Abstract
The fungal pathogen, Colletotrichum higginsianum, causes a disease called anthracnose on various cruciferous plants. Here, we characterized a Saccharomyces cerevisiae CDC25 ortholog in C. higginsianum, named ChCDC25 (CH063_04363). The ChCDC25 deletion mutants were defective in mycelial growth, conidiation, conidial germination, appressorial formation, and invasive hyphal growth on Arabidopsis leaves, resulting in loss of virulence. Furthermore, deletion of ChCDC25 led to increased sensitivity to cell wall stress and resulted in resistance to osmotic stress. Exogenous cyclic adenosine monophosphate (cAMP) and IBMX treatments were able to induce appressorial formation in the ChCDC25 mutants, but abnormal germ tubes were still formed. The results implied that ChCDC25 is involved in pathogenicity by regulation of cAMP signaling pathways in C. higginsianum. More importantly, we found that ChCDC25 may interact with Ras2 and affects Ras2 protein abundance in C. higginsianum. Taken together, ChCDC25 regulates infection-related morphogenesis and pathogenicity of C. higginsianum. This is the first report to reveal functions of a CDC25 ortholog in a hemibiotrophic phytopathogen.
Highlights
Colletotrichum higginsianum is an important hemibiotrophic fungal pathogen that causes anthracnose disease on various cruciferous plants (Narusaka et al, 2004; O’Connell et al, 2004)
Gene expression levels of ChCDC25 were assessed at different developmental stages: C. higginsianum mycelia grown for 3 days on potato dextrose broth (PDB), conidia collected from 7-day-old potato dextrose agar (PDA), and Arabidopsis leaves inoculated with Ch-1 and incubated for different intervals (24, 48, and 72 h)
These results indicated that CDC25 proteins are diverse among different plant pathogenic fungi
Summary
Colletotrichum higginsianum is an important hemibiotrophic fungal pathogen that causes anthracnose disease on various cruciferous plants (Narusaka et al, 2004; O’Connell et al, 2004). Bluhm et al (2007) demonstrated that Ras proteins switch between active (GTP-bound) and inactive (GDP-bound) states to regulate signal transduction cascades. In Saccharomyces cerevisiae, CDC25 acts as a RasGEF in regulation of Ras proteins to affect cell cycle, growth, and proliferation (Broach, 1991; Boy-Marcotte et al, 1996). In Colletotrichum orbiculare, CoIra, a GAP, plays a critical role in conidial germination, appressorial formation, appressorial penetration, and pathogenicity by regulating cyclic adenosine monophosphate (cAMP)–PKA and MAPK signaling pathways through inactivation of CoRas (Harata and Yasuyuki, 2014). In Ustilago maydis, the CDC25 homolog Sql is an activator of Ras, dispensable for vegetative growth but required for pathogenic development (Müller et al, 2003). Our results showed that ChCDC25 was localized in the cytoplasm and regulated vegetative growth, conidiation, appressorial formation, stress responses, and pathogenicity of C. higginsianum. Our data suggested that ChCDC25 can interact especially with Ras and affected Ras protein abundance in C. higginsianum
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