Role of calcineurin and Mpk1 in regulating the onset of mitosis in budding yeast

Mizunuma, Masaki; Hirata, Dai; Miyahara, Katsunori; Tsuchiya, Eiko; Miyakawa, Tokichi

doi:10.1038/32695

Cited by 127 publications

(166 citation statements)

References 24 publications

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“…The functions of ESP1, CLB2, MIH1 and CDC20 as regulators of mitosis have been extensively characterized (Baum et al, 1988;Russell et al, 1989;Sethi et al, 1991;Surana et al, 1991;Visintin et al, 1997;Ciosk et al, 1998;Shirayama et al, 1998;Uhlmann et al, 1999). ZDS2 and ZDS1 are required for G 2 /M progression and SWE1 function and can suppress mutations in numerous genes, mostly cell cycle regulators (Bi and Pringle, 1996;Ma et al, 1996;Schwer and Shuman, 1996;Yu et al, 1996;Mizunuma et al, 1998;Roy and Runge, 2000, and references within). DHH1 is a non-essential DEAD-box helicase that has been implicated in SWE1 function (Strahl-Bolsinger and Tanner, 1993;Warbick and Glover, 1994;Moriya and Isono, 1999), translation (Ladomery et al, 1997), transcription (Hata et al, 1998) and cell cycle arrest under stressful conditions (Maekawa et al, 1994;Bergkessel and Reese, unpublished).…”

Section: Isolation Of High Copy Suppressors Of the Taf68-9 Mutantmentioning

confidence: 99%

“…The predicted outcomes of the overexpression of ZDS2, CLB2, ZDS1 and MIH1 would be an increase in G 2 /M cyclin-dependent kinase activity and the increased rate of G 2 /M progression. ZDS2 and ZDS1 are likely positive regulators of the cell cycle (Bi and Pringle, 1996;Ma et al, 1996;Yu et al, 1996;Mizunuma et al, 1998) by inhibiting the function of SWE1, a negative regulator of mitosis (Booher et al, 1993). CLB2 is a mitotic cyclin, and overexpression will directly enhance CDK activity (Surana et al, 1991).…”

Section: Genetic Links Between Tafs and Cdksmentioning

confidence: 99%

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Genetic analysis of TAF68/61 reveals links to cell cycle regulators

Reese

Green

2001

Yeast

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In yeast, inactivation of certain TBP-associated factors (TAF II s) results in arrest at specific stages of the cell cycle. In some cases, cell cycle arrest is not observed because overlapping defects in other cellular processes precludes the manifestation of an arrest phenotype. In the latter situation, genetic analysis has the potential to reveal the involvement of TAF II s in cell cycle regulation. In this report, a temperature-sensitive mutant of TAF68/61 was used to screen for high-copy dosage suppressors of its growth defect. Ten genes were isolated: TAF suppressor genes, TSGs 1-10. Remarkably, most TSGs have either a genetic or a direct link to control of the G 2 /M transition. Moreover, eight of the 10 TSGs can suppress a CDC28 mutant specifically defective for mitosis (cdc28-1N) but not an allele defective for passage through start. The identification of these genes as suppressors of cdc28-1N has identified four unreported suppressors of this allele. Moreover, synthetic lethality is observed between taf68-9 and cdc28-1N. The isolation of multiple genes involved in the control of a specific phase of the cell cycle argue that the arrest phenotypes of certain TAF II mutants reflect their role in specifically regulating cell cycle functions.

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Section: Isolation Of High Copy Suppressors Of the Taf68-9 Mutantmentioning

confidence: 99%

Section: Genetic Links Between Tafs and Cdksmentioning

confidence: 99%

Genetic analysis of TAF68/61 reveals links to cell cycle regulators

Reese

Green

2001

Yeast

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“…1A, B). As Erk5 activity has been associated with cell cycle progression, 14,24 we synchronised the cells in G1/S phase by incubating them with thymidine and then stained them with propidium iodide (PI) for cytofluorometric evaluation of the cell cycle. The PI profiles showed that a fraction of shErk5 cells were polyploid (Fig.…”

Section: Thymidine Generates Lethal Dna Damage In Erk5-depleted Jurkamentioning

confidence: 99%

Erk5 contributes to maintaining the balance of cellular nucleotide levels and erythropoiesis

et al. 2015

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An adequate supply of nucleotides is essential for accurate DNA replication, and inappropriate deoxyribonucleotide triphosphate (dNTP) concentrations can lead to replication stress, a common source of DNA damage, genomic instability and tumourigenesis. Here, we provide evidence that Erk5 is necessary for correct nucleotide supply during erythroid development. Mice with Erk5 knockout in the haematopoietic lineage showed impaired erythroid development in bone marrow, accompanied by altered dNTP levels and increased DNA mutagenesis in erythroid progenitors as detected by exome sequencing. Moreover, Erk5-depleted leukemic Jurkat cells presented a marked sensitivity to thymidine-induced S phase stalling, as evidenced by increased H2AX phosphorylation and apoptosis. The increase in thymidine sensitivity correlated with a higher dTTP/dCTP ratio. These results indicate that Erk5 is necessary to maintain the balance of nucleotide levels, thus preventing dNTP misincorporation and DNA damage in proliferative erythroid progenitors and leukemic Jurkat T cells.

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“…Mck1p plays a role in mitotic chromosomal segregation specific to CDEIII function (Shero and Hieter, 1991), acts in the transcription of IME1 at the beginning of meiosis (Neigeborn and Mitchell, 1991), and is important for inducing the cell cycle delay in response to Ca 2ϩ (Mizunuma et al, 2001). Mds1p/Rim11p plays a role in expression of meiotic genes by phosphorylating Ime1p and Ume6p (Bowdish et al, 1994;Xiao and Mitchell, 2000).…”

Section: Introductionmentioning

confidence: 99%

Yeast Glycogen Synthase Kinase-3 Activates Msn2p-dependent Transcription of Stress Responsive Genes

Hirata

Andoh²,

Asahara

et al. 2003

MBoC

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The yeast Saccharomyces cerevisiae has four genes, MCK1, MDS1 (RIM11), MRK1, and YOL128c, that encode homologues of mammalian glycogen synthase kinase 3 (GSK-3). A gsk-3 null mutant in which these four genes are disrupted showed growth defects on galactose medium. We isolated several multicopy suppressors of this growth defect. Two of them encoded Msn2p and phosphoglucomutase (PGM). Msn2p is a transcription factor that binds to the stress-response element (STRE). PGM is an enzyme that interconverts glucose-1 phosphate and glucose-6 phosphate and is regulated by Msn2p at the transcriptional level. Expression of the mRNAs of PGM2 and DDR2, whose promoter regions possess STRE sequences, on induction by heat shock or salt stress was reduced not only in an msn2 msn4 (msn2 homologue) double mutant but also in the gsk-3 null mutant. STRE-dependent transcription was greatly inhibited in the gsk-3 null mutant or mck1 mds1 double mutant, and this phenotype was suppressed by the expression of Mck1p but not of a kinase-inactive form of Mck1p. Although Msn2p accumulated in the nucleus of the gsk-3 null mutant as well as in the wild-type strain under various stress conditions, its STRE-binding activity was reduced in extracts prepared from the gsk-3 null mutant or mck1 mds1 double mutant. These results suggest that yeast GSK-3 promotes formation of a complex between Msn2p and DNA, which is required for the proper response to different forms of stress. Because neither Msn2p–GSK-3 complex formation nor GSK-3–dependent phosphorylation of Msn2p could be detected, the regulation of Msn2p by GSK-3 may be indirect

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Role of calcineurin and Mpk1 in regulating the onset of mitosis in budding yeast

Cited by 127 publications

References 24 publications

Genetic analysis of TAF68/61 reveals links to cell cycle regulators

Genetic analysis of TAF68/61 reveals links to cell cycle regulators

Erk5 contributes to maintaining the balance of cellular nucleotide levels and erythropoiesis

Yeast Glycogen Synthase Kinase-3 Activates Msn2p-dependent Transcription of Stress Responsive Genes

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