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Eukaryotic Cell, March 2009, p. 362-372, Vol. 8, No. 3
1535-9778/09/$08.00+0     doi:10.1128/EC.00317-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Transcriptional Regulation of an Iron-Inducible Gene by Differential and Alternate Promoter Entries of Multiple Myb Proteins in the Protozoan Parasite Trichomonas vaginalis{triangledown}

Hong-Ming Hsu,1,2,{dagger} Shiou-Jeng Ong,2,{dagger} Ming-Chun Lee,2,{ddagger} and Jung-Hsiang Tai1*

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

Received 18 September 2008/ Accepted 31 December 2008

Iron-inducible transcription of a malic enzyme gene (also reputed to be ap65-1) in Trichomonas vaginalis was previously shown to involve a Myb1 repressor and a Myb2 activator, each of which may preferentially select two closely spaced promoter sites, MRE-1/MRE-2r, which comprises overlapping promoter elements, and MRE-2f. In the present study, an iron-inducible ~32-kDa Myb3 nuclear protein was demonstrated to bind only the MRE-1 element. Changes in the iron supply, which produced antagonistic effects on the levels of Myb2 and Myb3 expression, also resulted in temporal and alternate entries of Myb2 and Myb3 into the ap65-1 promoter. Repression or activation of basal and iron-inducible ap65-1 transcription was detected in transfected cells when Myb3 was, respectively, substantially knocked down or overexpressed. In the latter case, increased Myb3 promoter entry was detected with concomitant decrease in Myb2 promoter entry under specific conditions, while Myb3 promoter entry was inhibited under all test conditions in cells overexpressing Myb2. In contrast, concomitant promoter entries by Myb2 and Myb3 diminished in cells overexpressing Myb1, except that Myb3 promoter entry was slightly affected under prolonged iron depletion. Together, these results suggest that Myb2 and Myb3 may coactivate basal and iron-inducible ap65-1 transcription against Myb1 through conditional and competitive promoter entries.


* Corresponding author. Mailing address: Division of Infectious Diseases, Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan 115. Phone: 886-2-26523934. Fax: 886-2-27858847. E-mail: taijh{at}gate.sinica.edu.tw

{triangledown} Published ahead of print on 16 January 2009.

{dagger} These authors contributed equally.

{ddagger} Present address: Beckman Coulter, Taiwan, Inc., Rm. 216 8F, Tun-Hwa S. Rd. Sec. 2, Taipei, Taiwan 106.


Eukaryotic Cell, March 2009, p. 362-372, Vol. 8, No. 3
1535-9778/09/$08.00+0     doi:10.1128/EC.00317-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.