The yeast TEM1 gene, which encodes a GTP-binding protein, is involved in termination of M phase.

Shirayama, Masaki; Matsui, Yasuji; Toh‐e, Akio

doi:10.1128/mcb.14.11.7476

Cited by 167 publications

(158 citation statements)

References 48 publications

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“…Although TEM1 is an essential gene, LTE1 is not (29). Strains deleted for LTE1 arrest only at low temperatures (29), whereas at 25°C they merely show a transient delay at telophase (26). Thus, although Lte1p is not strictly required for cell cycle progression, it is required for efficient progression.…”

Section: Overexpression Identifies Genes That Are Helpful For Cell Cyclementioning

confidence: 99%

“…Activation of Tem1p is believed to be necessary for release of the Cdc14p phosphatase from the nucleolus, allowing it to dephosphorylate its substrates and promote mitotic exit (9,28). Although TEM1 is an essential gene, LTE1 is not (29). Strains deleted for LTE1 arrest only at low temperatures (29), whereas at 25°C they merely show a transient delay at telophase (26).…”

Section: Overexpression Identifies Genes That Are Helpful For Cell Cyclementioning

confidence: 99%

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A large-scale overexpression screen in Saccharomyces cerevisiae identifies previously uncharacterized cell cycle genes

Stevenson

Kennedy

Harlow

2001

Proc. Natl. Acad. Sci. U.S.A.

109

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We have undertaken an extensive screen to identify Saccharomyces cerevisiae genes whose products are involved in cell cycle progression. We report the identification of 113 genes, including 19 hypothetical ORFs, which confer arrest or delay in specific compartments of the cell cycle when overexpressed. The collection of genes identified by this screen overlaps with those identified in loss-of-function cdc screens but also includes genes whose products have not previously been implicated in cell cycle control. Through analysis of strains lacking these hypothetical ORFs, we have identified a variety of new CDC and checkpoint genes.C ell cycle studies performed with Saccharomyces cerevisiae have served as a guideline for understanding eukaryotic cell cycle progression. In particular, the now classic screens by Hartwell and colleagues (1-6) to identify temperature-sensitive mutants with specific arrest points throughout the cell division cycle (cdc) have shed light on numerous aspects of cell cycle, including progression through START (e.g., CDC28), regulation of DNA replication (e.g., CDC6), and control of mitosis (e.g., CDC14).Although the cumulative cdc screens performed to date have been extensive, Hartwell and colleagues proposed that there may be additional CDC genes that are difficult or impossible to uncover by using a recessive loss-of-function approach (6). Reasons for this difficulty were speculated to include: (i) a lack of susceptibility of the gene product to generation of a temperature-sensitive allele; (ii) the presence in the genome of a closely related gene with similar or redundant function (e.g., cyclins); (iii) the presence of CDC genes that are helpful but not absolutely required for cell cycle progression; and (iv) the assumption of a morphologically homogeneous terminal phenotype for all cdc mutants (6). In addition, it has since become apparent that protein degradation during the cell cycle is a highly regulated process that contributes to many stages of cell cycle progression. A change in turnover of some encoded gene products can lead to cell cycle arrest (7-9). Such genes would likely escape detection in the cdc screens.In an effort to complement the original cdc screens and in the interest of uncovering new CDC genes from within the categories described above, we undertook an extensive overexpression screen to identify genes that cause an alteration in cell cycle progression. By using this approach, we expected to uncover genes whose overexpression leads to hypermorphic, antimorphic, or neomorphic effects. Many of these genes should be involved at some level in the yeast cell cycle. To further delineate these putative cell cycle genes, we analyzed all of the initial positives by a variety of other assays to establish their roles in cell cycle control.We used a conditional overexpression approach with a S. cerevisiae cDNA library under control of the GAL1 promoter (10). A second smaller screen was performed by using a sheared genomic library under GAL1 control (11). Several previous studi...

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Section: Overexpression Identifies Genes That Are Helpful For Cell Cyclementioning

confidence: 99%

Section: Overexpression Identifies Genes That Are Helpful For Cell Cyclementioning

confidence: 99%

A large-scale overexpression screen in Saccharomyces cerevisiae identifies previously uncharacterized cell cycle genes

Stevenson

Kennedy

Harlow

2001

Proc. Natl. Acad. Sci. U.S.A.

109

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“…In budding yeast, there are many additional genes that have roles in the ending of mitosis. These include DBF2, DBF20, CDC5, and CDC15, which encode protein kinases, CDC14, which encodes a protein phosphatase, TEM1 and LTE1, encoding a guanosine triphosphate-binding protein and G-nucleotide exchange factor, respectively (Johnston et al, 1990;Schweitzer and Philippsen, 1991;Wan et al, 1992;Kitada et al, 1993;Shirayama et al, 1994;Toyn and Johnston, 1994). The multiple genetic interactions found among these genes (references above and our unpublished observations) suggest that the corresponding gene products act in a common signaling pathway regulating the M/G1 transition perhaps by controlling the deactivation of the B cyclin kinase.…”

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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“…Loss of function of the MEN causes cells to arrest in late anaphase͞ telophase, similar to the arrest caused by overexpression of non-degradable B-type cyclin (10). Components of the MEN interact genetically with each other and act upstream of Cdc14 as suggested by epistasis studies (8,(11)(12)(13)(14)(15)(16)(17). Lte1, a putative guanine-nucleotide exchange factor (GEF), and Tem1, a GTPbinding protein, are likely to be at the top of this pathway (12,15,18).…”

mentioning

confidence: 99%

Protein kinase Cdc15 activates the Dbf2-Mob1 kinase complex

Mah

Jang

Deshaies

2001

Proc. Natl. Acad. Sci. U.S.A.

188

206

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Exit from mitosis in budding yeast requires inactivation of cyclindependent kinases through mechanisms triggered by the protein phosphatase Cdc14. Cdc14 activity, in turn, is regulated by a group of proteins, the mitotic exit network (MEN), which includes Lte1, Tem1, Cdc5, Cdc15, Dbf2͞Dbf20, and Mob1. The direct biochemical interactions between the components of the MEN remain largely unresolved. Here, we investigate the mechanisms that underlie activation of the protein kinase Dbf2. Dbf2 kinase activity depended on Tem1, Cdc15, and Mob1 in vivo. In vitro, recombinant protein kinase Cdc15 activated recombinant Dbf2, but only when Dbf2 was bound to Mob1. Conserved phosphorylation sites Ser-374 and Thr-544 (present in the human, Caenorhabditis elegans, and Drosophila melanogaster relatives of Dbf2) were required for DBF2 function in vivo, and activation of Dbf2-Mob1 by Cdc15 in vitro. Although Cdc15 phosphorylated Dbf2, Dbf2-Mob1, and Dbf2(S374A͞T544A)-Mob1, the pattern of phosphate incorporation into Dbf2 was substantially altered by either the S374A T544A mutations or omission of Mob1. Thus, Cdc15 promotes the exit from mitosis by directly switching on the kinase activity of Dbf2. We propose that Mob1 promotes this activation process by enabling Cdc15 to phosphorylate the critical Ser-374 and Thr-544 phosphoacceptor sites of Dbf2.

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The yeast TEM1 gene, which encodes a GTP-binding protein, is involved in termination of M phase.

Cited by 167 publications

References 48 publications

A large-scale overexpression screen in Saccharomyces cerevisiae identifies previously uncharacterized cell cycle genes

A large-scale overexpression screen in Saccharomyces cerevisiae identifies previously uncharacterized cell cycle genes

Swi5 Controls a Novel Wave of Cyclin Synthesis in Late Mitosis

Protein kinase Cdc15 activates the Dbf2-Mob1 kinase complex

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