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ARS Home » Pacific West Area » Davis, California » Crops Pathology and Genetics Research » Research » Publications at this Location » Publication #247474
Title: TRANSCRIPTIONAL ANALYSIS OF THE REPONSE OF NEUROSPORA CRASSA TO PHYTOSHINGOSINE REVEALS LINKS TO MITOCHRONDRIAL FUNCTION

Author
item VIDEIRA, ARNALDO - University Of Portugal
item Kasuga, Takao
item TIAN, CHAOGUANG - University Of California
item LEMOS, CATARINA - University Of Portugal
item CASTRO, ANA - University Of Portugal
item GLASS, N. LOUISE - University Of California

Submitted to: Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/9/2009
Publication Date: 9/1/2009
Citation: Videira, A., Kasuga, T., Tian, C., Lemos, C., Castro, A., Glass, N. 2009. TRANSCRIPTIONAL ANALYSIS OF THE REPONSE OF NEUROSPORA CRASSA TO PHYTOSHINGOSINE REVEALS LINKS TO MITOCHRONDRIAL FUNCTION. Microbiology. 155: 3134-3141.

Interpretive Summary: Phytosphingosine (PHS) is a class of lipid derived from plants. It has been shown that PHS induces programmed cell death (PCD) in a filamentous model fungus Neurospora crassa by an unknown mechanism. To determine the relationship between treatment with PHS and PCD, we determined changes in global gene expression levels in N. crassa in response to PHS treatment. We found that genes encoding mitochondrial proteins were suppressed by PHS treatment. This suggests that repression of mitochondrial genes might be related to the death-inducing effects of PHS. As a way to identify new components required for PHS-induced death, we analyzed the PHS-sensitivity of 24 strains carrying deletions in genes that showed a significant decrease in expression pattern when wild-type was exposed to the PHS. Two additional mutants showing increased resistance to PHS were identified and both encode predicted mitochondrial proteins, further supporting the role of the mitochondria in PHS-induced PCD.

Technical Abstract: Treatment of Neurospora crassa cells with phytosphingosine (PHS) induces programmed cell death (PCD) by an unknown mechanism. To determine the relationship between treatment with PHS and PCD, we determined changes in global gene expression levels in N. crassa during a time course of PHS treatment. Most genes having differential expression levels compared to untreated samples showed an increase in relative expression level upon PHS exposure. However, we found that genes encoding mitochondrial proteins were highly enriched among ~100 genes that showed a relative decrease in expression levels after PHS treatment, suggesting that repression of these genes might be related to the death-inducing effects of PHS. Since mutants in respiratory chain complex I are more resistant to both PHS and hydrogen peroxide than the wild type strain, possibly related to the production of reactive oxygen species (ROS), we also compared gene expression profiles of a complex I mutant (nuo14) and wild-type in response to H2O2. Genes with higher expression levels in the mutant, in the presence of H2O2, are also significantly enriched in genes encoding mitochondrial proteins. These data suggest that complex I mutants cope better with drug-induced decrease in expression of genes encoding mitochondrial proteins and may explain their increased resistance to both PHS and H2O2. As a way to identify new components required for PHS-induced death, we analyzed the PHS-sensitivity of 24 strains carrying deletions in genes that showed a significant alteration in expression pattern when wild-type was exposed to the sphingolipid. Two additional mutants showing increased resistance to PHS were identified and both encode predicted mitochondrial proteins, further supporting the role of the mitochondria in PHS-induced PCD.