4.6 Article

Herbicide atrazine activates SF-1 by direct affinity and concomitant co-activators recruitments to induce aromatase expression via promoter II

Journal

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 355, Issue 4, Pages 1012-1018

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2007.02.062

Keywords

aromatase; steroidogenic factor 1; atrazine; endocrine disruption

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The popular herbicide atrazine is an endocrine disruptor that demasculinizes and feminizes several species of animals, and co-relates with breast and reproductive disorders in mammalians. We recently reported that atrazine induces human aromatase gene expression via promoter II (ArPII) in a steroidogenic factor 1 (SF-1)-dependent manner. Here, we show that knockdown of SF-1 abolishes ArPII induction by atrazine in H295R cells, which harbor high SF-I expression and are originally atrazine-responsive. Conversely, exogenous SF-1 enables atrazine to induce ArPII in the otherwise non-responsive KGN cells. Atrazine's effect is independent from protein kinase A and LRH-1, a close relative of SF-1. However, it binds directly to the SF-1, and concomitantly, enhances interactions of SF-1 with co-activator TIF2, and renders more SF-1 binding to ArPII chromatin. Intriguingly, LBD mutations do not alter SF-1's ability to mediate atrazine stimulation, suggesting that atrazine interacts with SF-1 via a region(s) other than the ligand binding pocket. These data suggest that atrazine binds to and activates SF-1 to induce ArPII. (c) 2007 Elsevier Inc. All rights reserved.

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