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Integr Comp Biol. 2008 Sep;48(3):419-27. doi: 10.1093/icb/icn034. Epub 2008 May 9.

A proposed role of the sulfotransferase/sulfatase pathway in modulating yolk steroid effects.

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1
Department of Biological Sciences, Campus Box 4120, Illinois State University, Normal, IL 61790-4120, USA.

Abstract

Steroid hormones have long been studied by behavioral ecologists as a nongenetic means whereby females can influence the development of their offspring. In oviparous vertebrates, steroids are present in the yolk at the time of oviposition and have been shown to affect numerous traits of the offspring. To date, most studies have focused on the functional relationship between yolk steroids and offspring development. In this article we used a mechanistic approach to investigate the effects of yolk steroids in an attempt to decipher how lipophilic steroids may make it from the lipid-rich yolk to the developing embryo. First, we examined the distribution of radioactive and nonradioactive estradiol following the exogenous application of each to developing eggs of the red-eared slider. Second, we quantified sulfotransferase activity in various components of the egg as a potential mechanism for the metabolism of steroids. Results indicate that exogenous estradiol is converted to a water-soluble form during the first 15 days of development, concurrent with an increase of sulfotransferase activity in the yolk and extra-embryonic membranes. Based on these data, we propose a mechanistic model based upon the sulfotransferase/sulfatase pathway as a means through which developing eggs can convert steroids to a water-soluble form that can be transported to the embryo. These sulfonated steroids may then serve as precursors for subsequent steroid production via sulfatase activity. This model utilizes a mechanism known to be important for the modulation of maternal steroid signals in placental mammals, at the same time addressing several previously unanswered questions regarding the mechanisms underlying the effects of yolk steroids.

PMID:
21669803
DOI:
10.1093/icb/icn034

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