Abstract:

The Deepwater Horizon oil spill (April 20, 2010 to July 15, 2010) was responsible for the release of ~ 4 to 5 million barrels of crude oil in to the Gulf of Mexico and contaminating the coastline of Louisiana, Mississippi, Alabama and Florida. The aryl hydrocarbon receptor (AHR) pathway is considered to be the ‘master regulator’ of the molecular response to hydrocarbon exposure. In vertebrates, the AHR pathway regulates a battery of phase I and phase II metabolic genes responsible for the biotransformation of hydrocarbons to water soluble, and potentially less toxic metabolites. The AHR pathway is also known to crosstalk with the NRF2 pathway (‘master regulator’ of the oxidative stress response) to assist in ameliorating oxidative stress caused by hydrocarbon biotransformation. The classic molecular biomarker for vertebrate hydrocarbon exposure is induction of the cytochrome P450 1A (CYP1A) gene regulated by the AHR. However, these pathways (AHR and NRF2) are best characterized in vertebrate models and any conservation of function between vertebrates and invertebrates is poorly understood. To investigate the activation of these pathways in a classic invertebrate monitoring species, hatchery raised oysters (Crassostrea virginica) were routinely deployed over the period of one year at three different oysters reefs near Mobile Bay, AL – Grand Bay, Fort Morgan and Orange Beach. Oysters were deployed for a period of two months and sample five times during the 12 month monitoring program – May, August and November of 2010, and Feb and May of 2011. After collection of the oysters at the end of each deployment, gill and digestive gland tissue was removed by dissection and Total RNA was isolated from each individual tissue. Gene expression profiling of selected biomarkers consisting with hydrocarbon toxicity was performed on six biological replicates (per deployment site and collection date), with each replicate consisting of pooled equivalent amounts of RNA from four individual oysters.

Suggested Citation:

Jenny, Matthew and William Walton. 2015. Growth and quantitative PCR data from oysters (Crassotrea virginica) deployed along the northern Gulf of Mexico coast, May 2010 - June 2011. Distributed by: GRIIDC, Harte Research Institute, Texas A&M University–Corpus Christi. doi:10.7266/N7CR5R80

Purpose:

We will define exposure and quantify effects of oil exposure and recovery on oysters by testing a variety of indicators (under pre-, during, and post-spill conditions) on field deployed oysters, including gross biological measures (growth and/or survival) and physiological “stress” responses (biomarker gene expression). We will link these responses to oil exposure directly via hydrocarbon body burden in oyster tissues. In the case of gene regulation, individual tissues (gill and digestive gland) will be analyzed to account for differential response among tissues.

Data Parameters and Units:

Growth Measurements: SH – Shell height; SL – Shell Length; SW – Shell width; WWW – whole wet weight; DSW – dried shell weight; DTW – dried tissue weight; CI – condition index Gene Expression Real-Time PCR Key: CV7 – Beta-Actin; CV66 – Glutathione S-transferase (GST) pi; CV73 – GST theta; CV78F/79R – Superoxide Dismutase; CV80 – cytochrome P450 1A (CYP1A) like #1; CV82 – CYP1A like #2; CV83 – aryl hydrocarbon receptor; CV85 – multidrug resistance protein transporter #1; CV86 – multidrug resistance protein transporter #2

Instruments:

BioRad MyiQ2 Real-time PCR Thermocycler

Individual Files: