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Disorders of Sex Development (DSD) are conditions with diverse pathophysiology in which development of �gonadal sex� is
divergent. Albeit DSD has been studied widely, diagnosis remains still undefined in over 50% of patients with 46, XY DSD.
Many epidemiological and animal studies have suspected environment endocrine disrupting chemicals to be involved in DSD.
Therefore, we hypothesize that a significant number of DSD are caused by the combination of genetic variants and endocrine
disruptors. Androgenic compounds work by binding to androgen receptors, which further bind to androgen response elements
(ARE) and switch on specific genes. We have generated several transgenic zebrafish lines in which five-tandem AREs drive
expression of YFP. Thus, validate the use of zebrafish as in vivo biosensor model for testing disruption of androgen action due to
exposure to EDCs and therefore a possible cause for 46 XY DSD. In this study, response of 5XARE: YFP construct was studied
in vitro and in vivo. In vitro results confirmed that construct is responsive to human androgen receptor, however, efficiency of
zebrafish androgen receptor to bind human androgen response element awaits future. The in vivo response of construct cannot
be assessed as random increase and decrease in YFP expression was observed after exposure to anti-androgen and androgen
ligands. This variability is likely either due to multiple insertions within individual lines or time point at which treatments were
performed. However, repeat experiments are required to confirm this finding. In future, embryos having YFP expression in
androgen responsive tissue will be selected, out crossed with wild type and treated within 24 hours post fertilization.