Abstract Title

Session S-08C: Occurrences and Impacts of Emerging Contaminants

Keywords

Emerging Contaminants and Emergencies

Start Date

2-5-2014 8:30 AM

End Date

2-5-2014 10:00 AM

Description

Concern over human and wildlife health has brought increased attention to a group of emerging environmental contaminants referred to as endocrine disrupting compounds (EDCs). While progress has been made in describing the effects of these compounds, there are still gaps in our understanding of alternative modes of action and physiological effects outside of the reproductive axis, particularly in invertebrates. One way that EDCs may elicit these changes is through disruptions to normal epigenetic mechanisms. Epigenetics refers to heritable processes that alter gene activity without manipulating the underlying DNA sequence. Epigenetic marks, such as DNA methylation, are important regulators of gene expression in both plants and animals. This research aims to characterize alternative modes of action of endocrine disrupting compounds by utilizing molecular tools to examine epigenetic and physiological changes in Pacific oysters (Crassostrea gigas) exposed to the synthetic estrogen, 17α-ethinyl estradiol (EE2). In this experiment, juvenile oysters were exposed to EE2 during gonad maturation. Sex-ratio and size were evaluated after two months of exposure. Results of this exposure include a trend toward more females in the EE2 exposed. In addition, the EE2 exposed females were significantly larger than unexposed females. To investigate the molecular underpinnings of this phenotype, DNA methylation profiles of control and EE2 exposed females were directly compared using a DNA tiling microarray (MBD-ChIP) in order to test the hypothesis that invertebrate DNA methylation patterns will be altered upon exposure to EDCs. This analysis revealed a suite of genes that were differentially methylated in response to EE2. Functional annotations of these genes indicate that a number of biological pathways outside of the reproductive axis are being affected by exposure to EE2.

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May 2nd, 8:30 AM May 2nd, 10:00 AM

A molecular framework to identify novel modes of action of endocrine disrupting compounds in shellfish

Room 606

Concern over human and wildlife health has brought increased attention to a group of emerging environmental contaminants referred to as endocrine disrupting compounds (EDCs). While progress has been made in describing the effects of these compounds, there are still gaps in our understanding of alternative modes of action and physiological effects outside of the reproductive axis, particularly in invertebrates. One way that EDCs may elicit these changes is through disruptions to normal epigenetic mechanisms. Epigenetics refers to heritable processes that alter gene activity without manipulating the underlying DNA sequence. Epigenetic marks, such as DNA methylation, are important regulators of gene expression in both plants and animals. This research aims to characterize alternative modes of action of endocrine disrupting compounds by utilizing molecular tools to examine epigenetic and physiological changes in Pacific oysters (Crassostrea gigas) exposed to the synthetic estrogen, 17α-ethinyl estradiol (EE2). In this experiment, juvenile oysters were exposed to EE2 during gonad maturation. Sex-ratio and size were evaluated after two months of exposure. Results of this exposure include a trend toward more females in the EE2 exposed. In addition, the EE2 exposed females were significantly larger than unexposed females. To investigate the molecular underpinnings of this phenotype, DNA methylation profiles of control and EE2 exposed females were directly compared using a DNA tiling microarray (MBD-ChIP) in order to test the hypothesis that invertebrate DNA methylation patterns will be altered upon exposure to EDCs. This analysis revealed a suite of genes that were differentially methylated in response to EE2. Functional annotations of these genes indicate that a number of biological pathways outside of the reproductive axis are being affected by exposure to EE2.