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Originally published In Press as doi:10.1074/jbc.M007504200 on October 12, 2000

J. Biol. Chem., Vol. 276, Issue 3, 2062-2068, January 19, 2001
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De Novo Activation of the beta -Phaseolin Promoter by Phosphatase or Protein Synthesis Inhibitors*

Guofu LiDagger , Kenneth J. Bishop, and Timothy C. Hall§

From the Institute of Developmental and Molecular Biology and Department of Biology, Texas A & M University, College Station, Texas 77843-3155

The promoter for the phaseolin (phas) bean seed protein gene adopts an inactive chromatin structure in leaves of transgenic tobacco. This repressive architecture, which confers stringent spatial regulation, is disrupted upon transcriptional activation during embryogenesis in a process that requires the presence of both a transcription factor (PvALF) and abscisic acid (ABA). Toward determining the need for de novo synthesis of proteins other than PvALF in transcriptional activation we explored the effect of several eukaryotic protein synthesis inhibitors. Surprisingly, cycloheximide (CHX), emetine, and verrucarin A were able to induce transcription from the phas promoter in tobacco and bean leaf tissue in the absence of either PvALF or ABA. This induction was decreased by the replication inhibitors hydroxyurea and aphidicolin but not by genistein or mimosine. Since protein phosphatases and kinases are essential components of the ABA signal transduction pathway, it is conceivable that CHX is also capable of inducing phosphorylation of proteins usually involved in ABA-mediated activation. Interestingly, okadaic acid, an inhibitor of serine/threonine phosphatase, also strongly activated transcription from the phas promoter. In contrast, the protein synthesis inhibitors anisomycin and puromycin did not activate transcription from the phas promoter, nor did the tyrosine phosphatase inhibitors phenylarsine oxide and sodium orthovanadate. These discrete but different results on transcriptional activation may reflect specific modes of action of the inhibitors, or they may reflect differential interactions of the inhibitors or of downstream events resulting from inhibitor activity with presently unknown components of the transcriptional activation system.


* This work was supported by Grant MCB99-74706 from the National Science Foundation.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger Present address: Sangamo Biosciences Inc., 501 Canal Blvd., Suite A100, Richmond, CA 94804.

§ To whom correspondence should be addressed. Fax: 979-862-4098; E-mail: tim@idmb.tamu.edu.


Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.


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M. B. Chandrasekharan, G. Li, K. J. Bishop, and T. C. Hall
S Phase Progression Is Required for Transcriptional Activation of the {beta}-Phaseolin Promoter
J. Biol. Chem., November 14, 2003; 278(46): 45397 - 45405.
[Abstract] [Full Text] [PDF]




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