SPO12andSIT4suppress mutations inDBF2, which encodes a cell cycle protein kinase that is periodically expressed

Parkes, Vincent; Johnston, Leland H.

doi:10.1093/nar/20.21.5617

Cited by 38 publications

(60 citation statements)

References 23 publications

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“…Reiser et al the FEAR network such as Spo12 or Cdc5 can, when overproduced, suppress the temperature-sensitive lethality of MEN mutants (Parkes and Johnston, 1992;Jaspersen et al, 1998;Stegmeier et al, 2002). We found that overexpression of SPO12 suppressed the proliferation defect of cdc15-2 mutants as well as of cdc15-2 pbs2⌬ mutants ( Figure 5C).…”

Section: Regulation Of Cdc14 Localization By Stressmentioning

confidence: 51%

The Stress-activated Mitogen-activated Protein Kinase Signaling Cascade Promotes Exit from Mitosis

Reiser

D’Aquino

et al. 2006

MBoC

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In budding yeast, a signaling network known as the mitotic exit network (MEN) triggers exit from mitosis. We find that hypertonic stress allows MEN mutants to exit from mitosis in a manner dependent on the high osmolarity glycerol (HOG) mitogen-activated protein (MAP) kinase cascade. The HOG pathway drives exit from mitosis in MEN mutants by promoting the activation of the MEN effector, the protein phosphatase Cdc14. Activation of Cdc14 depends on the Cdc14 early anaphase release network, a group of proteins that functions in parallel to the MEN to promote Cdc14 function. Notably, exit from mitosis is promoted by the signaling branch defined by the Sho1 osmosensing system, but not by the Sln1 osmosensor of the HOG pathway. Our results suggest that the stress MAP kinase pathway mobilizes programs to promote completion of the cell cycle and entry into G 1 under unfavorable conditions.

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Section: Regulation Of Cdc14 Localization By Stressmentioning

confidence: 51%

The Stress-activated Mitogen-activated Protein Kinase Signaling Cascade Promotes Exit from Mitosis

Reiser

D’Aquino

et al. 2006

MBoC

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“…There are a number of genes, encoding regulatory proteins, that, when mutated, cause a cell cycle arrest similar to mob1 mutants. There is an extensive array of genetic interactions linking them together, suggesting that they belong to a common pathway (Pringle and Hartwell, 1981;Wickner et al, 1987;Johnston et al, 1990;Parkes and Johnston, 1992;Kitada et al, 1993;Molero et al, 1993;Spevak et al, 1993;Keng et al, 1994;Shirayama et al, 1994aShirayama et al, , 1994bShirayama et al, , 1996Toyn and Johnston, 1994). We have begun to establish that MOB1 shares genetic interactions with several members of this class of genes.…”

Section: Discussionmentioning

confidence: 99%

MOB1, an Essential Yeast Gene Required for Completion of Mitosis and Maintenance of Ploidy

Luca

Winey

1998

MBoC

166

200

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Mob1p is an essential Saccharomyces cerevisiaeprotein, identified from a two-hybrid screen, that binds Mps1p, a protein kinase essential for spindle pole body duplication and mitotic checkpoint regulation. Mob1p contains no known structural motifs; however MOB1 is a member of a conserved gene family and shares sequence similarity with a nonessential yeast gene,MOB2. Mob1p is a phosphoprotein in vivo and a substrate for the Mps1p kinase in vitro. Conditional alleles ofMOB1 cause a late nuclear division arrest at restrictive temperature. MOB1 exhibits genetic interaction with three other yeast genes required for the completion of mitosis,LTE1, CDC5, and CDC15 (the latter two encode essential protein kinases). Most haploid mutantmob1 strains also display a complete increase in ploidy at permissive temperature. The mechanism for the increase in ploidy may occur through MPS1 function. One mob1strain, which maintains stable haploidy at both permissive and restrictive temperature, diploidizes at permissive temperature when combined with the mps1–1 mutation. Strains containingmob2Δ also display a complete increase in ploidy when combined with the mps1-1 mutation. Perhaps in addition to, or as part of, its essential function in late mitosis, MOB1 is required for a cell cycle reset function necessary for the initiation of the spindle pole body duplication.

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“…It is well established that the preliminary events of S phase occur in late mitosis (for example see Cocker et al, 1996). Deletion of SPO12 and SIC1 both lead to a slight protraction of M phase (Donovan et al, 1994;Parkes and Johnston, 1992) and perhaps, in the absence of Pho85, defects occur in the M-G1 transition leading to the observed temperature sensitivity in the double mutants.…”

Section: Discussionmentioning

confidence: 99%

“…We have used Dbf2 as a probe to study the events of late mitosis (Johnston et al, 1990;Parkes and Johnston, 1992;Donovan et al, 1994;Johnston, 1993, 1994). One approach was to isolate dosage suppressors of dbf2 ts alleles, which normally cause arrest in telophase.…”

Section: Introductionmentioning

confidence: 99%

Swi5 Controls a Novel Wave of Cyclin Synthesis in Late Mitosis

Aerne¹,

Johnson²,

Toyn³

et al. 1998

MBoC

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We have shown previously that the Swi5 transcription factor regulates the expression of the SIC1 Cdk inhibitor in late mitosis. This suggests that Swi5 might control other genes with roles in ending mitosis. We identified a gene with a Swi5-binding site in the promoter that encoded a protein with high homology to Pcl2, a cyclin-like protein that associates with the Cdk Pho85. This gene, PCL9, is indeed regulated by Swi5 in late M phase, the only cyclin known to be expressed at this point in the cell cycle. The Pcl9 protein is associated with a Pho85-dependent protein kinase activity, and the protein is unstable with peak levels occurring in late M phase. PCL2 is already known to be expressed in late G1 and we find that, in addition, it is also regulated by Swi5 in telophase. The expression of PCL2 and PCL9 at this stage of the cell cycle implies a role for the Pho85 Cdk at the end of mitosis. Consistent with this a synthetic interaction was observed between pho85⌬ and strains deleted for SIC1, SWI5, and SPO12. These and other studies support the notion that the M/G1 switch is a major cell cycle transition.

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SPO12andSIT4suppress mutations inDBF2, which encodes a cell cycle protein kinase that is periodically expressed

Cited by 38 publications

References 23 publications

The Stress-activated Mitogen-activated Protein Kinase Signaling Cascade Promotes Exit from Mitosis

The Stress-activated Mitogen-activated Protein Kinase Signaling Cascade Promotes Exit from Mitosis

MOB1, an Essential Yeast Gene Required for Completion of Mitosis and Maintenance of Ploidy

Swi5 Controls a Novel Wave of Cyclin Synthesis in Late Mitosis

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