The yeast repeated element sigma contains a hormone-inducible promoter.

Arsdell, S W Van; Stetler, Gary L.; Thorner, Jeremy

doi:10.1128/mcb.7.2.749

Cited by 70 publications

(51 citation statements)

References 24 publications

(34 reference statements)

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“…Shifting the cells to the restrictive temperature led to further activation of the pathway, as illustrated by increased FUSI transcription and cell cycle arrest. Similar results were obtained when the mRNA levels of a second pheromone-inducible transcript, sigma (48) b a-Factor (a-F; 2 pLg/ml) was added to cells grown at 23°C.…”

Section: Methodssupporting

confidence: 63%

Mutations in cell division cycle genes CDC36 and CDC39 activate the Saccharomyces cerevisiae mating pheromone response pathway.

Lopes¹,

Ho²,

Reed³

1990

Mol. Cell. Biol.

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Conditional mutations in the genes CDC36 and CDC39 cause arrest in the Gl phase of the Saccharomyces cerevisiae cell cycle at the restrictive temperature. We present evidence that this arrest is a consequence of a mutational activation of the mating pheromone response. cdc36 and cdc39 mutants expressed pheromoneinducible genes in the absence of pheromone and conjugated in the absence of a mating pheromone receptor.On the other hand, cells lacking the G. subunit or overproducing the Ga, subunit of the transducing G protein that couples the receptor to the pheromone response pathway prevented constitutive activation of the pathway in cdc36 and cdc39 mutants. These epistasis relationships imply that the CDC36 and CDC39 gene products act at the level of the transducing G protein. The CDC36 and CDC39 gene products have a role in cellular processes other than the mating pheromone response. A mating-type heterozygous diploid cell, homozygous for either the cdc36 or cdc39 mutation, does not exhibit the Gl arrest phenotype but arrests asynchronously with respect to the cell cycle. A similar asynchronous arrest was observed in cdc36 and cdc39 cells where the pheromone response pathway had been inactivated by mutations in the transducing G protein. Furthermore, cdc36 and cdc39 mutants, when grown on carbon catabolite-derepressing medium, did not arrest in Gl and did not induce pheromone-specific genes at the restrictive temperature.

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Section: Methodssupporting

confidence: 63%

Mutations in cell division cycle genes CDC36 and CDC39 activate the Saccharomyces cerevisiae mating pheromone response pathway.

Lopes¹,

Ho²,

Reed³

1990

Mol. Cell. Biol.

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“…duced by the pheromone response (Van Arsdell et al 1987;Clark et al 1988). Thus, Ste7p may have evolved However, relatively wild-type levels of IN and cDNA were observed at 6 hr.…”

Section: Analysis Of Ty3 Cdna In Mutant Strains: Subsequentmentioning

confidence: 99%

Host Factors That Affect Ty3 Retrotransposition in Saccharomyces cerevisiae

et al. 2004

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The retrovirus-like element Ty3 of Saccharomyces cerevisiae integrates at the transcription initiation region of RNA polymerase III. To identify host genes that affect transposition, a collection of insertion mutants was screened using a genetic assay in which insertion of Ty3 activates expression of a tRNA suppressor. Fifty-three loci were identified in this screen. Corresponding knockout mutants were tested for the ability to mobilize a galactose-inducible Ty3, marked with the HIS3 gene. Of 42 mutants tested, 22 had phenotypes similar to those displayed in the original assay. The proteins encoded by the defective genes are involved in chromatin dynamics, transcription, RNA processing, protein modification, cell cycle regulation, nuclear import, and unknown functions. These mutants were induced for Ty3 expression and assayed for Gag3p protein, integrase, cDNA, and Ty3 integration upstream of chromosomal tDNA Val(AAC) genes. Most mutants displayed differences from the wild type in one or more intermediates, although these were typically not as severe as the genetic defect. Because a relatively large number of genes affecting retrotransposition can be identified in yeast and because the majority of these genes have mammalian homologs, this approach provides an avenue for the identification of potential antiviral targets.

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“…RNA was isolated from -20 OD units of log-phase cells as described (Van Ardell et al 1987). Glyoxal denaturation of the RNA was followed by electrophoresis through a sodium phosphate-agarose gel (pH 7.0).…”

Section: Analysis Of Al Mrnamentioning

confidence: 99%

The origin recognition complex has essential functions in transcriptional silencing and chromosomal replication.

Fox¹,

Loo²,

Dillin³

et al. 1995

Genes Dev.

174

162

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The role of the origin recognition complex (ORC) was investigated in replication initiation and in silencing. Temperature-sensitive mutations in ORC genes caused defects in replication initiation at chromosomal origins of replication, as measured by two-dimensional (2-D) origin-mapping gels, fork migration analysis, and plasmid replication studies. These data were consistent with ORC functioning as a eukaryotic replication initiator. Some origins displayed greater replication initiation deficiencies in orc mutants than did others, revealing functional differences between origins. Alleles of ORC5 were isolated that were defective for silencing but not replication, indicating that ORC's role in silencing could be separated from its role in replication. In temperature-sensitive orc mutants arrested in mitosis, temperature-shift experiments caused a loss of silencing, indicating both that ORC had functions outside of the S phase of the cell cycle and that ORC was required for the maintenance of the silenced state.[Key Words: ORC; silencing; cell cycle; replication; position effect; SIR; yeast; genetics]Received September 22, 1994; revised version accepted March 9, 1995.A central issue in eukaryotic DNA replication is the nature of events at replication origins, the positions on chromosomes at which DNA replication initiates. Replication initiation is a key control point in cell cycle progression, and identification of the proteins responsible for initiation at chromosomal origins is crucial to understanding the regulation of DNA replication in vivo. The yeast origin recognition complex (ORC) is a six-subunit protein complex that was purified based on its ability to bind specifically to yeast origins in vitro (Bell and Stillman 1992). Recent studies indicate that ORC is the best candidate for the yeast replication initiator {Bell and

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The yeast repeated element sigma contains a hormone-inducible promoter.

Cited by 70 publications

References 24 publications

Mutations in cell division cycle genes CDC36 and CDC39 activate the Saccharomyces cerevisiae mating pheromone response pathway.

Mutations in cell division cycle genes CDC36 and CDC39 activate the Saccharomyces cerevisiae mating pheromone response pathway.

Host Factors That Affect Ty3 Retrotransposition in Saccharomyces cerevisiae

The origin recognition complex has essential functions in transcriptional silencing and chromosomal replication.

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