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Eukaryotic Cell, February 2006, p. 391-399, Vol. 5, No. 2
1535-9778/06/$08.00+0     doi:10.1128/EC.5.2.391-399.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Multifarious Transcriptional Regulation of Adhesion Protein Gene ap65-1 by a Novel Myb1 Protein in the Protozoan Parasite Trichomonas vaginalis

Shiou-Jeng Ong,1 Hong-Ming Hsu,1 Hsing-Wei Liu,2 Chien-Hsin Chu,1 and Jung-Hsiang Tai2*

Department of Parasitology, College of Medicine, National Taiwan University,1 Division of Infectious Diseases, Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, Republic of China2

Received 2 September 2005/ Accepted 16 November 2005

The transcription efficiency of an adhesion protein gene, ap65-1, in Trichomonas vaginalis varies with changes in the iron supply and with the growth stage. In the present study, two Myb recognition elements, MRE-1/MRE-2r and MRE-2f, were found to play antagonistic roles in regulating the iron-inducible activity of an ap65-1 reporter gene. Intriguingly, either of these elements was shown to be sufficient to repress basal activity, but together they were also shown to activate growth-related activity of the reporter gene in iron-depleted cells. A myb1 gene which encodes a 24-kDa protein containing a Myb-like R2R3 DNA binding domain was identified from Southwestern screening of MRE-2f-binding proteins. The Myb1 protein was detected as a major 35-kDa protein which exhibited variations in nuclear concentration with changes in the iron supply. A recombinant Myb1 protein was shown to differentially interact with MRE-1/MRE-2r and MRE-2f in vitro. Overexpression of hemagglutinin-tagged Myb1 in T. vaginalis resulted in repression or activation of ap65-1 transcription in iron-depleted cells at an early and a late stage of cell growth, respectively, while iron-inducible ap65-1 transcription was constitutively repressed. The hemagglutinin-tagged Myb1 protein was found to constantly occupy the chromosomal ap65-1 promoter at a proximal site, but it also selected two more distal sites only at the late growth stage. Together, these observations suggest that Myb1 critically regulates multifarious ap65-1 transcription, possibly via differential selection of multiple promoter sites upon environmental changes.


* Corresponding author. Mailing address: Division of Infectious Diseases, Institute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan. Phone: 886-2-26523934. Fax: 886-2-27858847. E-mail: taijh{at}gate.sinica.edu.tw.


Eukaryotic Cell, February 2006, p. 391-399, Vol. 5, No. 2
1535-9778/06/$08.00+0     doi:10.1128/EC.5.2.391-399.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.




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