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Regulation of the transcriptional response to oxidative stress in fungi: similarities and differences
Journal article   Open access   Peer reviewed

Regulation of the transcriptional response to oxidative stress in fungi: similarities and differences

W Scott Moye-Rowley
Eukaryotic cell, Vol.2(3), pp.381-389
06/2003
DOI: 10.1128/EC.2.3.381-389.2003
PMCID: PMC161443
PMID: 12796283
url
https://doi.org/10.1128/EC.2.3.381-389.2003View
Published (Version of record) Open Access

Abstract

While dealing with oxidative stress is a common necessity for fungi, different organisms rely on different mechanisms to detoxify ROS and ensure their survival. S. pombe cells have an elaborate signaling network that activates a downstream transcription factor in response to oxidative stress. The finding of histidine kinases that may serve as the sensors for ROS indicates that important information will soon be forthcoming to explain how this signaling network detects changes in the oxidative environment of a cell. S. cerevisiae cells do not express the analogous histidine kinases seen in S. pombe, consistent with different requirements for oxidant sensing in these two yeasts. An intriguing feature of the S. pombe histidine kinases is the presence of PAS domains in these proteins (12). PAS domains have been demonstrated to serve as redox sensors in several different systems (reviewed in reference 83). Unlike S. cerevisiae Sln1p, the S. pombe Mak kinases do not appear to have transmembrane domains and may function as cytoplasmic sensors of redox status. S. cerevisiae cells appear to rely on direct oxidant sensing by transcriptional regulators such as Yap1p. In opposition to the more selective appearance of the histidine kinase sensor pathway, all fungal species examined appear to express a transcription factor similar to S. cerevisiae Yap1p. Additionally, Hsf1p and Skn7p gene homologues can be found in S. pombe and C. albicans genomic sequences and are likely present in all fungi. The ubiquitous presence of these transcriptional regulators emphasizes the nonnegotiable status of these proteins as key components in the response to redox challenge. These transcription factors also provide insight into the complex nature of the response to various oxidants in the cell. The most information about the oxidant-specific defects that appear in the presence of a compromised form of one of these gene regulators comes from studies with S. cerevisiae (summarized in Table 1). Loss of the YAP1 gene causes cells to acquire an extremely oxidative-stress-sensitive phenotype for many but not all oxidants. Peroxide and dlamide sensitivity increases greatly in cells lacking Yap1p, but resistance to menadione, a free radical generator, does not appear to increase in Δyap1 strains (72). Removal of the SKN7 gene dramatically enhances peroxide sensitivity but appears to increase tolerance to diamide challenge (56). Finally, functionally compromised forms of Hsflp fail to support wild-type peroxide or menadione resistance. These findings illustrate the complicated and interacting nature of the antioxidant genes regulated by these transcription factors. A better understanding of this web of target genes and the effects of their gene products on redox balance will be a major experimental step towards understanding how a eukaryotic cell survives oxidative stress.
 Fungal Proteins - genetics Fungi - physiology Gene Expression Regulation, Fungal Models, Biological Oxidative Stress - genetics Saccharomyces cerevisiae - physiology Transcription Factors - physiology Transcription, Genetic

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