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Molecular and Cellular Biology, March 1999, p. 2408-2415, Vol. 19, No. 3
Departament de Bioquímica i Biologia
Molecular,
Received 23 July 1998/Returned for modification 5 October
1998/Accepted 8 December 1998
Yeast cells overexpressing the Ser/Thr protein phosphatase Ppz1
display a slow-growth phenotype. These cells recover slowly from
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
The Yeast Ser/Thr Phosphatases Sit4 and Ppz1 Play
Opposite Roles in Regulation of the Cell Cycle
-factor or nutrient depletion-induced G1 arrest, showing a considerable delay in bud emergence as well as in the expression of
the G1 cyclins Cln2 and Clb5. Therefore, an excess of the
Ppz1 phosphatase interferes with the normal transition from
G1 to S phase. The growth defect is rescued by
overexpression of the HAL3/SIS2 gene, encoding a negative
regulator of Ppz1. High-copy-number expression of HAL3/SIS2
has been reported to improve cell growth and to increase expression of
G1 cyclins in sit4 phosphatase mutants. We show
here that the described effects of HAL3/SIS2 on
sit4 mutants are fully mediated by the Ppz1
phosphatase. The growth defect caused by overexpression of
PPZ1 is intensified in strains with low G1
cyclin levels (such as bck2
or cln3
mutants), whereas mutation of PPZ1 rescues the synthetic
lethal phenotype of sit4 cln3 mutants. These results reveal
a role for Ppz1 as a regulatory component of the yeast cell cycle,
reinforce the notion that Hal3/Sis2 serves as a negative modulator of
the biological functions of Ppz1, and indicate that the Sit4 and Ppz1
Ser/Thr phosphatases play opposite roles in control of the
G1/S transition.
*
Corresponding author. Mailing address: Dept.
Bioquímica i Biologia Molecular, Fac. Veterinària,
Universidad Autònoma de Barcelona, Bellaterra 08193, Barcelona,
Spain. Phone: 34-93-5812182. Fax: 34-93-5812006. E-mail:
J.Arino{at}CC.UAB.ES.
Molecular and Cellular Biology, March 1999, p. 2408-2415, Vol. 19, No. 3
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
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