Relationship of the Two APRT Gene Products from saccharomyces Cerevisiae

1998 ◽  
pp. 309-314
Author(s):  
Timothy R. Crother ◽  
Milton W. Taylor
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Gene Products ◽  
Aprt Gene ◽  
Relationship Of

scholarly journals The immunosuppressant SR 31747 blocks cell proliferation by inhibiting a steroid isomerase in Saccharomyces cerevisiae.

1996 ◽  
Vol 16 (6) ◽  
pp. 2719-2727 ◽  
Author(s):  
S Silve ◽  
P Leplatois ◽  
A Josse ◽  
P H Dupuy ◽  
C Lanau ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Proliferation ◽  
Gene Product ◽  
In Vitro Assays ◽  
Gene Products ◽  
Yeast Saccharomyces Cerevisiae ◽  
Isomerase Activity ◽  
Encoding Gene ◽  
Resistant Mutants

SR 31747 is a novel immunosuppressant agent that arrests cell proliferation in the yeast Saccharomyces cerevisiae, SR 31747-treated cells accumulate the same aberrant sterols as those found in a mutant impaired in delta 8- delta 7-sterol isomerase. Sterol isomerase activity is also inhibited by SR 31747 in in vitro assays. Overexpression of the sterol isomerase-encoding gene, ERG2, confers enhanced SR resistance. Cells growing anaerobically on ergosterol-containing medium are not sensitive to SR. Disruption of the sterol isomerase-encoding gene is lethal in cells growing in the absence of exogenous ergosterol, except in SR-resistant mutants lacking either the SUR4 or the FEN1 gene product. The results suggest that sterol isomerase is the target of SR 31747 and that both the SUR4 and FEN1 gene products are required to mediate the proliferation arrest induced by ergosterol depletion.

Two systems of glucose repression of the GAL1 promoter in Saccharomyces cerevisiae

1990 ◽  
Vol 10 (9) ◽  
pp. 4757-4769
Author(s):  
J S Flick ◽  
M Johnston
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Base Pair ◽  
Glucose Repression ◽  
Gene Products ◽  
Gal1 Promoter ◽  
Base Pair Fragment ◽  
Common Signal ◽  
Multiple Sequences ◽  
Pair Fragment ◽  
Gal1 Gene

Expression of the GAL1 gene in Saccharomyces cerevisiae is strongly repressed by growth on glucose. We show that two sites within the GAL1 promoter mediate glucose repression. First, glucose inhibits transcription activation by GAL4 protein through UASG. Second, a promoter element, termed URSG, confers glucose repression independently of GAL4. We have localized the URSG sequences responsible for glucose repression to an 87-base-pair fragment located between UASG and the TATA box. Promoters deleted for small (20-base-pair) segments that span this sequence are still subject to glucose repression, suggesting that there are multiple sequences within this region that confer repression. Extended deletions across this region confirm that it contains at least two and possibly three URSG elements. To identify the gene products that confer repression upon UASG and URSG, we have analyzed glucose repression mutants and found that the GAL83, REG1, GRR1, and SSN6 genes are required for repression mediated by both UASG and URSG. In contrast, GAL82 and HXK2 are required only for UASG repression. A mutation designated urr1-1 (URSG repression resistant) was identified that specifically relieves URSG repression without affecting UASG repression. In addition, we observed that the SNF1-encoded protein kinase is essential for derepression of both UASG and URSG. We propose that repression of UASG and URSG is mediated by two independent pathways that respond to a common signal generated by growth on glucose.

The HML mating-type cassette of Saccharomyces cerevisiae is regulated by two separate but functionally equivalent silencers

1989 ◽  
Vol 9 (11) ◽  
pp. 4621-4630
Author(s):  
D J Mahoney ◽  
J R Broach
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mating Type ◽  
Binding Sites ◽  
The Other ◽  
Functional Domains ◽  
Gene Products ◽  
Cis Acting ◽  
Full Expression ◽  
Mating Type Genes ◽  
Chromosome Iii

Mating-type genes resident in the silent cassette HML at the left arm of chromosome III are repressed by the action of four SIR gene products, most likely mediated through two cis-acting sites located on opposite sides of the locus. We showed that deletion of either of these two cis-acting sites from the chromosome did not yield any detectable derepression of HML, while deletion of both sites yielded full expression of the locus. In addition, each of these sites was capable of exerting repression of heterologous genes inserted in their vicinity. Thus, HML expression is regulated by two independent silencers, each fully competent for maintaining repression. This situation was distinct from the organization of the other silent locus, HMR, at which a single silencer served as the predominant repressor of expression. Examination of identifiable domains and binding sites within the HML silencers suggested that silencing activity can be achieved by a variety of combinations of various functional domains.

The RAD7 and RAD16 genes, which are essential for pyrimidine dimer removal from the silent mating type loci, are also required for repair of the nontranscribed strand of an active gene in Saccharomyces cerevisiae

1994 ◽  
Vol 14 (9) ◽  
pp. 6135-6142
Author(s):  
R Verhage ◽  
A M Zeeman ◽  
N de Groot ◽  
F Gleig ◽  
D D Bang ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mating Type ◽  
Excision Repair ◽  
Complementation Group ◽  
Pyrimidine Dimer ◽  
Gene Products ◽  
Pyrimidine Dimers ◽  
Nucleotide Excision ◽  
Active Genes ◽  
Silent Mating Type Loci

The rad16 mutant of Saccharomyces cerevisiae was previously shown to be impaired in removal of UV-induced pyrimidine dimers from the silent mating-type loci (D. D. Bang, R. A. Verhage, N. Goosen, J. Brouwer, and P. van de Putte, Nucleic Acids Res. 20:3925-3931, 1992). Here we show that rad7 as well as rad7 rad16 double mutants have the same repair phenotype, indicating that the RAD7 and RAD16 gene products might operate in the same nucleotide excision repair subpathway. Dimer removal from the genome overall is essentially incomplete in these mutants, leaving about 20 to 30% of the DNA unrepaired. Repair analysis of the transcribed RPB2 gene shows that the nontranscribed strand is not repaired at all in rad7 and rad16 mutants, whereas the transcribed strand is repaired in these mutants at a fast rate similar to that in RAD+ cells. When the results obtained with the RPB2 gene can be generalized, the RAD7 and RAD16 proteins not only are essential for repair of silenced regions but also function in repair of nontranscribed strands of active genes in S. cerevisiae. The phenotype of rad7 and rad16 mutants closely resembles that of human xeroderma pigmentosum complementation group C (XP-C) cells, suggesting that RAD7 and RAD16 in S. cerevisiae function in the same pathway as the XPC gene in human cells. RAD4, which on the basis of sequence homology has been proposed to be the yeast XPC counterpart, seems to be involved in repair of both inactive and active yeast DNA, challenging the hypothesis that RAD4 and XPC are functional homologs.

Screening for Theileria parva secretory gene products by functional analysis in Saccharomyces cerevisiae

2000 ◽  
Vol 109 (1) ◽  
pp. 81-87 ◽  
Author(s):  
Susan Musembi ◽  
Rozmin Janoo ◽  
Bali Sohanpal ◽  
Horace Ochanda ◽  
Onesmo ole-MoiYoi ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Functional Analysis ◽  
Gene Products ◽  
Theileria Parva

scholarly journals TWO RECESSIVE SUPPRESSORS OF SACCHAROMYCES CEREVISIAE CHO1 THAT ARE UNLINKED BUT FALL IN THE SAME COMPLEMENTATION GROUP

Genetics ◽  
1985 ◽  
Vol 111 (1) ◽  
pp. 1-6
Author(s):  
Katharine D Atkinson
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Meiotic Recombination ◽  
Genetic Locus ◽  
Complementation Group ◽  
Complementation Analysis ◽  
Gene Products ◽  
Chromosome X ◽  
Recessive Mutations ◽  
Recessive Mutant ◽  
Phenotypic Reversion

ABSTRACT Phenotypic reversion of ethanolamine-requiring Saccharomyces cerevisiae cho 1 mutants is predominantly due to recessive mutations at genes unlinked to the chromosome V cho 1 locus. The recessive suppressors do not correct the primary cho 1 defect in phosphatidylserine synthesis but circumvent it with a novel endogenous supply of ethanolamine. One suppressor (eam1) was previously mapped to chromosome X, and 135 suppressor isolates were identified as eam1 alleles by complementation analysis. Additional meiotic recombination studies have identified a second genetic locus, eam2, that falls in the eam1 complementation group but maps close to the centromere of chromosome IV. Although the normal EAM1 and EAM2 alleles are fully dominant over recessive mutant alleles, their dominance fails in diploids heterozygous for defects in both genes simultaneously. The unusual complementation pattern could be explained by interaction of the gene products in formation of the same enzyme.

Multiple GCD genes required for repression of GCN4, a transcriptional activator of amino acid biosynthetic genes in Saccharomyces cerevisiae

1986 ◽  
Vol 6 (11) ◽  
pp. 3990-3998
Author(s):  
S Harashima ◽  
A G Hinnebusch
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Amino Acid ◽  
Lacz Gene ◽  
Gene Products ◽  
Wild Type ◽  
Double Mutation ◽  
Double Stranded Rna ◽  
Amino Acid Availability ◽  
Genes Encoding ◽  
New Alleles

GCN4 encodes a positive regulator of multiple unlinked genes encoding amino acid biosynthetic enzymes in Saccharomyces cerevisiae. Expression of GCN4 is coupled to amino acid availability by a control mechanism involving GCD1 as a negative effector and GCN1, GCN2, and GCN3 as positive effectors of GCN4 expression. We used reversion of a gcn2 gcn3 double mutation to isolate new alleles of GCD1 and mutations in four additional GCD genes which we designate GCD10, GCD11, GCD12, and GCD13. All of the mutations lead to constitutive derepression of HIS4 transcription in the absence of the GCN2+ and GCN3+ alleles. By contrast, the gcd mutations require the wild-type GCN4 allele for their derepressing effect, suggesting that each acts by influencing the level of GCN4 activity in the cell. Consistent with this interpretation, mutations in each GCD gene lead to constitutive derepression of a GCN4::lacZ gene fusion. Thus, at least five gene products are required to maintain the normal repressed level of GCN4 expression in nonstarvation conditions. Interestingly, the gcd mutations are pleiotropic and also affect growth rate in nonstarvation conditions. In addition, certain alleles lead to a loss of M double-stranded RNA required for the killer phenotype. This pleiotropy suggests that the GCD gene products contribute to an essential cellular function, in addition to, or in conjunction with, their role in GCN4 regulation.

scholarly journals Saccharomyces cerevisiae kinesin- and dynein-related proteins required for anaphase chromosome segregation.

1995 ◽  
Vol 128 (4) ◽  
pp. 617-624 ◽  
Author(s):  
W S Saunders ◽  
D Koshland ◽  
D Eshel ◽  
I R Gibbons ◽  
M A Hoyt
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Chromosome Segregation ◽  
Motor Proteins ◽  
Cytoplasmic Dynein ◽  
Gene Products ◽  
Loss Of Function ◽  
Direct Role ◽  
Double Deletion ◽  
Different Types ◽  
Related Proteins

The Saccharomyces cerevisiae kinesin-related gene products Cin8p and Kip1p function to assemble the bipolar mitotic spindle. The cytoplasmic dynein heavy chain homologue Dyn1p (also known as Dhc1p) participates in proper cellular positioning of the spindle. In this study, the roles of these motor proteins in anaphase chromosome segregation were examined. While no single motor was essential, loss of function of all three completely halted anaphase chromatin separation. As combined motor activity was diminished by mutation, both the velocity and extent of chromatin movement were reduced, suggesting a direct role for all three motors in generating a chromosome-separating force. Redundancy for function between different types of microtubule-based motor proteins was also indicated by the observation that cin8 dyn1 double-deletion mutants are inviable. Our findings indicate that the bulk of anaphase chromosome segregation in S. cerevisiae is accomplished by the combined actions of these three motors.

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