Mutation of CRE1 in Fusarium oxysporum reverts the pathogenicity defects of the FRP1 deletion mutant.

The F-box protein Frp1 is required for pathogenicity of Fusarium oxysporum f. sp. lycopersici towards tomato. The Delta frp1 mutant is deficient in expression of genes for cell wall-degrading enzymes (CWDEs) and ICL1, encoding a key enzyme for the assimilation of C2 carbon sources. An explanation for the inability of the Delta frp1 mutant to express these genes may be found in constitutive carbon catabolite repression. Cre1 is the transcriptional repressor in filamentous fungi known to repress several CWDE genes and other genes required for assimilation of non-sugar carbon sources. Here, we demonstrate that Frp1 and Cre1 both control the repression/derepression state of such genes. The replacement of CRE1 with GST::CRE1 resulted in a derepressed phenotype in wild-type background, suggesting that this replacement affects Cre1 function. Strikingly, in the Delta frp1 mutant the replacement of CRE1 with GST::CRE1 restored pathogenicity, growth on ethanol and expression of ICL1 and CWDE genes. A GFP-Cre1 fusion protein is not degraded nor exported out of the nucleus during growth on ethanol, a derepressing carbon source, suggesting that Cre1 is not likely a target of Frp1 for degradation by the proteasome. We conclude that both proteins function together to regulate transcription of carbon source utilization genes.