Faculty Opinions recommendation of Interdependent nuclear accumulation of budding yeast Cdt1 and Mcm2-7 during G1 phase.

p25rum1 and p40SIC1 are specific inhibitors of p34(cdc2/CDC28) kinase complexes with B-type cyclins that play a central role in the regulation of the G1 phase of the cell cycle. We show here that low levels of expression of SIC1 in Schizosaccharomyces pombe rescues all the phenotypes of cells lacking the rum1+ gene. In addition, high level expression of SIC1 in S. pombe induces extra rounds of DNA replication without mitosis, a phenotype very similar to the overexpression of rum1+. Transient expression of rum1+ in S. cerevisiae restores the G1 arrest phenotype of cdc4 sic1Delta double mutants. Overproduction of rum1+ in Saccharomyces cerevisiae causes a cell cycle block in G1 with a phenotype similar to inactivation of all the Clb cyclins. Finally, we have mapped the cyclin interacting domain and Cdk inhibitory domain to a region of about 80 amino acids in p25rum1 that has significant homology to the C-terminal domain of p40SIC1. All these observations suggest that fission yeast p25rum1 and budding yeast p40SIC1 define a family of Cdk inhibitors that specifically down regulate cyclin B/Cdk1 during the G1 phase of the cell cycle.

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The duration of mitosis and daughter cell size are modulated by nutrients in budding yeast

The Journal of Cell Biology ◽

10.1083/jcb.201609114 ◽

2017 ◽

Vol 216 (11) ◽

pp. 3463-3470 ◽

Cited By ~ 29

Author(s):

Ricardo M. Leitao ◽

Douglas R. Kellogg

Keyword(s):

Cell Cycle ◽

Cell Size ◽

Daughter Cell ◽

Slow Growth ◽

Budding Yeast ◽

Size Control ◽

G1 Phase ◽

Large Reduction ◽

Duration Of Mitosis ◽

Cell Cycle Entry

The size of nearly all cells is modulated by nutrients. Thus, cells growing in poor nutrients can be nearly half the size of cells in rich nutrients. In budding yeast, cell size is thought to be controlled almost entirely by a mechanism that delays cell cycle entry until sufficient growth has occurred in G1 phase. Here, we show that most growth of a new daughter cell occurs in mitosis. When the rate of growth is slowed by poor nutrients, the duration of mitosis is increased, which suggests that cells compensate for slow growth in mitosis by increasing the duration of growth. The amount of growth required to complete mitosis is reduced in poor nutrients, leading to a large reduction in cell size. Together, these observations suggest that mechanisms that control the extent of growth in mitosis play a major role in cell size control in budding yeast.

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Treatment of the budding yeast Saccharomyces cerevisiae with the lipid peroxidation product 4-HNE provokes a temporary cell cycle arrest in G1 phase

Free Radical Biology and Medicine ◽

10.1016/s0891-5849(98)00110-5 ◽

1998 ◽

Vol 25 (6) ◽

pp. 682-687 ◽

Cited By ~ 32

Author(s):

Willibald Wonisch ◽

Sepp D. Kohlwein ◽

Jörg Schaur ◽

Franz Tatzber ◽

Helmut Guttenberger ◽

...

Keyword(s):

Saccharomyces Cerevisiae ◽

Cell Cycle ◽

Lipid Peroxidation ◽

Cell Cycle Arrest ◽

Budding Yeast ◽

G1 Phase ◽

Lipid Peroxidation Product ◽

Yeast Saccharomyces Cerevisiae ◽

Cycle Arrest ◽

Peroxidation Product

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Cdc28 Activates Exit from Mitosis in Budding Yeast

The Journal of Cell Biology ◽

10.1083/jcb.149.7.1361 ◽

2000 ◽

Vol 149 (7) ◽

pp. 1361-1376 ◽

Cited By ~ 60

Author(s):

Adam D. Rudner ◽

Kevin G. Hardwick ◽

Andrew W. Murray

Keyword(s):

Cell Cycle ◽

Kinase Activity ◽

Budding Yeast ◽

G1 Phase ◽

Phosphorylation Sites ◽

Cyclin Dependent Kinase ◽

Anaphase Promoting Complex ◽

Reduced Activity

The activity of the cyclin-dependent kinase 1 (Cdk1), Cdc28, inhibits the transition from anaphase to G1 in budding yeast. CDC28-T18V, Y19F (CDC28-VF), a mutant that lacks inhibitory phosphorylation sites, delays the exit from mitosis and is hypersensitive to perturbations that arrest cells in mitosis. Surprisingly, this behavior is not due to a lack of inhibitory phosphorylation or increased kinase activity, but reflects reduced activity of the anaphase-promoting complex (APC), a defect shared with other mutants that lower Cdc28/Clb activity in mitosis. CDC28-VF has reduced Cdc20- dependent APC activity in mitosis, but normal Hct1- dependent APC activity in the G1 phase of the cell cycle. The defect in Cdc20-dependent APC activity in CDC28-VF correlates with reduced association of Cdc20 with the APC. The defects of CDC28-VF suggest that Cdc28 activity is required to induce the metaphase to anaphase transition and initiate the transition from anaphase to G1 in budding yeast.

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The duration of mitosis and daughter cell size are modulated by nutrients in budding yeast

10.1101/080648 ◽

2016 ◽

Cited By ~ 1

Author(s):

Ricardo M. Leitao ◽

Douglas R. Kellogg

Keyword(s):

Cell Cycle ◽

Cell Size ◽

Daughter Cell ◽

Slow Growth ◽

Budding Yeast ◽

Size Control ◽

G1 Phase ◽

Large Reduction ◽

Duration Of Mitosis ◽

Cell Cycle Entry

AbstractThe size of nearly all cells is modulated by nutrients. Thus, cells growing in poor nutrients can be nearly half the size of cells in rich nutrients. In budding yeast, cell size is thought to be controlled almost entirely by a mechanism that delays cell cycle entry until sufficient growth has occurred in G1 phase. Here, we show that most growth of a new daughter cell occurs in mitosis. When the rate of growth is slowed by poor nutrients, the duration of mitosis is increased, which suggests that cells compensate for slow growth in mitosis by increasing the duration of growth. The amount of growth required to complete mitosis is reduced in poor nutrients, leading to a large reduction in cell size. Together, these observations suggest that mechanisms that control the extent of growth in mitosis play a major role in cell size control in budding yeast.

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