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  4. Activation of multifarious transcription of an adhesion protein ap65-1 gene by a novel Myb2 protein in the protozoan parasite Trichomonas vaginalis
 
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Activation of multifarious transcription of an adhesion protein ap65-1 gene by a novel Myb2 protein in the protozoan parasite Trichomonas vaginalis

Journal
Journal of Biological Chemistry
Journal Volume
282
Journal Issue
9
Pages
6716-6725
Date Issued
2007
Author(s)
Ong S.-J.
HONG-MING HSU  
Liu H.-W.
Chu C.-H.
Tai J.-H.
DOI
10.1074/jbc.M610484200
URI
https://www.scopus.com/inward/record.uri?eid=2-s2.0-34250373772&doi=10.1074%2fjbc.M610484200&partnerID=40&md5=435acafc50ce723615ba5ab0a4e48671
https://scholars.lib.ntu.edu.tw/handle/123456789/506732
Abstract
Multifarious transcription of the adhesion protein ap65-1 gene in the human pathogen, Trichomonas vaginalis, is critically regulated by the coordination of two similar but opposite oriented DNA regulatory regions, MRE-1/MRE-2r and MRE-2f, both of which are binding sites for multiple Myb-like proteins. In the present study, MRE-1/MRE-2r was demonstrated to be composed of multiple overlapping promoter elements, among which the entire region is required for growth-related ap65-1 transcription, and the 5′-MRE-1 antagonizes the suppressive activity of the 3′-MRE-2r in iron-inducible transcription. The recombinant Myb2 protein derived from a previously identified myb2 gene was demonstrated to recognize distinct sequence contexts in MRE-2r and MRE-2f, whereas Myb2 in the nuclear lysate preferentially binds to MRE-2f to MRE-2r. Iron repletion resulted in persistent repression of the myb2 gene, and temporal activation/deactivation of Myb2 promoter entry, which was also activated by prolonged iron depletion. The hemagglutinin-tagged Myb2 when overexpressed during iron-depleted conditions facilitated basal and growth-related ap65-1 transcription to a level that was achieved in iron-replete cells, whereas iron-inducible ap65-1 transcription was abolished with knockdown of Myb2. These findings demonstrated that Myb2 is involved in activation of growth-related and iron-inducible transcription of the ap65-1 gene, possibly through differential promoter selection in competition with other Myb proteins. © 2007 by The American Society for Biochemistry and Molecular Biology, Inc.
Type
journal article

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