ARNT2 Is Not Required for TCDD Developmental Toxicity in Zebrafish

ARNT2 is not required for TCDD developmental toxicity in zebrafish.

ZfAHR2 has been identified as the receptor that is essential for mediating the developmental toxicity caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in zebrafish. One form of zfARNT2, zfARNT2b, forms a functional heterodimer with zfAHR2 that specifically recognizes XREs in gel shift experiments and induces XRE-driven transcription in COS-7 cells treated with TCDD. However, it has not been...

Ischemia is not required for arteriogenesis in zebrafish embryos.

OBJECTIVE The role of ischemia in collateral vessel development (arteriogenesis) is a contentious issue that cannot be addressed using mammalian models. To investigate this, we developed models of arteriogenesis using the zebrafish embryo, which gains sufficient oxygenation via diffusion to prevent ischemia in response to arterial occlusion. METHODS AND RESULTS We studied gridlock mutant embr...

Identification of zebrafish ARNT1 homologs: TCDD toxicity in the developing zebrafish requires ARNT1

Sox9b is required for epicardium formation and plays a role in TCDD-induced heart malformation in zebrafish.

Activation of the transcription factor aryl hydrocarbon receptor by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) prevents the formation of the epicardium and leads to severe heart malformations in developing zebrafish (Danio rerio). The downstream genes that cause heart malformation are not known. Because TCDD causes craniofacial malformations in zebrafish by downregulating the sox9b gene, we hyp...

Zebrafish as a model for developmental toxicity assessment

The zebrafish embryo has emerged as promising alternative model for traditional in vivo developmental toxicological screening due to their advantageous characteristics as their small size and transparency. In this paper, we reviewed the applicability of the zebrafish embryo model in some relevant areas to human toxicology as developmental toxicity, cardiovascular toxicity and neurotoxicity (beh...