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The conserved SKN‐1/Nrf antioxidant response has complex interactions with the heat shock response (880.4)
Author(s) -
Tang Lanlan,
Choe Keith
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.880.4
Subject(s) - heat shock factor , caenorhabditis elegans , heat shock , biology , transcription factor , cellular stress response , hsf1 , heat shock protein , chromatin immunoprecipitation , microbiology and biotechnology , microarray analysis techniques , gene , genetics , signal transduction , regulation of gene expression , hsp70 , gene expression , fight or flight response , promoter
Numerous inducible gene pathways have been defined as coordinating defense and repair in response to one of many types of stress. A major challenge now is to begin understanding how these pathways interact to optimize homeostasis, mitigate competition for common substrates, and avoid incompatibilities. In animals ranging from nematodes to mammals, the transcription factor SKN‐1/Nrf controls the expression of over 50 detoxification and antioxidation genes in response to oxidants and electrophiles. Surprisingly, we find that while SKN‐1/Nrf activity is beneficial for survival of oxidants and reactive small molecules, it is strongly detrimental to survival of heat stress. Genome‐wide chromatin‐immunoprecipitation and microarray data from the genetic model Caenorhabditis elegans suggest that SKN‐1/Nrf negatively regulates several genes within the heat shock response, including heat‐shock transcription factor 1 (HSF‐1). We also find that high temperature has complex effects on the SKN‐1/Nrf pathway; it causes accumulation of the factor in the nucleus, but interferes with induction of many target genes. Therefore, our early work suggests that there may be multiple interactions between conserved responses to oxidants and heat that influence signaling and functional outcomes of both pathways. Grant Funding Source : NSF grant IOS‐1120130