Identification of a gene necessary for cell cycle arrest by a negative growth factor of yeast: FAR1 is an inhibitor of a G1 cyclin, CLN2

Chang, Fred; Herskowitz, Ira

doi:10.1016/0092-8674(90)90503-7

Cited by 386 publications

(352 citation statements)

References 48 publications

Supporting

Mentioning

345

Contrasting

Unclassified

Order By: Relevance

“…Therefore, one might not expect FAR1 to play a role in the white cell response, because the role FAR1 plays in the analogous mating process of S. cerevisiae is in the polarization of cells in a gradient of pheromone and G1 arrest (Chang and Herskowitz, 1990;Valtz et al, 1995;Butty et al, 1998). However, in supplemental data to Roberts et al (2000), it was reported that STE12 was not up-regulated by pheromone in a far1⌬ mutant, indicating that Far1p played a role in the up-regulation of pheromone-induced genes.…”

Section: Opaque Cell Pheromone Response Of Far1⌬mentioning

confidence: 74%

“…Therefore, we considered the possibility that Far1p may also be involved in the up-regulation of genes by pheromone in the white cell response. The far1⌬ mutant of S. cerevisiae shmoos in response to ␣-pheromone, but the shmoos do not polarize in a gradient of pheromone, and far1⌬ cells are not blocked in G1 by pheromone (Chang and Herskowitz, 1990;Dorer et al, 1995;Valtz et al, 1995). The far1⌬ mutant of S. cerevisiae is capable of mating, but the frequency of mating is significantly reduced, presumably because far1⌬ cells cannot efficiently find partners because they are defective in chemotropism (Valtz et al, 1995).…”

mentioning

confidence: 99%

See 1 more Smart Citation

The Same Receptor, G Protein, and Mitogen-activated Protein Kinase Pathway Activate Different Downstream Regulators in the Alternative White and Opaque Pheromone Responses ofCandida albicans

Song

Sahni

Daniels

et al. 2008

MBoC

251

View full text Add to dashboard Cite

Candida albicans must undergo a switch from white to opaque to mate. Opaque cells then release mating type-specific pheromones that induce mating responses in opaque cells. Uniquely in C. albicans, the same pheromones induce mating-incompetent white cells to become cohesive, form an adhesive basal layer of cells on a surface, and then generate a thicker biofilm that, in vitro, facilitates mating between minority opaque cells. Through mutant analysis, it is demonstrated that the pathways regulating the white and opaque cell responses to the same pheromone share the same upstream components, including receptors, heterotrimeric G protein, and mitogen-activated protein kinase cascade, but they use different downstream transcription factors that regulate the expression of genes specific to the alternative responses. This configuration, although common in higher, multicellular systems, is not common in fungi, and it has not been reported in Saccharomyces cerevisiae. The implications in the evolution of multicellularity in higher eukaryotes are discussed. INTRODUCTIONBoth single cell organisms and the individual cells of multicellular organisms must respond to a variety of environmental signals (Dorsky et al., 2000;Balázsi and Oltvai, 2005). In addition, in higher eukaryotes different cell types frequently respond to the same signal in unique ways (Rincón and Pedraza-Alva, 2003;Bacci et al., 2005;Dailey et al., 2005). In most cases, different signals interact with unique surface receptors that activate different signal transduction pathways, as has been demonstrated in Saccharomyces cerevisiae (Leberer et al., 1997;Gustin et al., 1998;Madhani and Fink, 1998;Elion, 2000). The mitogen-activated protein (MAP) kinase pathways have evolved as highly efficient, multipurpose signal transduction systems. S. cerevisiae uses multiple MAP kinase pathways, each one for a distinct signaling system, including the mating process, the filamentation process, cell wall integrity, ascospore formation, and osmoregulation (Levin and Errede, 1995;Gustin et al., 1998;Saito and Tatebayashi, 2004;Chen and Thorner, 2007). Several of these pathways share a limited number of components, but all are presumed to use different receptors to elicit very different responses. In the mating process of S. cerevisiae, a cells release a-factor that interacts with the a-receptor on ␣ cells, and ␣ cells release ␣-factor that interacts with the ␣-receptor on a cells. These alternative signals are then transduced through the same heterotrimeric G protein to activate the same MAP kinase pathway, which in turn activates the same downstream regulators that elicit similar mating responses, including G1 arrest, polarization, and shmooing (Sprague et al., 1983;Bender and Sprague, 1986;Leberer et al., 1997). Other fungi, including Magnaporthe grisea (Dixon et al., 1999;Zhao et al., 2005b) Neurospora crassa (Li et al., 2005), and Cryptococcus neoformans (Davidson et al., 2003;Kraus et al., 2003;Bahn et al., 2005) also use MAP kinase pathways for a variety of responses...

show abstract

Section: Opaque Cell Pheromone Response Of Far1⌬mentioning

confidence: 74%

mentioning

confidence: 99%

The Same Receptor, G Protein, and Mitogen-activated Protein Kinase Pathway Activate Different Downstream Regulators in the Alternative White and Opaque Pheromone Responses ofCandida albicans

Song

Sahni

Daniels

et al. 2008

MBoC

251

View full text Add to dashboard Cite

show abstract

“…Up-regulation of the transcription of pheromone-dependent genes in early G 1 may reflect a mechanism that ensures the proper timing of the cell cycle arrest. Expression of the Far1 protein, which is thought to specifically inhibit the G 1 cyclins Cln1 and Cln2, is restricted to early G 1 (17,18,61). After START, Far1 is degraded and the cell is committed to undergo a mitotic cell division cycle (62).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of the G1-cyclin Gene CLN2Represses the Mating Pathway in Saccharomyces cerevisiaeat the Level of the MEKK Ste11

Wassmann¹,

Ammerer

1997

Journal of Biological Chemistry

View full text Add to dashboard Cite

Basal and induced transcription of pheromonedependent genes is regulated in a cell cycle-dependent way. FUS1, a gene strongly induced after pheromone treatment, shows high mRNA levels in mitosis and early G 1 phase of the cell cycle, a decrease in G 1 after START and again an increase in S phase. Overexpression of CLN2 was shown to repress the transcript number of pheromone-dependent genes (1). We asked whether the activities of components of the mating pathway fluctuate during the cell cycle. We were also interested in determining at what level Cln2 represses the signal transduction machinery. Here we show that the activity of the mitogen-activated protein kinase Fus3 indeed fluctuates during the cell cycle, reflecting the oscillations of the gene transcripts. CLN2 overexpression represses Fus3 kinase activity, independently of the phosphatase Msg5. Additionally, we show that the activity of the MEK Ste7 also fluctuates during the cell cycle. Increased Cln2 levels repress the ability of hyperactive STE11 alleles to induce the pathway. G protein-independent activation of Ste11 caused by an rga1 pbs2 mutation is resistant to high levels of Cln2 kinase. Therefore our results suggest that Cln2-dependent repression of the mating pathway occurs at the level of Ste11.

show abstract

“…The CLN proteins are the cyclins that activate CDC28 at START (Sudbery et al, 1980;Cross, 1988Cross, , 1990Nash et al, 1988;Hadwiger et al, 1989;Richardson et al, 1989;Wittenberg et al, 1990), and some signals that regulate START may act by modulating CLN protein function (Chang and Herskowitz, 1990;Wittenberg et al, 1990;Cross and Tinkelenberg, 1991 Pines and Hunter, 1991). Cyclin A is synthesized in S phase and is associated with the CDC2 protein in S-phase cells (Giordano et al, 1989;Pines and Hunter, 1990).…”

Section: Introductionmentioning

confidence: 99%

Activation of the p34 CDC2 protein kinase at the start of S phase in the human cell cycle.

Marraccino

Firpo

Roberts

1992

MBoC

View full text Add to dashboard Cite

Using a protocol for selecting cells on the basis of both size and age (with respect to the preceding mitosis), we isolated highly synchronous human G1 cells. With this procedure, we demonstrated that the p34 CDC2 kinase was activated at the start of S phase. Cyclin A synthesis began at the same time, and activation of the p34 CDC2 kinase at the start of S phase was, at least in part, due to its association with cyclin A. Furthermore, cells synchronized in late G1 by exposure to the drug mimosine contain active cyclin A/p34 CDC2 kinase, indicating that p34 CDC2 activation can occur before DNA synthesis begins. Thus, the cyclin A/CDC2 complex, which previously has been shown to be sufficient to start SV40 DNA synthesis in vitro, assembles and is activated at the start of S phase in vivo.

show abstract

Identification of a gene necessary for cell cycle arrest by a negative growth factor of yeast: FAR1 is an inhibitor of a G1 cyclin, CLN2

Cited by 386 publications

References 48 publications

The Same Receptor, G Protein, and Mitogen-activated Protein Kinase Pathway Activate Different Downstream Regulators in the Alternative White and Opaque Pheromone Responses ofCandida albicans

The Same Receptor, G Protein, and Mitogen-activated Protein Kinase Pathway Activate Different Downstream Regulators in the Alternative White and Opaque Pheromone Responses ofCandida albicans

Overexpression of the G1-cyclin Gene CLN2Represses the Mating Pathway in Saccharomyces cerevisiaeat the Level of the MEKK Ste11

Activation of the p34 CDC2 protein kinase at the start of S phase in the human cell cycle.

Contact Info

Product

Resources

About