wild type during nitroge\nn starvation; defective in vacuolar protein degradation duri\nng nitrogen starvation; defective in sporulation\n mMND1:needed for Meiotic Nuclear Divisions,,Null mutant is viable;\n arrests after DNA-replication but before nuclear divisions \nafter shift to sporulation medium.\n mSRC1:Spliced mRNA and Cell cycle regulated gene,,Null mutant is v\niable and shows normal growth in standard media; expression \nis induced at G2/M transition.\n mLEU1:leucine biosynthesis,isopropylmalate isomerase,Leucine requi\nring\n mAMA1:Required for sporulation, highly induced during sporulation;\n activator of meiotic anaphase promoting complex,,Null mutan\nt is viable; homozygous null mutant does not sporulate but d\noes not exhibit any vegetative phenotype.\n COMP.KO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mSOL1:Multicopy Suppressor Of los1,,Null mutant is viable\n mYOL024W:Unknown ,, Unknown\n mCDC20:Required for onset of anaphase,anaphase promoting complex (A\nPC) subunit,Null mutant is inviable; conditional alleles sho\nw cell cycle arrest in G2\n mCDA1:Required for proper formation of the ascospore wall,chitin d\neacetylase,Null mutant is viable, mutants spores disrupted f\nor both cda1 and cda2 fail to emit natural fluorescence and \nare sensitive to hydrolyrtic enzymes, ether, and heat shock\n mNEJ1:Hypothetical ORF,Mating-type regulated component of NHEJ,Nul\nl mutant is viable, defective in NHEJ\n mCDA2:Required for proper formation of the ascospore wall,chitin d\neacetylase,Null mutant is viable, mutant spores disrupted fo\nr both cda1 and cda2 fail to emit natural fluorescence and a\nre sensitive to hydrolyrtic enzymes, ether, and heat shock\n mCDC23:Required for mitosis and RNA synthesis,,unable to complete G\n(sub)2/M transition\n mYBR184W:Unknown ,, Unknown\n mSPO11:Dispensable for mitosis, premeiotic DNA synthesis, spindle p\nole body duplication, meiosis I, meiosis II & spores. Requir\ned for chromosome pairing seen by in situ hybridization, dou\nble strand breaks, synaptonemal complexes.,early meiosis-spe\ncific recombination protein,Null mutant is viable, sporulati\non defective; spo11 executes meiosis I early, is rescued by \nspo13 and is epistatic to rad52 spo13; and is classified as \nan early recombination function. It fails to form any recomb\nination intermediates and is partially suppressed by X-irrad\niation (by induced double strand breaks), in meiosis. The sp\no11-1 temperature sensitive mutant is double strand break-, \nrecombination-, and exhibits tripartite synaptonemal complex\n structures at a restrictive temperature, suggesting synapto\nnemal complex formation may be partially independent of doub\nle strand breaks and recombination. mRNA is induced early in\n meiosis; meiosis-specific regulation is dependent on a URS1\n element within the coding region.\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 mCDC26:component of anaphase-promoting complex; required for ubiqui\ntination of Clb2p and Clb3p, is a nuclear protein, and is in\nduced by heat shock,,thermosensitive cell growth (lethal at \nhigh temperature)\n mSPO13:Spo13 acts as a transcriptional activator in a one-hybrid as\nsay (see Henninger et al (1996) SPO13 and control of meiotic\n chromosome segregation in Saccharomyces cerevisiae),,Null m\nutant is viable, defective for sporulation; loss of function\n results in a single division during meiosis (with some chro\nmosomes segregating reductionally or aberrantly depending on\n strain background), occurring slightly earlier or at the ti\nme of wild type meiosis I, and dyad asci containing two dipl\noid spores. spo13 rescues the meiotic lethality of early Rec\n- mutants and Rec+ haploids. Gain of function causes a CDC28\n-dependent arrest at M-phase in mitosis and a delay in MI nu\ncleardivision.\n mCDC27:Protein required for cell cycle,anaphase promoting complex (\nAPC) subunit,Null mutant is inviable. Some conditional allel\nes overreplicate their DNA.\n mSPO16:Early meiotic protein required for efficient spore formation\n,,sporulation defective\n mYHL012W:Unknown ,, Unknown\n mSSP1:Involved in the control of meiotic nuclear divisions & spore\n formation; dispensable for mitosis, premeiotic DNA synthesi\ns, recombination, meiosis I, meiosis II, & initiation of pro\nspore walls; required for spore wall elongation,,Null mutant\n is viable; spo3-1 at a semi-permissive temperature produces\n asci with one or two randomly packaged haploid spores; at a\n restrictive temperature, prospore walls grow and close prio\nr to the completion of meiosis II, resulting in immature ane\nuploid and/or anucleate spores. Multinucleate cells completi\nng meiosis II, but blocked in spore development, bud and res\nume division in return to growth assay.\n mSPO19:sporulation-defective; SPO19 was found as a weak high-copy s\nuppressor of the spo1-1 ts mutation. The gene is specificall\ny induced late in meiosis (Primig et al. (2000) Nat Genet 26\n:415-423),meiosis-specific GPI-protein,Null mutant is viable\n; unable to form spores\n mSSP2:Sporulation Specific,,Null mutant is viable, fails to sporul\nate\n mMNE1:similar to Lucilia illustris mitochondria cytochrome oxidase\n,,\n mYPL033C:Unknown ,, Unknown\n mHOP1:Meiosis-specific protein involved in homologous chromosome s\nynapsis and chiasmata formation,DNA binding protein,decrease\nd levels of meiotic crossing over and intragenic recombinati\non between markers on homologous chromosomes\n mEMI2:Unknown ,, Unknown\n mHOP2:HOmologous Pairing,meiosis-specific gene required for the pa\niring of similar chromosomes,Null mutant is viable; homozygo\nus hop2 null diploids arrest in meiotic prophase prior to th\ne first meiotic division\n mCNM67:chaotic nuclear migration; predicted mass is 67kDa,,Null mut\nant is viable but shows slow growth and a nuclear migration \ndefect\n mMAM1:monopolin; involved in chromosome attachment to meiotic spin\ndle,Monopolin,Null mutant is viable; sister kinetochores ori\nent towards opposite spindle poles in meiosis I (as opposed \nto wt where homologous kinetochores orient towards the oppos\nite spindle poles and sister kinetochores orient towards the\n same spindle pole)\n mPCT1:phosphorylcholine transferase; or cholinephosphate cytidylyl\ntransferase,cholinephosphate cytidylyltransferase , phosphor\nylcholine transferase,Null mutant is viable\n mHXT10:high-affinity hexose transporter,high affinity hexose transp\norter,\n mYGL230C:Unknown ,, Unknown\n mHXT14:High-affinity hexose transporter,hexose transporter,\n mYGR226C:Unknown ,, Unknown\n Cond962:t9_g/r_ratio\n mSPO20:DBF2 Interacting Protein; SNAP 25 homolog,DBF2 interacting p\nrotein , SNAP 25 homolog,Null mutant is viable, other mutant\n fails to form spores\n mSPO21:sporulation defective,,meiosis proficient, fails to form spo\nres\n mYNL155W:Unknown ,, Unknown\n mHST1:Homolog of SIR2,,Overexpression restores transcriptional sil\nencing in a sir2 mutant\n mHST3:Homolog of SIR2,,hst3 hst4 double mutant has defects in telo\nmeric silencing, cell cycle progression, radiation resistanc\ne, and genomic stability\n mHST4:Homolog of SIR2,,hst3 hst4 double mutant has defects in telo\nmeric silencing, cell cycle progression, radiation resistanc\ne, and genomic stability\n mYJL160C:Unknown ,, Unknown\n mHFM1:C4 zinc finger DNA-binding protein of low sequence specifici\nty in vitro; Probable 119 kD DNA/RNA helicase family member,\nC4 zinc finger DNA-binding protein of low sequence specifici\nty in vitro; Probable 119 kDa DNA/RNA helicase family member\n,Null mutant is viable\n mYFL012W:Unknown ,, Unknown\n mYNL170W:Unknown ,, Unknown\n mYBR063C:Unknown ,, Unknown\n mRED1:Required for full chr. pairing & chr. condensation seen by i\nn situ hybridization, axial elements, stable localization of\n Hop1p & synaptonemal complexes; at HIS2 required for normal\n levels of double strand breaks,meiosis-specific protein inv\nolved in similar chromosome synapsis and chiasmata formation\n; localizes to chromosome cores independently of Mei4p and S\npo11p; mRNA is induced in meiosis,Null mutant is viable; exh\nibits reduced meiotic interchromosomal crossing over; red1 i\ns rescued by spo13 and epistatic to rad52; mek1 and hop1 are\n on the same pathway as red1, which is independent of the me\nr1 pathway by epistasis analysis; RED1 suppresses double str\nand break repair in dmc1 mutants\n mCDC3:involved in proper bud growth,,Null mutant is inviable; othe\nr mutants show abnormal cell-wall deposition and bud growth,\n inability to complete cytokinesis, and failure to form the \nring of 10nm filaments in the neck region of budding cells.\n mCDC5:CDC5 is dispensable for premeiotic DNA synthesis and recombi\nnation, but required for tripartite synaptonemal complexes, \nhaploidization, and spores,protein kinase,Null mutant is inv\niable. cdc5(ts) mutants form synaptonemal complexes lacking \ncentral elements and arrest either at meiosis I with broken \nspindles or at meiosis II with short spindles. Late shifts t\no a restrictive temperature result in reductional dyads; eac\nh spore contains an entire meiosis II short spindle with uns\neparated chromatids. In some strains at semi-permissive temp\nerature, chromosomes segregate reductionally or equationally\n depending upon the centromere.\n mYNL019C:Unknown ,, Unknown\n mMPC54:Meiotic Plaque Component,,Null: viable. Other phenotypes: sp\norulation deficient.\n mSTO1:Large subunit of the nuclear cap-binding protein complex,Lar\nge subunit of the nuclear cap-binding protein complex,defect\nive growth on fermentable carbon sources and supression of t\nop1-hpr1\n mGAS4:Unknown ,, Unknown\n mYLL032C:Unknown ,, Unknown\n mYNL033W:Unknown ,, Unknown\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 mYUH1:ubiquitin hydrolase,ubiquitin hydrolase,\n mYOR298W:Unknown ,, Unknown\n mALG9:catalyzes the transfer of mannose from Dol-P-Man to lipid-li\nnked oligosaccharides,mannosyltransferase,accumulation of li\npid-linked Man6GlcNAc2; hypoglycosylation of secreted protei\nns\n mSPC110:may be involved in connecting nuclear microtubules to the sp\nindle pole body,interacts with Spc42p, calmodulin, and a 35 \nkDa protein , spindle pole body component , interacts with S\npc42p, calmodulin, and a 35 kDa protein , spindle pole body \ncomponent,Null mutant is inviable\n mYDR065W:Unknown ,, Unknown\n mYGL138C:Unknown ,, Unknown\n mMSH4:dispensable for DNA repair, required for full levels of reci\nprocal exchange and spore viability,meiosis specific protein\n, E.coli MutS protein, localizes to discrete sites on meioti\nc chromosomes,Null mutant is viable, has no apparent defect \nin mismatch repair, wild-type levels of gene conversion and \npostmeiotic segregation\n mMSH5:dispensable for DNA repair and meiotic intrachromosomal reci\nprocal recombination, required for full reciprocal recombina\ntion between homologs, and spore viability,mutS homolog,Null\n mutant is viable. Diploids lacking the MSH5 gene display de\ncreased levels of spore viability, increased levels of meios\nis I chromosome nondisjuction, and decreased levels of recip\nrocal exchange between, but not within, homologs. Gene conve\nrsion is not reduced. Msh5 mutants are phenotypically simila\nr to mutants in the meiosis-specific gene MSH4. msh5 is epis\ntatic to msh4, suggesting they act in the same pathway.\n mREC102:Dispensable for mitotic recombination, DNA damage repair, ax\nial elements & meiotic chromosome condensation; required for\n wild-type level of chromosome pairing seen by in situ hybri\ndization, tripartite synaptonemal complexes,23 kDa protein c\nontaining a putative leucine zipper , meiosis specific recom\nbination protein,Reduced meiotic recombination; inviable spo\nres; mutant is rescued by spo13 and is epistatic to rad52\n mIRS4:Increased rDNA silencing,,Null mutant is viable and shows in\ncreased rDNA silencing\n mREC104:meiosis-specific recombination gene, dispensable for mitotic\n recombination and axial elements in meiosis, required for t\nripartite synaptonemal complexes, meiotic recombination and \nspore viability; classified as an early recombination gene,m\neiosis-specific protein,Null mutant is viable, rec104 mutant\ns exhibit reduced meiotic DNA recombination, executes meiosi\ns I early; rec104 is rescued by spo13 and is epistatic to ra\nd52 spo13\n Cond936:12h\n mYOR255W:Unknown ,, Unknown\n mNMT1:N-myristoyl transferase,N-myristoyl transferase,Null mutant \nis inviable\n mGAT3:The amino acid sequence of this ORF is very homologous to th\nat of GAT4/YIR013C.,,\n mGAT4:very short and so far mRNA can't be detected,very short and \nso far mRNA can't be detected,being investigated\n mDIN7:DNA-damage inducible gene,,\n mYDL186W:Unknown ,, Unknown\n mYGL015C:Unknown ,, Unknown\n mYBR064W:Unknown ,, Unknown\n mPCH2:Pachytene CHeckpoint,ATPase (putative),Null mutant is viable\n and bypasses meiotic arrest of zip1 mutant, resulting in ch\nromosome segregation defects\n mYJR107W:Unknown ,, Unknown\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mYPR140W:Unknown ,, Unknown\n mYCL048W:Unknown ,, Unknown\n mAPC11:subunit of the Anaphase Promoting Complex; all known APC sub\nunits co-immunoprecipitate with epitope-tagged Apc11p,anapha\nse promoting complex (APC) subunit,Null mutant is inviable a\nt 25 C\n mMRL1:Mannose 6-phosphate Receptor Like,,\n mREC114:meiosis-specific recombination gene; dispensable for mitotic\n recombination and axial elements in meiosis but required fo\nr synaptonemal complexes, meiotic recombination, and spore v\niability; classified as an early recombination gene,early sp\norulation protein,reduced meiotic recombination, rec114 muta\nnts execute meiosis I early, are rescued by spo13 and are ep\nistatic to rad52 spo13\n mYFR032C:Unknown ,, Unknown\n mCTS2:chitinase,Sporulation-specific chitinase,Null mutant fails t\no form mature asci, synthesis of spore wall surface layers i\ns affected.\n mIME2:Positive regulator of meiosis, dispensable for mitosis, stim\nulates early, middle and late gene expression and negatively\n regulates IME1,,Null mutant is viable, homozygous null muta\nnts are sporulation defective. High copy IME2 stimulates mei\notic recombination without starvation and permits meiosis in\n an ime1 null background\n mYMR118C:Unknown ,, Unknown\n mYNL319W:Unknown ,, Unknown\n mSLZ1:sporulation-specific protein with a leucine zipper motif, re\ngulated by the transcription factor Ume6 and expressed early\n in meiosis,,\n mREV3:DNA polymerase zeta, which is unique in its ability to bypas\ns thymine dimers during replication, is composed of Rev3p an\nd Rev7p.,DNA polymerase zeta subunit,The null mutant is viab\nle and resists ultraviolet (UV) mutagenesis in both haploid \nand homozygous mutant diploid cells. Other antimutator pheno\ntypes are also observed.\n mYOR214C:Unknown ,, Unknown\n mPIG1:Putative type 1 phosphatase regulatory subunit; interacts wi\nth Gsy2p,similar to Gac1p, a putative type 1 protein phospha\ntase targeting subunit,Null mutant is viable; gac1 pig1 doub\nle mutant has more severe glycogen-deficient phenotype than \ngac1 mutant\n mREV7:Protein required for mutagenesis by physical and chemical ag\nents,DNA polymerase zeta (pol-zeta) subunit,Null mutant is v\niable\n mPIG2:Interacts with Gsy2p,30% identity to YER054C/GIP2,Null mutan\nt is viable and shows no detectable changes in glycogen meta\nbolism\n mMPS1:Required for spindle pole body duplication and a mitotic che\nckpoint function.,,Null mutant is inviable. Eliminating the \nexpression of MPS1 causes accumulation of non-viable cells w\nith less than a 1 N DNA content. Allele-specific suppression\n and synthetic lethal interactions occur between mps1 and cd\nc37. Overexpression of Mps1p induces modification of Mad1p a\nnd arrests wild-type yeast cells in mitosis with morphologic\nally normal spindles. mps1 does not arrest in the absence of\n spindle pole body duplication and monopolar spindle formati\non, or nocodozole treatment. Required for sporulation.\n mMDM30:Unknown ,, Unknown\n mMPS2:Monopolar spindle two, encodes a membrane protein localized \nat the nuclear envelope and the spindle pole body throughout\n the cell cycle. The protein is approximately 45 kDa, and co\nntains a coiled-coil motif and a hydrophobic domain.,,Null m\nutant is inviable, however some null spore clones can surviv\ne with abnormal ploidy; the mps2-1 mutant is incapable of pr\noper duplication of the SPB, resulting in a defective pole t\nhat only nucleates cytoplasmic microtubules. Overexpression \nof MPS2 in a cim5-1 ts mutant is toxic to cells.\n Meiosis.Series0:The core meiotic transcriptome in budding yeasts. Nat Genet\n. 2000 Dec;26(4):415-23.\n mYDR438W:Unknown ,, Unknown\n mYIL112W:Unknown ,, Unknown\n mSPO69:Required for sporulation; highly induced during sporulation.\n,S. pombe REC8 homolog,Null mutant is viable, does not under\ngo meiotic division and is unable to sporulate. The null mut\nant also exhibits a loss of sister chromatid cohesion, an ab\nsence of the synaptonemal complex, and chaotic chromosome se\ngregation.\n mYGL081W:Unknown ,, Unknown\n mICT1:Increased Copper Tolerance; Similar to Ecm18p,,\n mYNL116W:Unknown ,, Unknown\n mGRR1:F box protein with several leucine rich repeats,,Null mutant\n is viable, resistant to high levels of divalent cations, se\nnsitive to sulfite, and defective in high affinity glucose t\nransport and glucose repression; null mutant also exibits an\n elongated cell morphology\n mYOL131W:Unknown ,, Unknown\n mHPR5:Required for proper timing of committment to meiotic recombi\nnation and the transition from Meiosis I to Meiosis II,DNA h\nelicase,Null mutant is viable, radiation (ultraviolet or ion\nizing sensitive), loss of function results in RAD52-dependen\nt hyperrecombination suggesting recombination suppression oc\ncurs by antagonizing the Rad52 recombinational repair pathwa\ny; wild-type suppresses mitotic recombination; some mutant a\nlleles have lower spore viability which is not rescued by sp\no13, suggesting they affect a late recombination function; h\npr5 mutations are rad6 suppressors\n mPES4:Suppressor of DNA polymerase epsilon mutation,poly(A) bindin\ng protein , similar to YHR015W,\n mDON1:prospore membrane localizing protein,,\n mECM8:ExtraCellular Mutant,,A Tn3 insertion into this gene causes \nhypersensitivity to the cell surface polymer perturbing agen\nt calcofluor white.\n mYKL107W:Unknown ,, Unknown\n mYEL023C:Unknown ,, Unknown\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 Cond940:6h\n mSPO71:Product of gene unknown,,Null mutant is viable; upon sporula\ntion, null mutants undergo both meiotic divisions but do not\n form a spore wall.\n mSPO74:Protein involved in sporulation,,undergoes meiotic nuclear d\nivisions but does not form spores\n mSPO77:Hypothetical ORF,,Undergoes meiotic nuclear divisions but do\nes not form spores\n mYLR343W:Unknown ,, Unknown\n mYNL095C:Unknown ,, Unknown\n Cond934:8h\n mYDR374C:Unknown ,, Unknown\n mORC1:binds to origins of replication and thereby directs DNA repl\nication and is also involved in transcriptional silencing,or\nigin recognition complex (ORC) 120 kDa (largest) subunit , s\nimilar to Cdc6p, Cdc18p, and Sir3p and to proteins from K. l\nactis, S. pombe, and humans,\n Cond961:t7_g/r_ratio\n mULP2:Product of gene unknown,,Null mutant is viable but exhibits \ntemperature-sensitive growth, abnormal cell morphology, decr\neased plasmid and chromosome stability, and a severe sporula\ntion defect as well as hypersensitivity to DNA-damaging agen\nts, hydroxyurea, and benomyl. SMT4/ULP2 was also isolated as\n a high copy suppressor of a temperature sensitive mutation \nin MIF2, a putative centromere protein gene\n mHEF3:Translational elongation factor EF-3B,Translation elongation\n factor 3 (EF-3),\n Cond935:10h\n mYNL205C:Unknown ,, Unknown\n mYKR089C:Unknown ,, Unknown\n mKNH1:46% identical at amino acid level to Kre9p; located extracel\nlularly,KRE9 homolog,Null mutant is viable; overexpression s\nuppresses kre9 mutation; knh1 kre9 double mutant is inviable\n mGNP1:high-affinity glutamine permease,high affinity glutamine per\nmease,Null mutant is viable but shows reduced glutamine tran\nsport and is therefore resistant to the glutamine analog L-g\nlutamic acid gamma-monohydroxamate; overexpression induces s\nensitivity to heat shock\n mGNA1:involved in UDP-N-acetylglucosamine biosynthesis,glucosamine\n-phosphate N-acetyltransferase,Null mutatn is inviable\n mCDH1:CDC20 homolog 1,required for Clb2 and Ase1 degradation,Null \nmutant is viable but defective in Clb2p and Ase1p degradatio\nn; deletion of cdh1 causes pheromone resistance and is synth\netically lethal with sic1 deletion; overexpression causes ec\ntopic degradation of Clb2p and Ase1p\n mYKL050C:Unknown ,, Unknown\n Sporulation.Series0:The transcriptional program of sporulation in budding yeast.\n Science. 1998 Oct 23;282(5389):699-705.\n mPRM6:pheromone-regulated membrane protein,,\n mGIP1:Glc7-interacting protein.,,sporulation defective\n mYLR054C:Unknown ,, Unknown\n mYER085C:Unknown ,, Unknown\n mRIM4:Regulator of IMe2 expression,RNA-binding protein of the RRM \nclass (putative),Null mutant is viable. Homozygous null dipl\noid fails to sporulate, does not form meiosis I or II spindl\nes, and exhibits reduced expression of early and middle spor\nulation-specific genes. Null mutant is suppressed by hyperac\ntive Ime2p derivative, but not by overexpression IME1\n mYDR317W:Unknown ,, Unknown\n mYOL047C:Unknown ,, Unknown\n mYJR119C:Unknown ,, Unknown\n mYBR250W:Unknown ,, Unknown\n mSTU2:May play a role in attachment, organization, and/or dynamics\n of microtubule ends at the spindle pole body,,Null mutant i\ns inviable; stu2 mutations can suppress cold-sensitivity of \ntub2-423 mutants\n mMEI5:Meiotic protein required for synapsis and meiotic recombinat\nion,,\n mPFS1:Prospore Formation at Selected spindle poles,,Null mutant is\n viable; homozygous null diploid accumulates nonsister-spore\n dyads, normal meiotic spindles\n Cond938:2h\n mEXO1:Protein that complements a drug-hypersensitive mutation,exon\nuclease,Mutants demonstrate sensitivity to cycloheximide, bl\neomycin, actinomycin D, 5-fluorouracil, and several other an\ntibiotics, as well as irregular shapes and sensitivity to zy\nmolase digestion\n mYJL043W:Unknown ,, Unknown\n mYFL040W:Unknown ,, Unknown\n mYDR042C:Unknown ,, Unknown\n mSPR1:Sporulation regulated genes,exo-1,3-beta-glucanase, sporulat\nion-specific,Fail to hydrolyze p-nitrophenyl-beta-D-glucanas\ne or laminarin; mutant spores exhibit reduced thermoresistan\nce\n
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Computational Genomics Lab, Tel-Aviv uniresity