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1 Center for Environmental Health Sciences, Dartmouth Medical School, Hanover, New Hampshire, United States; Mt. Desert Island Biological Laboratory, Salisbury Cove, Maine, United States; Biological Sciences, Dartmmouth College, Hanover, New Hampshire, United States
2 Mt. Desert Island Biological Laboratory, Salisbury Cove, Maine, United States
3 Mt. Desert Island Biological Laboratory, Salisbury Cove, Maine, United States; Physiology, Dartmouth Medical School, Hanover, New Hampshire, United States
4 Physiology, Dartmouth Medical School, Hanover, New Hampshire, United States
5 Center for Environmental Health Sciences, Dartmouth Medical School, Hanover, New Hampshire, United States; Pharmacology and Toxicology, Dartmouth Medical School, Hanover, New Hampshire, United States
6 Physiology, Dartmouth Medical School, Hanover, New Hampshire, United States; Center for Environmental Health Sciences, Dartmouth Medical School, Hanover, New Hampshire, United States; Mt. Desert Island Biological Laboratory, Salisbury Cove, Maine, United States
* To whom correspondence should be addressed. E-mail: bruce.a.stanton{at}dartmouth.edu.
Killifish are euryhaline teleosts that adapt to rapid changes in the salinity of the seawater. It is generally accepted that acclimation to seawater is mediated by cortisol activation of the glucocorticoid receptor (GR), which stimulates CFTR mRNA expression and CFTR mediated Cl- secretion by the gill. Because there is no direct evidence in killifish that the GR stimulates CFTR gene expression, Q-PCR studies were conducted to test the hypothesis that cortisol activation of GR up-regulates CFTR mRNA expression, and that this response is required for acclimation to seawater. Inhibition of the GR by RU486 prevented killifish from acclimating to increased salinity, and blocked the increase in CFTR mRNA. By contrast, inhibition of the mineralocorticoid receptor by spironolactone had no effect on acclimation to seawater. Thus, acclimation to increased salinity in killifish requires signaling via the GR and includes an increase in CFTR gene expression. Because arsenic, a toxic metalloid that naturally occurs in the aquatic environment, has been shown to disrupt GR transcriptional regulation in avian and mammalian systems, studies were also conducted to determine whether arsenic disrupts cortisol-mediated activation of CFTR gene expression in this in vivo fish model and thereby blocks the ability of killifish to acclimate to increased salinity. Arsenic prevented acclimation to seawater and decreased CFTR protein abundance. However, arsenic did not disrupt the GR-induced increase in CFTR mRNA. Thus, arsenic blocks acclimation to seawater in killifish by a mechanism that does not disrupt GR-mediated induction of CFTR gene expression.
This article has been cited by other articles:
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  G. R. Scott, D. W. Baker, P. M. Schulte, and C. M. Wood Physiological and molecular mechanisms of osmoregulatory plasticity in killifish after seawater transfer J. Exp. Biol., August 1, 2008; 211(15): 2450 - 2459. [Abstract] [Full Text] [PDF]
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 D. S. Miller, J. R. Shaw, C. R. Stanton, R. Barnaby, K. H. Karlson, J. W. Hamilton, and B. A. Stanton MRP2 and Acquired Tolerance to Inorganic Arsenic in the Kidney of Killifish (Fundulus heteroclitus) Toxicol. Sci., May 1, 2007; 97(1): 103 - 110. [Abstract] [Full Text] [PDF]
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