The fission yeast cdc18+ gene product couples S phase to START and mitosis

doi:10.1016/0092-8674(93)90427-R

Cell

Volume 74, Issue 2, 30 July 1993, Pages 371-382

https://doi.org/10.1016/0092-8674(93)90427-R Get rights and content

Abstract

Commitment to the cell cycle in fission yeast requires the function of the cdc10⁺ transcriptional activator at START. The product of the cdc18⁺ gene is a major downstream target of cdc10⁺, and transcription of cdc18⁺ is activated by cdc10⁺ during passage through START. The cdc18⁺ function is required for entry into S phase. In addition, the product of the cdc18⁺ gene is part of the checkpoint control that prevents mitosis from occurring until S phase is completed. Thus, cdc18⁺ plays a key role in coupling S phase to START and mitosis.

References (57)

B.J. Andrews et al.
Identification of a DNA binding factor involved in cell cycle control of the yeast HO gene
Cell
(1989)
N. Barbet et al.
Versatile shuttle vectors and genomic libraries for use with Schizosaccharomyces pombe
Gene
(1992)
G. Basi et al.
TATA box mutations in the Schizosaccharomyces pombe nmt1 promoter affect transcription efficiency but not the transcription start point or thiamine repressibility
Gene
(1993)
D.M. Becker et al.
High efficiency transformation of yeast by electroporation
Meth. Enzymol.
(1991)
L. Breeden et al.
Cell cycle control of the yeast HO gene: cis- and trans-activating regulators
Cell
(1987)
M. Caligiuri et al.
Sct1 functions in partnership with cdc10 in a transcription complex that activates cell cycle START and inhibits differentiation
Cell
(1993)
J. Culotti et al.
Genetic control of the cell division cycle in yeast. III. Seven genes controlling nuclear division
Exp. Cell Res.
(1971)
T. Enoch et al.
Mutation of fission yeast cell cycle control genes abolishes dependence of mitosis on DNA replication
Cell
(1990)
L.H. Hartwell
Sequential function of gene products relative to DNA synthesis in the yeast cell cycle
J. Mol. Biol.
(1976)
S. Moreno et al.
Molecular genetic analysis of the fission yeast Schizosaccharomyces pombe
Meth. Enzymol.
(1991)

K. Nasmyth et al.

The role of SWI4 and SWI6 in the activity of G1 cyclins in yeast

Cell

(1991)

J. Ogas et al.

Transcriptional activation of CLN1, CLN2, and a putative new G1 cyclin (HCS26) by SWI4, a positive regulator of G1-specific transcription

Cell

(1991)

S. Uzawa et al.

The fission yeast cut1⁺ gene regulates spindle pole body duplication and has homology to the budding yeast ESP1 gene

Cell

(1990)

C. Wittenberg et al.

G1-specific cyclins of S. cervisiae: cell cycle periodicity, regulation by mating pheromone, and association with the p34^CDC28 protein kinase

Cell

(1990)

C. Zhou et al.

Molecular cloning of Saccharomyces cerevisiae CDC6 gene: isolation, identification and sequence analysis

J. Biol. Chem.

(1989)

F. Al-Khodairy et al.

DNA repair mutants defining G2 checkpoint pathways in Schizosaccharomyces pombe

EMBO J.

(1992)

B.J. Andrews et al.

The yeast SWI4 protein contains a motif present in developmental regulators and is part of a complex involved in cell-cycle dependent transcription

Nature

(1989)

S. Aves et al.

Cloning, sequencing and transcriptional control of the Schizosaccharomyces pombe cdc1O “start” gene

EMBO J.

(1985)

L. Breeden et al.

Similarity between cell cycle genes of budding and fission yeast and the Notch gene of Drosophila

Nature

(1987)

D. Broek et al.

Involvement of p34^cdc2 in establishing the dependency of S phase on mitosis

Nature

(1991)

A. Bueno et al.

Dual functions of CDC6: a yeast protein required for DNA replication also inhibits nuclear division

EMBO J.

(1992)

L. Dirick et al.

A central role for SWI6 in moldulated cell cycle Start-specific transcription in yeast

Nature

(1992)

T. Enoch et al.

Mitotic checkpoint control in fission yeast

T. Enoch et al.

Fission yeast genes involved in coupling mitosis to completion of DNA replication

Genes Dev.

(1992)

M.J. Fernandez-Sarabia et al.

SIT4 protein phosphatase is required for the normal accumulation of SWI4, CLN1, CLN2 and HCS26 RNAs during late G₁

Genes Dev.

(1992)

S.L. Forsburg et al.

Cell cycle regulation in the yeasts Saccharomyces cerevisiae and Schizosaccharomyces pombe

Annu. Rev. Cell Biol.

(1991)

C.B. Gordon et al.

A cell cycle responsive transcriptional control element and a negative control element in the gene encoding DNA polymerase α in Saccharomyces cerevisiae

C.B. Gordon et al.

The cdc22 gene of Schizosaccharomyces pombe encodes a cell cycle regulated transcript

EMBO J.

(1986)

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ArticleThe fission yeast cdc18+ gene product couples S phase to START and mitosis

Abstract

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Fission yeast genes involved in coupling mitosis to completion of DNA replication

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Article
The fission yeast cdc18⁺ gene product couples S phase to START and mitosis

Involvement of p34^cdc2 in establishing the dependency of S phase on mitosis

SIT4 protein phosphatase is required for the normal accumulation of SWI4, CLN1, CLN2 and HCS26 RNAs during late G₁