Molecular cloning and transcriptional analysis of the start gene <i>CDC25</i>
 of <i>Saccharomyces cerevisiae</i>

Martegani, Enzo; Baroni, Maurizio D.; Frascotti, Gianni; Alberghina, Lilia

doi:10.1002/j.1460-2075.1986.tb04505.x

Cited by 51 publications

(25 citation statements)

References 40 publications

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“…Adenylyl cyclase seems to be a primary target of systems that monitor the presence or absence of key nutritional compounds (Tatchell et al, 1985;Tripp et al, 1986;Boy-Marcotte et al, 1987;Mbonyi et al, 1988). The nutritional sensory systems whose existence is suggested by these observations do not appear to act directly on adenylyl cyclase but rather through intermediary proteins, three of which, encoded by the two RAS genes (Toda et at., 1985), and the CDC25 gene (Camonis et al, 1986;Martegani et al, 1986;Broek et al, 1987;Daniel et al, 1987), have been identified.…”

Section: Introductionmentioning

confidence: 99%

cAMP- and RAS-independent Nutritional Regulation of Plasma-membrane H+-ATPase Activity in Saccharomyces cerevisiae

Mazón

Behrens²,

Portillo³

et al. 1989

Microbiology

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Section: Introductionmentioning

confidence: 99%

cAMP- and RAS-independent Nutritional Regulation of Plasma-membrane H+-ATPase Activity in Saccharomyces cerevisiae

Mazón

Behrens²,

Portillo³

et al. 1989

Microbiology

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“…Nine dif ferent plasmids were isolated. Five of these nine con tained known genes: Three plasmids contained TPKl, which is one of the three genes that encode the catalytic subunits of the cAPK (Toda et al 1987a); one contained CDC25 itself (Camonis et al 1986;Martegani et al 1986b;Broek et al 1987;Robinson et al 1987); and the other contained CYRl, which encodes adenylyl cyclase (Kataoka et al 1985a). From restriction mapping and Southern hybridization data, the remaining four plasmids did not contain CDC25, RASl,RAS2,CYRl,TPKl,TPK2,or TPK3, all genes capable of suppressing cdc25^^ when they are carried on multicopy yeast plasmids.…”

mentioning

confidence: 99%

SCH9, a gene of Saccharomyces cerevisiae that encodes a protein distinct from, but functionally and structurally related to, cAMP-dependent protein kinase catalytic subunits.

Toda¹,

Cameron²,

Sass³

et al. 1988

Genes Dev.

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162

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A new gene, SCH9, was isolated from Saccharomyces cerevisiae by its ability to complement a cdc25^^ mutation. Sequence analysis indicates that it encodes a 90,000-dalton protein with a carboxy-terminal domain homologous to yeast and mammalian cAMP-dependent protein kinase catalytic subunits. In addition to suppressing loss of CDC25 function, multicopy plasmids containing SCH9 suppress the growth defects of strains lacking the RAS genes, the CYRl gene, which encodes adenylyl cyclase, and the TPK genes, which encode the cAMP-dependent protein kinase catalytic subunits. Cells lacking SCH9 grow slowly and have a prolonged Gi phase of the cell cycle. This defect is suppressed by activation of the cAMP effector pathway. We propose that SCH9 encodes a protein kinase that is part of a growth control pathway which is at least partially redundant with the cAMP pathway.

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“…We have previously cloned the CDC25 gene (2,28), and we have used the cloned sequence to construct different isogenic strains in order to study the interactions between the CDC25 and RAS2 gene products. In (48).…”

mentioning

confidence: 99%

Cell size modulation by CDC25 and RAS2 genes in Saccharomyces cerevisiae.

Baroni¹,

Martegani²,

Monti³

et al. 1989

Mol. Cell. Biol.

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A detailed kinetic analysis of the cell cycle of cdc25-1, RAS2 al-19, or cdc25-1lRAS2'a1-19 mutants during exponential growth is presented. At the permissive temperature (24°C), cdc25-1 cells show a longer GIl/ unbudded phase of the cell cycle and have a smaller critical cell size required for budding without changing the growth rate in comparison to an isogenic wild type. The RAS2'a"''9 mutation efficiently suppresses the ts growth defect of the cdc25-1 mutant at 36°C and the increase of GI phase at 24°C. Moreover, it causes a marked increase of the critical cell mass required to enter into a new cell division cycle compared with that of the wild type. Since the critical cell mass is physiologically modulated by nutritional conditions, we have also studied the behavior of these mutants in different media. The increase in cell size caused by the RAS2VaIl9 mutation is evident in all tested growth conditions, while the effect of cdc25-1 is apparently more pronounced in rich culture media. CDC25 and RAS2 gene products have been showed to control cell growth by regulating the cyclic AMP metabolic pathway. Experimental evidence reported herein suggests that the modulation of the critical cell size by CDC25 and RAS2 may involve adenylate cyclase.The budding yeast Sacchlaromnyces cerevisiae is a microorganism used as a model eucaryote for the study of the regulation of cell cycle and of cell growth. S. cerei'isiae has a major cell cycle control point in the regulatory area called start, located in G1. At start, a yeast cell integrates many intracellular and environmental signals and then is committed to continue proliferation or is switched to differentiation pathways such as sporulation, conjugation, or entry into the stationary phase (36).At start, a critical cell size for budding and for entering the S phase is required (9,20); this requirement allows for the coordination between growth, which is normally the ratelimiting process in most physiological conditions (1,20), and nuclear division cycle events. The G1 phase is delayed until this critical mass is reached, which determines a major control mechanism of cell cycle progression (1. 16, 24, 48).The critical cell mass required for budding is strictly related to the nutritional conditions of the cells. Indeed, poor media and low growth rates correspond to smaller critical sizes until a minimum size for budding has been reached and it cannot be further reduced at longer generation times (19,25,47,48 (5,7,39,46), that share extensive homology with the mammalian ras proteins (21). A mechanism mediated by the activation of cAMP-dependent protein kinases positively regulates the cell growth and inhibits differentiating pathways associated with nutrient depletion, such as sporulation or entrance into the GO phase (33). In fact, all the mutations that inactivate this mechanism, thereby reducing the ability to increase intracellular cAMP levels ((dc25, (dc135, rasl. ras2), arrest growth in a manner that mimics nutrient starvation (17, 22, 30). If the inactivation is onl...

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Molecular cloning and transcriptional analysis of the start gene CDC25 of Saccharomyces cerevisiae

Cited by 51 publications

References 40 publications

cAMP- and RAS-independent Nutritional Regulation of Plasma-membrane H+-ATPase Activity in Saccharomyces cerevisiae

cAMP- and RAS-independent Nutritional Regulation of Plasma-membrane H+-ATPase Activity in Saccharomyces cerevisiae

SCH9, a gene of Saccharomyces cerevisiae that encodes a protein distinct from, but functionally and structurally related to, cAMP-dependent protein kinase catalytic subunits.

Cell size modulation by CDC25 and RAS2 genes in Saccharomyces cerevisiae.

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