Regulation of p34CDC28 tyrosine phosphorylation is not required for entry into mitosis in S. cerevisiae

Amon, Angelika; Surana, Uttam; Muroff, Ivor; Nasmyth, Kim

doi:10.1038/355368a0

Cited by 285 publications

(225 citation statements)

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“…In budding yeast, however, the DNA damage checkpoint pathway does not control cell cycle progression by inactivating the Cdk1 equivalent, Cdc28 (5). Instead, this checkpoint pathway induces a mitotic arrest by inhibiting the metaphase to anaphase transition.…”

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confidence: 99%

Two Distinct Pathways for Inhibiting Pds1 Ubiquitination in Response to DNA Damage

Agarwal

Tang

et al. 2003

Journal of Biological Chemistry

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The presence of DNA damage activates a conserved cellular response known as the DNA damage checkpoint pathway. This pathway induces a cell cycle arrest that persists until the damage is repaired. Consequently, the failure to arrest in response to DNA damage is associated with genomic instability. In budding yeast, activation of the DNA damage checkpoint pathway leads to a mitotic cell cycle arrest. Following the detection of DNA damage, the checkpoint signal is transduced via the Mec1 kinase, which in turn activates two kinases, Rad53 and Chk1 that act in parallel pathways to bring about the cell cycle arrest. The downstream target of Rad53 is unknown. The target of Chk1 is Pds1, an inhibitor of anaphase initiation whose degradation is a prerequisite for mitotic progression. Pds1 degradation is dependent on its ubiquitination by the anaphase-promoting complex/cyclosome ubiquitin ligase, acting in conjunction with the Cdc20 protein (APC/C Cdc20 ). Previous studies showed that the Rad53 and Chk1 pathways independently lead to Pds1 stabilization but the mechanism for this was unknown. In the present study we show that both the Chk1 and the Rad53 pathways inhibit the APC/ C Cdc20 -dependent ubiquitination of Pds1 but they affect different steps of the process: the Rad53 pathway inhibits the Pds1-Cdc20 interaction whereas Chk1-dependent phosphorylation of Pds1 inhibits the ubiquitination reaction itself. Finally, we show that once the DNA damage is repaired, Pds1 dephosphorylation is involved in the recovery from the checkpoint induced cell cycle arrest.

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confidence: 99%

Two Distinct Pathways for Inhibiting Pds1 Ubiquitination in Response to DNA Damage

Agarwal

Tang

et al. 2003

Journal of Biological Chemistry

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“…About 100 transformants were obtained, and among 11 randomly selected for sequencing, one was found to include both mutations. As expected, the cdc28-A18F19 strain grows normally and is resistant to overexpression of the Schizosaccharomyces pombe weel + gene from a GAL promoter (Amon et al, 1992). Overall, longer flanking regions may result in higher rates of successful mutagenesis; however, the length limitations for efficient PCR amplifications have to be considered.…”

Section: Marking the Genomic Cdc28 Locusmentioning

confidence: 61%

“…In order to determine whether the predicted difficulty with integrating mutations distant from the marker might preclude general use of this technique, we tested the use of fusion PCR to introduce aminoterminal T18A and Y19F mutations in the chromosomal CDC28 ORF along with the 3k selectable marker. This mutation would be expected to have no vegetative growth phenotype on an otherwise wild-type background (Amon et al, 1992). The cdc28-A18F19 coding sequence was amplified from plasmid p3303 using primers x228F and +1125R, and the marker and flanking regions from genomic DNA using primers +932F and +1342R (Figure 2).…”

Section: Marking the Genomic Cdc28 Locusmentioning

confidence: 99%

Marker‐fusion PCR for one‐step mutagenesis of essential genes in yeast

Kitazono¹,

Tobe²,

Kalton³

et al. 2001

Yeast

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We describe a one-step gene replacement method based on fusion PCR that can be used to mutagenize essential genes at their endogenous locus. Marker-fusion PCR can facilitate transfer of alleles between strains as well as PCR-based techniques, such as site-directed and error-prone PCR mutagenesis, all without cloning or strain constructions. With this method, PCR is used to fuse a mutagenized fragment to an overlapping fragment containing a selectable marker flanked by regions of homology to the target. By transforming yeast with these PCR products, specific mutations are introduced at the endogenous locus through homologous recombination. We tested the 'marker-fusion PCR' method using the budding yeast CDC28 gene and were able to efficiently introduce site-directed mutations and integrate genomic or plasmid-borne mutant alleles. As a further application for this method, we used a spiked oligonucleotide to randomize the coding sequence for a single domain of CDC28 and were able to construct highly mutagenized libraries for this region.

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“…Which pathways converge on the Wee1 and Cdc25 regulators depends on the biology of the organism. For example, in budding yeast, instead of entry to mitosis (Amon et al 1992), it is used earlier in the cell cycle to arrest cells should synthesis of the bud be perturbed (the morphogenesis checkpoint) (Lew and Reed 1995). In many systems, unreplicated or damaged DNA activates "checkpoint" pathways that tip the balance in favor of Wee1 and against Cdc25 to prevent mitosis (reviewed in Langerak 2011).…”

Section: Entry To Mitosis Cyclin B -Cyclin-dependent Kinase (Cdk): Thmentioning

confidence: 99%

The Biochemistry of Mitosis

Wieser

Pines

2015

Cold Spring Harb Perspect Biol

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In this article, we will discuss the biochemistry of mitosis in eukaryotic cells. We will focus on conserved principles that, importantly, are adapted to the biology of the organism. It is vital to bear in mind that the structural requirements for division in a rapidly dividing syncytial Drosophila embryo, for example, are markedly different from those in a unicellular yeast cell. Nevertheless, division in both systems is driven by conserved modules of antagonistic protein kinases and phosphatases, underpinned by ubiquitin-mediated proteolysis, which create molecular switches to drive each stage of division forward. These conserved control modules combine with the self-organizing properties of the subcellular architecture to meet the specific needs of the cell. Our discussion will draw on discoveries in several model systems that have been important in the long history of research on mitosis, and we will try to point out those principles that appear to apply to all cells, compared with those in which the biochemistry has been specifically adapted in a particular organism.

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Regulation of p34CDC28 tyrosine phosphorylation is not required for entry into mitosis in S. cerevisiae

Cited by 285 publications

References 22 publications

Two Distinct Pathways for Inhibiting Pds1 Ubiquitination in Response to DNA Damage

Two Distinct Pathways for Inhibiting Pds1 Ubiquitination in Response to DNA Damage

Marker‐fusion PCR for one‐step mutagenesis of essential genes in yeast

The Biochemistry of Mitosis

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