Developmental and tissue-specific expression of AHR1, AHR2, and ARNT2 in dioxin-sensitive and -resistant populations of the marine fish Fundulus heteroclitus
Wh. Powell et al., Developmental and tissue-specific expression of AHR1, AHR2, and ARNT2 in dioxin-sensitive and -resistant populations of the marine fish Fundulus heteroclitus, TOXICOL SCI, 57(2), 2000, pp. 229-239
Fundulus heteroclitus is a well-characterized marine fish model for studyin
g aryl hydrocarbon toxicity. The F. heteroclitus population in New Bedford
Harbor (NBH), a Superfund site in southeastern Massachusetts, exhibits heri
table resistance to the toxic effects of planar halogenated aromatic hydroc
arbons (PHAHs), including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TC DD) and p
olychlorinated biphenyls (PCBs). To investigate the role of the aryl hydroc
arbon receptor (AHR) signal transduction pathway in PHAH resistance, we mea
sured the relative levels of AHR1, AHR2, and ARNT2 mRNA in whole embryos at
different developmental stages and in dissected tissues of adults, compari
ng expression of these genes in NBH fish with fish from a reference site (S
corton Creek, MA [SC]). Expression of both AHR1 and AHR2 mRNA increased dur
ing development, achieving maximum levels Drier to hatching. Maximal embryo
nic expression of AHR1 was delayed relative to AHR2. Whole NBH and SC embry
os exhibited no discernable differences in expression of these genes. As we
have previously observed, adult SC fish expressed AHR2 and ARNT2 mRNA in a
ll tissues examined, while AHR1 was expressed predominantly in brain, heart
, and gonads. In contrast, AHR1 mRNA was widely expressed in NBH fish, appe
aring with unusual abundance in gill, gut, kidney, liver, and spleen. This
AHR1 expression pattern was not observed in the lab-reared progeny of NBH f
ish, demonstrating that constitutive AHR1 expression in gill, gut, kidney,
liver, and spleen is not a heritable phenotype. Furthermore, widespread AHR
1 expression was not induced in reference-site fish by TCDD or PCB mixtures
, suggesting that aberrant AHR1 expression is not simply a normal physiolog
ical response of contaminant exposure. These results identify ubiquitous AH
R1 expression as an attribute unique to feral NBH F. heteroclitus, and they
represent a first step in determining the regulatory mechanisms underlying
this expression pattern and its possible role in TCDD resistance.