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Molecular and Cellular Biology, May 2005, p. 3914-3922, Vol. 25, No. 10
0270-7306/05/$08.00+0     doi:10.1128/MCB.25.10.3914-3922.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

The H1 Phosphorylation State Regulates Expression of CDC2 and Other Genes in Response to Starvation in Tetrahymena thermophila

Yali Dou ,{dagger},{ddagger} Xiaoyuan Song,{ddagger} Yifan Liu,{dagger} and Martin A. Gorovsky*

Department of Biology, University of Rochester, Rochester, New York 14627

Received 18 November 2004/ Returned for modification 13 January 2005/ Accepted 16 February 2005

In Tetrahymena thermophila, highly phosphorylated histone H1 of growing cells becomes partially dephosphorylated when cells are starved in preparation for conjugation. To determine the effects of H1 phosphorylation on gene expression, PCR-based subtractive hybridization was used to clone cDNAs that were differentially expressed during starvation in two otherwise-isogenic strains differing only in their H1s. H1 in A5 mutant cells lacked phosphorylation, and H1 in E5 cells mimicked constitutive H1 phosphorylation. Sequences enriched in A5 cells included genes encoding proteases. Sequences enriched in E5 cells included genes encoding cdc2 kinase and a Ser/Thr kinase. These results indicate that H1 phosphorylation plays an important role in regulating the pattern of gene expression during the starvation response and that its role in transcription regulation can be either positive or negative. Treatment of starved cells with a phosphatase inhibitor caused CDC2 gene overexpression. Expression of the E5 version of H1 in starved cells containing endogenous, wild-type H1 caused the wild-type H1 to remain highly phosphorylated. These results argue that Cdc2p is the kinase that phosphorylates Tetrahymena H1, establish a positive feedback mechanism between H1 phosphorylation and CDC2 expression, and indicate that CDC2 gene expression is regulated by an H1 phosphatase.


* Corresponding author. Mailing address: Department of Biology, University of Rochester, Rochester, NY 14627. Phone: (585) 275-6988. Fax: (585) 275-2070. E-mail: goro{at}mail.rochester.edu.

{dagger} Present address: The Rockefeller University, New York, NY 10021.

{ddagger} Y.D. and X.S. were equal contributors to this paper.


Molecular and Cellular Biology, May 2005, p. 3914-3922, Vol. 25, No. 10
0022-538X/05/$08.00+0     doi:10.1128/MCB.25.10.3914-3922.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.




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