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At least 19 recordsLinked to original sources
PubMed1992

The Saccharomyces cerevisiae NPS1 gene, a novel CDC gene which encodes a 160 kDa nuclear protein involved in G2 phase control.

We have cloned the gene NPS1 (nuclear protein of Saccharomyces) which encodes a nuclear protein of mol. wt 156 735 Daltons (1359 amino acids) essential for cell growth. NPS1 contains a 2 kb sequence that is highly homologous to the S. cerevisiae SNF2/GAM1 gene known as a transcriptional regulator for multiple genes. However, the NPS1 gene was found to have a distinct function from SNF2/GAM1. The growth of the cells carrying a nps1 delta :: URA3 deletion allele and galactose-inducible NPS1 on a plasmid was arrested under NPS1-repressed conditions with a cell cycle arrest phenotype, being arrested at the large-bud stage with a single nucleus that had a DNA content of G2/M phase. When the arrested cells were further incubated under NPS1-repressed conditions, re-replication of DNA occurred in some of the arrested cells without passage through mitosis. In the predicted amino acid sequence of NPS1, sequences homologous to the catalytic domain of protein kinases were found. We constructed a mutation which results in the substitution of a highly conserved lysine residue (Lys792) in the presumed ATP-binding site of this kinase-like domain with a glutamic acid codon. The mutant gene failed to rescue the growth defect caused by NPS1 disruption, suggesting that Lys792 is essential for the function of NPS1.

Amino Acid Sequence↗
PubMed1996

Characterization of a novel CDC gene (ORC1) partly homologous to CDC6 of Saccharomyces cerevisiae.

A novel cell cycle gene was identified by a computer search for genes partly homologous to known CDC genes, CDC6 of Saccharomyces cerevisiae and CDC18 of Schizosaccharomyces pombe, using the nucleotide sequence data base for S. cerevisiae produced by the Yeast Sequencing Project. The protein sequence coded by the cloned gene was found to be identical to that of purified ORC1 protein. Disruption of the gene and subsequent tetrad analysis revealed that the gene was essential for growth. The function of the gene product was analyzed by depleting the protein from the cell using a mutant haploid strain containing the disrupted ORC1 gene on the chromosome and a galactose-inducible gene coding for HA-tagged ORC1 protein on a single copy plasmid. The HA-tagged protein was expressed during growth in the presence of galactose but began to decrease rapidly upon depletion of galactose. Analysis of the cell cycle progression of the mutant cells by FACS after the removal of galactose from the medium, and microscope observations of cells and their nuclei revealed that the normal progression of 2N cells was immediately impeded as the ORC1 protein started to decrease. This was blocked completely in the cells that had progressed to the S phase under conditions deficient in ORC1 protein followed by cell death. Two-dimensional gel analysis of the replication intermediates after the galactose removal revealed that the depletion of ORC1 protein caused a decrease in the frequency of initiation of chromosomal replication, eventually resulting in the inhibition of replication as a whole. The function of the ORC1 protein in the cell cycle progression of S. cerevisiae is discussed in light of current information on ORC.

Cell Division↗
PubMed1992

A new cdc gene required for S phase entry of Schizosaccharomyces pombe encodes a protein similar to the cdc 10+ and SWI4 gene products.

We have isolated a new cell division cycle gene (res1+) required for entry into S phase, as a multicopy dual suppressor of the pat1 and cdc10 mutants of the fission yeast Schizosaccharomyces pombe. The res1+ gene specifies a 72 kDa protein with two copies of the cdc10/SWI6 motif. A disruptant of res1+ grows poorly at 30 degrees C with severe heat- and cold-sensitivities, and completely arrests in G1 at 36 degrees C and 23 degrees C. The arrested disruptant retains a full conjugation ability. In addition to the cdc10/SWI6 motif, Res1 and SWI4 proteins share a remarkable homology in their amino-terminal region, whereas Cdc10 and SWI6 do so in their carboxy-terminal region. Moreover, the amino-terminal region is essential for the function of Res1 as it is for the function of SWI4. Furthermore, analogous to the relationship of SWI4 to SWI6, the res1+ gene effectively rescues cdc10 mutants, but the cdc10+ gene cannot rescue the res1- phenotype. Thus, striking similarities exist in both structural and functional relationships between Res1 and SWI4, and between Cdc10 and SWI6. In view of the fact that SWI4 and SWI6 form a transcription factor complex and activate promoters containing the SWI4/SWI6 dependent cell-cycle box, Res1 might be a putative association partner of Cdc10 which appears to be involved at least in the activation of promoters containing a MluI cell-cycle box.

Amino Acid Sequence↗
PubMed1993

Evidence for two cell division cycle (CDC) genes that govern yeast bud emergence in the pathogenic fungus Wangiella dermatitidis.

Strains Mc2 and Mc3 are morphological mutants of the melanized, pathogenic fungus Wangiella dermatitidis. These strains possess temperature-sensitive (ts) mutations designated mcm2 and mcm3, respectively. At the restrictive temperature (37 degrees C), uninucleate yeast cells of strains Mc2 and Mc3 cease budding and initiate an isotropic mode of cellular development, which is reflected in the formation of a multicellular and multinucleate morphology. Because W. dermatitidis either lacks or has an undiscovered sexual cycle, parasexual methods of analysis were used to confirm that mcm2 and mcm3 define separate bud emergence control genes in the wild-type strain. Spheroplasts of albino auxotrophs derived from strains Mc2 and Mc3 were fused and then regenerated on minimal medium. The resulting fusion products grew as darkly pigmented, prototrophic colonies. When incubated at 37 degrees C, all fusion products exhibited polarized growth predominantly as uninucleate, budding yeasts and less frequently as pseudohyphae and moniliform hyphae. Subsequent analysis of cultures derived from albino, ts segregants, which were induced from fusion products by using methyl benzimidazole-2-yl-carbamate, revealed three types of cell populations. Two resembled those expressed by strain Mc2 or Mc3. The third consisted of a cell population unlike the former, suggesting the presence of both ts mutations in all cells. These results imply that yeast development in the fusion products resulted from intergenic complementation of mcm2 and mcm3, i.e., they are nonallelic. Because mcm2 and mcm3 are equivalent to certain cdc lesions in the yeast Saccharomyces cerevisiae, we have renamed the analogous genes defined by the mutations in W. dermatitidis as CDC1 and CDC2. To our knowledge, these are the first CDC genes identified in a dematiaceous fungus.

Alleles↗
PubMed1985

Suppression of temperature sensitive mutations in oncogene-related CDC genes in Saccharomyces cerevisiae by catabolite repression resistance and cytoplasmic petite mutations.

The "start" cell division control genes CDC36 and CDC28 have been reported to contain a certain sequence homology to tissue oncogenes (ets and some protein kinase encoding oncogenes respectively). Here we report that temperature sensitive mutations in these genes are suppressed in cytoplasmic "petite" mutants and catabolite repression resistant mutants.

Genes, Fungal↗
PubMed1984

Coupling between phosphatidylinositol metabolism and cdc 28 gene product of Saccharomyces cerevisiae. On the possible mechanism of cdc 28 gene action.

It was shown that the decrease in phosphatidylinositol (PI) content in cdc 28 G1-cells was due to a defect in inositol transport. This decrease in inositol transport was linked to microtubular function which was evident by the effect of a microtubular disrupting agent (colcemid) on inositol transport in stationary phase A364A cells. The involvement of PI in yeast G1 phase was further substantiated by the observation that o-phenanthroline, which blocks yeast cells in G1 phase, could inhibit inositol transport and PI levels as well. It is proposed that the regulation of PI metabolism is mediated by the gene cdc 28 and that microtubules may play a major role in the mechanism of action of this gene product.

Demecolcine↗
PubMed1989

The C-terminal part of a gene partially homologous to CDC 25 gene suppresses the cdc25-5 mutation in Saccharomyces cerevisiae.

In Saccharomyces cerevisiae, the product of the CDC25 gene is required for progression in the cell division cycle. It is necessary for cAMP production. It has been suggested that the CDC25 gene product acts through Ras proteins. We report the cloning of a DNA fragment from a new gene able to suppress the thermosensitive phenotype of the cdc25-5 mutation. It is unable to suppress the defect of a mutant of the adenylate cyclase gene or of the ras1, ras2ts double mutant. This DNA fragment prevents the drop in cAMP level in cdc25-5 mutant cells shifted to restrictive temperature. The complementing part of this fragment contains a truncated open reading frame (ORF) corresponding to the 3' end of a gene we named SCD25. The 584-amino acid sequence deduced from this ORF shares 45% identity with the 592-aa C-terminal part of the CDC25 ORF which is sufficient for complementation of cdc25 mutations. Some of the common sequences between these two genes are also partially homologous with the amino acid sequence of LTE1, another gene of S. cerevisiae. The capacity of the SCD25 fragment to suppress a cdc25 mutation and its homology to the C-terminal part of the CDC25 led us to propose that the CDC25 and the SCD25 C-terminal fragments each encode a protein domain which is capable in itself to support a similar biochemical function.

Amino Acid Sequence↗
PubMed1981

Cell division cycle mutants altered in DNA replication and mitosis in the fission yeast Schizosaccharomyces pombe.

A total of 59 new temperature sensitive cdc mutants are described which grow normally at 25 degrees C but become blocked at DNA replication or mitosis when incubated at 36 degrees C. Thirty-nine of the mutants are altered in cdc genes which have been identified previously. The remaining 20 mutants define 10 new cdc genes. These have been characterised physiologically, and 6 of the genes (cdc 17, 20, 21, 22, 23, 24) were found to be required for DNA replication, 2 for mitosis (cdc 27, 28), and 2 (cdc 18, 19), could not be unambiguously assigned to either DNA replication or mitosis but were definitely required for one or the other. Three genes, the previously identified cdc 10, and cdc 20, 22 are likely to be required for the initiation of DNA replication. Mutants in two genes, cdc 17, 24 undergo bulk DNA synthesis at 36 degrees C, but this DNA is defective. In the case of cdc 17 the defect is in the ligation of Okazaki fragments. cdc 23 is required for bulk DNA synthesis, whilst cdc 21 may possibly be required for the initiation of a particular sub-set of replicons. A previously isolated mutant cdc 13.117 is also further described. This mutant becomes blocked in the middle of mitosis with apparently condensed chromosomes.

Ascomycota↗
PubMed1990

Mitotic transmission of artificial chromosomes in cdc mutants of the yeast, Saccharomyces cerevisiae.

In the yeast, Saccharomyces cerevisiae, cell division cycle (CDC) genes have been identified whose products are required for the execution of different steps in the cell cycle. In this study, the fidelity of transmission of a 14-kb circular minichromosome and a 155-kb linear chromosome fragment was examined in cell divisions where specific CDC products were temporarily inactivated with either inhibitors, or temperature sensitive mutations in the appropriate CDC gene. All of the cdc mutants previously shown to induce loss of endogenous linear chromosomes also induced loss of a circular minichromosome and a large linear chromosome fragment in our study (either 1:0 or 2:0 loss events). Therefore, the efficient transmission of these artificial chromosomes depends upon the same trans factors that are required for the efficient transmission of endogenous chromosomes. In a subset of cdc mutants (cdc6, cdc7 and cdc16), the rate of minichromosome loss was significantly greater than the rate of loss of the linear chromosome fragment, suggesting that a structural feature of the minichromosome (nucleotide content, length or topology) makes the minichromosome hypersensitive to the level of function of these CDC gene products. In another subset of cdc mutants (cdc7 and cdc17), the relative rate of 1:0 events to 2:0 events differed for the minichromosome and chromosome fragment, suggesting that the type of chromosome loss event observed in these mutants was dependent upon chromosome structure. Finally, we show that 2:0 events for the minichromosome can occur by both a RAD52 dependent and RAD52 independent mechanism. These results are discussed in the context of the molecular functions of the CDC products.

Cell Division↗
PubMed1982

Mating-defective ste mutations are suppressed by cell division cycle start mutations in Saccharomyces cerevisiae.

Temperature-sensitive mutants which arrest in the G1 phase of the cell cycle have been described for the yeast Saccharomyces cerevisiae. One class of these mutants (carrying cdc28, cdc36, cdc37, or cdc39) forms a shmoo morphology at restrictive temperature, characteristic of mating pheromone-arrested wild-type cells. Therefore, one hypothesis to explain the control of cell division by mating factors states that mating pheromones arrest wild-type cells by inactivating one or more of these CDC gene products. A class of mutants (carrying ste4, ste5, ste7, ste11, or ste12) which is insensitive to mating pheromone and sterile has also been described. One possible function of the STE gene products is the inactivation of the CDC gene products in the presence of a mating pheromone. A model incorporating these two hypotheses predicts that such STE gene products will not be required for mating in strains carrying an appropriate cdc lesion. This prediction was tested by assaying the mating abilities of double mutants for all of the pairwise combinations of cdc and ste mutations. Lesions in either cdc36 or cdc39 suppressed the mating defect due to ste4 and ste5. Allele specificity was observed in the suppression of both ste4 and ste5. The results indicate that the CDC36, CDC39, STE4, and STE5 gene products interact functionally or physically or both in the regulation of cell division mediated by the presence or absence of mating pheromones. The cdc36 and cdc39 mutations did not suppress ste7, ste11, or ste12. Lesions in cdc28 or cdc37 did not suppress any of the ste mutations. Other models of CDC and STE gene action which predicted that some of the cdc and ste mutations would be alleles of the same locus were tested. None of the cdc mutations was allelic to the ste mutations and, therefore, these models were eliminated.

Cell Division↗
PubMed1986

The expression in meiosis of genes which are transcribed periodically in the mitotic cell cycle of budding yeast.

The mitotic cell cycle genes CDC 8, 9 and 21 in Saccharomyces cerevisiae, together with the histone H2A gene, are transcribed discontinuously in meiosis. Message from all four genes initially declines in amount, then increases abruptly to reach maximal levels during premeiotic DNA synthesis before again declining. This response occurs only in meiotic cells; in asporogenous diploids the transcript simply declines in amount. In contrast, message from four genes with no known specific meiotic function (including the actin gene) shows the same profile in both sporogenous and asporogenous diploids. In mitotic cells the three CDC genes appear to be transcribed at the same time in the cell cycle, whereas in meiosis their transcripts accumulate with different kinetics, suggesting either that they have different turnover rates in meiotic cells or that the timing of their transcription is different.

Actins↗
PubMed1982

Two cell division cycle mutants of Saccharomyces cerevisiae are defective in transmission of mitochondria to zygotes.

Mutations in CDC genes of S. cerevisiae disrupt the cell cycle at specific stages. The experiments reported here demonstrate that two CDC genes, CDC5 and CDC27, are necessary for mitochondrial segregation as well as for nuclear division. The defect in the transmission of mitochondria was revealed by the examination of uninucleate and binucleate progeny of transient heterokaryons generated by using the kar1-1 mutation that disrupts nuclear fusion. One of the parents lacked mitochondrial DNA (rho(0)) whereas the other parent had functional mitochondria (rho(+)). When the parents of the heterokaryon were both wild-type (CDC), nearly all progeny received mitochondria at 21 degrees and at 34 degrees . Thirty-four of the 36 cdc mutations tested had no defect in transmission of mitochondria to zygotic progeny in crosses in which one parent was a cdc mutant and the other parent was not (CDC). However, the cdc5 and cdc27 mutations prevented the transmission of mitochondria to cdc progeny at 34 degrees but not at 21 degrees ; CDC progeny received mitochondria at either temperature. This defect was observed in crosses of cdc5 or cdc27 by wild-type cells regardless of which parent donated mitochondria to the zygote. The defect in mitochondrial transmission cosegregated in meiotic tetrads with the defect in mitosis demonstrating that both are likely to be caused by the same temperature-sensitive mutation. These results indicate that the CDC5 and CDC27 gene products are essential in two motility-related processes: mitochondrial movement from the zygote to the progeny and in mitosis.-Furthermore, the results suggest that the function performed by the CDC5 and CDC27 gene products for mitochondrial transmission differ in some fundamental way from the function performed for mitosis. The function necessary for mitosis can be supplied to the cdc5 (or cdc27) nucleus by the CDC5 (or CDC27) nucleus in the same heterokaryon but the function necessary for mitochondrial transmission cannot. Perhaps the function needed for mitochondrial transmission must be performed in the cell cycle preceding the actual segregation of mitochondria whereas the function needed for nuclear segregation can be performed at the time that mitosis occurs.

Cell Cycle↗
PubMed1995

The normal cell cycle activation program is exploited during the infection of quiescent B lymphocytes by Epstein-Barr virus.

B lymphocytes in the peripheral circulation are maintained in a non-proliferative state. Antigen recognition stimulates limited proliferation, whereas infection with Epstein-Barr virus (EBV) results in continual proliferation and the outgrowth of immortal cell lines. Because it is not clear at which point in cell cycle the peripheral B lymphocytes are arrested, we characterized the expression of several cell cycle-associated genes in quiescent and stimulated cells. We show that the expression of four cell genes, cdc-2, cyclin E, CD23, and cyclin D2, are up-regulated approximately 100-fold as a result of EBV-mediated immortalization. Because these genes play a positive role in cell proliferation, we suggest that this regulatory switch contributes to controlling entry into the cell cycle. Transient stimulation of quiescent B lymphocytes with either a cocktail of anti-CD40, anti-IgM, and IL4, or EBV results in the rapid expression of the same four genes, suggesting that, after infection, EBV exploits the normal program of B-lymphocyte cell cycle activation.

Adult↗
PubMed1997

Identification, characterization, and chromosomal organization of cell division cycle genes in Caulobacter crescentus.

We report a detailed characterization of cell division cycle (cdc) genes in the differentiating gram-negative bacterium Caulobacter crescentus. A large set of temperature-sensitive cdc mutations was isolated after treatment with the chemical mutagen N-methyl-N'-nitro-N-nitrosoguanidine. Analysis of independently isolated mutants at the nonpermissive temperature identified a variety of well-defined terminal phenotypes, including long filamentous cells blocked at various stages of the cell division cycle and two unusual classes of mutants with defects in both cell growth and division. The latter strains are uniformly arrested as either short bagel-shaped coils or large predivisional cells. The polar morphology of these cdc mutants supports the hypothesis that normal cell cycle progression is directly responsible for developmental regulation in C. crescentus. Genetic and physical mapping of the conditional cdc mutations and the previously characterized dna and div mutations identified at least 21 genes that are required for normal cell cycle progression. Although most of these genes are widely scattered, the genetically linked divA, divB, and divE genes were shown by genetic complementation and physical mapping to be organized in one gene cluster at 3200 units on the chromosome. DNA sequence analysis and marker rescue experiments demonstrated that divE is the C. crescentus ftsA homolog and that the ftsZ gene maps immediately adjacent to ftsA. On the basis of these results, we suggest that the C. crescentus divA-divB-divE(ftsA)-ftsZ gene cluster corresponds to the 2-min fts gene cluster of Escherichia coli.

Amino Acid Sequence↗
PubMed1997

Expression of cell cycle genes during Sesbania rostrata stem nodule development.

Upon infection of Sesbania rostrata with Azorhizobium caulinodans, nodules are formed on roots and stems. Stem nodules develop from abundantly distributed dormant root primordia. To acquire more insight into the meristem organization during stem nodule development, the expression patterns of a mitotic B1-type cyclin gene (Sesro; CycB1;1), a cyclin-dependent kinase gene (Cdc-2-1Sr), and a histone H4 gene (H4-1Sr) of S. rostrata were followed by in situ hybridization. Cdc2-1Sr transcripts were found in all cells of uninfected and infected root primordia. In uninfected root primordia, Sesro;CycB1;1 transcripts were detected in a few cells of the apical root meristem whereas H4-1Sr transcripts were abundant in this region. Interestingly, after inoculation with A. caulinodans, H4-1Sr transcripts disappeared in the root meristem and a patchy pattern of Sesro;CycB1;1 and H4-1Sr expression appeared in the cortex of the root primordium, reflecting the formation of globular nodule primordia. When bacterial invasion started, a distal nodule meristem was delimited wherein Sesro;CycB1;1 and H4-1Sr expression was concentrated. Approximately 1 week after inoculation, meristem activity ceased, indicated by the loss of Sesro;CycB1;1 and H4-1Sr expression.

Amino Acid Sequence↗
PubMed1982

Preparation of product-specific antisera by gene fusion: antibodies specific for the product of the yeast cell-division-cycle gene CDC28.

Antisera with specificity for the product of a yeast cell-division-cycle (CDC) gene were prepared by immunizing rabbits to a novel hybrid polypeptide. A segment of the yeast gene CDC28 was fused to the Escherichia coli lacZ gene, which encodes beta-galactosidase, by insertion of yeast sequences into the plasmid pBGF1. pBGF1 contains the lac promoter-operator and most of the lacZ gene. An EcoRI site, 16 codons upstream from the carboxyterminus of the beta-galactosidase coding region, served as a convenient splicing site for the heterologous sequences. To insure that an open reading frame be maintained between the two gene segments for some portion of the fusions, the CDC28-encoding segments were first subjected to limited digestion with nuclease BAL31 to produce random junction points. A hybrid polypeptide encoded by such a continuous open reading frame was purified from E. coli by preparative SDS-polyacrylamide gel electrophoresis and used to immunize rabbits. The resulting antisera were shown to have specificity for CDC28 gene product synthesized by cell-free translation of yeast mRNA.

Antibodies↗