Abstract

Heat shock transcription factors (HSFs) are a family of transcription regulators. Although HSFs’ functions in controlling the transcription of the molecular chaperone heat shock proteins and resistance to stresses are well established, their effects on the pathogenicity of plant pathogenic fungi remain unknown. In this study, we analyze the role of CgHSF1 in the pathogenicity of Colletotrichum gloeosporioides and investigate the underlying mechanism. Failure to generate the Cghsf1 knock-out mutant suggested that the gene is essential for the viability of the fungus. Then, genetic depletion of the Cghsf1 was achieved by inserting the repressive promoter of nitrite reductase gene (PniiA) before its coding sequence. The mutant showed significantly decrease in the pathogenicity repression of appressorium formation, and severe defects in melanin biosynthesis. Moreover, four melanin synthetic genes were identified as direct targets of CgHSF1. Taken together, this work highlights the role of CgHSF1 in fungal pathogenicity via the transcriptional activation of melanin biosynthesis. Our study extends the understanding of fungal HSF1 proteins, especially their involvement in pathogenicity.

Highlights

  • The genus Colletotrichum spp. is a group of plant pathogenic fungi that can infect a wide range of plants worldwide [1]

  • We found that CgHSF1 depletion impairs the expression of melanin biosynthesis genes, compromises appressorium formation, and leads to the decrease in pathogenicity

  • The results showed that the fluorescence of the CK was located in both the cell nucleus and cytoplasm, whereas that of CgHSF1-sGFP was mainly located in the cell nucleus, as evidenced by the co-localization of 4′,6-diamidino-2-phenylindole (DAPI) staining (Figure 2B)

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Summary

Introduction

The genus Colletotrichum spp. is a group of plant pathogenic fungi that can infect a wide range of plants worldwide [1]. Colletotrichum higginsianum, Colletotrichum orbiculare, and C. gloeosporioides could adjust their strategies to switch between these stages by regulating the expression of virulence factors, such as effectors, secondary metabolite synthesis enzymes, and degradative enzymes [3,4]. Wor, a conserved fungal TF from Candida albicans, controls the white–opaque switching of cells and is required for virulence to humans [5,6]. In plant pathogenic fungi from the genus Fusarium, SGE1 proteins, the orthologs of Wor, regulate effector genes and secondary metabolite gene clusters [7,8,9,10], and are required for parasitic growth [11].

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