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Progress Reports: Boston University: Mechanisms and Impacts of PCB Resistant Fish

Superfund Research Program

Mechanisms and Impacts of PCB Resistant Fish

Project Leader: Mark E. Hahn (Woods Hole Oceanographic Institution)
Co-Investigators: Sibel I. Karchner (Woods Hole Oceanographic Institution), Neelakanteswar Aluru (Woods Hole Oceanographic Institution)
Grant Number: P42ES007381
Funding Period: 1995-2020
View this project in the NIH Research Portfolio Online Reporting Tools (RePORT)

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Progress Reports

Year:   2019  2018  2017  2016  2015  2014  2013  2012  2010  2009  2008  2007  2006  2005  2004  2003  2002  2001  2000  1999  1998  1997  1996  1995 

To investigate mechanisms for dioxin resistance in killifish, project investigators cloned and sequenced a killifish homolog of a mouse gene known as AHR repressor (AHRR). This protein inhibited the ability of dioxin to cause AHR1- or AHR2-dependent changes in gene expression. Additionally, the synthesis of AHRR was increased by treatment with dioxins or PCBs in an AHR-dependent manner. However, the expression of the AHRR gene was not increased in the dioxin-resistant New Bedford Harbor (NBH) fish.

Another possible resistance mechanism involves polymorphisms in AHR genes. We have identified 24 polymorphic sites among 7 AHR1 cDNA clones. The 7 alleles cluster in two groups (AHR1*1 and AHR1*2). Screening of NBH and control fish showed that the AHR1*1A and AHR1*1B alleles are under-represented in the NBH population, suggesting selection against fish possessing these alleles. We have begun to investigate the function of these alleles; initial results indicate that both proteins exhibit high-affinity binding of dioxins and can support dioxin-dependent activation of gene expression. Project investigators are now beginning a detailed survey of the structure and function of these alleles at NBH and other sites.

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