The key iron assimilation genesClFTR1,ClNPS6were crucial for virulence ofCurvularia lunatavia initiating its appressorium formation and virulence factors

Abstract

Summary Iron is virtually an essential nutrient for all organisms, to understand how iron contributes to virulence of plant pathogenic fungi, we identified ClFTR1 and ClNPS6 in maize pathogen Curvularia lunata (Cochliobolus lunatus) in this study. Disruption of ClNPS6 significantly impaired siderophore biosynthesis. ClFTR1 and ClNPS6 did mediate oxidative stress but had no significant impact on vegetative growth, conidiation, cell wall integrity and sexual reproduction. Conidial germination delayed and appressoria formation reduced in ΔClftr1 comparing with wild type (WT) CX‐3. Genes responsible for conidial germination, appressoria formation, non‐host selective toxin biosynthesis and cell wall degrading enzymes were also downregulated in the transcriptome of ΔClftr1 and ΔClnps6 compared with WT. The conidial development, toxin biosynthesis and polygalacturonase activity were impaired in the mutant strains with ClFTR1 and ClNPS6 deletion during their infection to maize. ClFTR1 and ClNPS6 were upregulated expression at 12–24 and 48–120 hpi in WT respectively. ClFTR1 positively regulated conidial germination, appressoria formation in the biotrophy‐specific phase. ClNPS6 positively regulates non‐host selective toxin biosynthesis and cell wall degrading enzyme activity in the necrotrophy‐specific phase. Our results indicated that ClFTR1 and ClNPS6 were key genes of pathogen known to conidia development and virulence factors.

Appressoria—Small but Incredibly Powerful Structures in Plant–Pathogen Interactions

“…Compared to wild-type (WT) CX-3, the Clftr1 deletion mutants caused delayed conidial germination and were reduced in appressoria formation. In addition, ∆Clftr1 and ∆Clnps6 mutants showed downregulation of several genes that were responsible for conidial germination, appressoria formation, non-host selective toxin biosynthesis, and cell wall-degrading enzymes [102]. ClNOX2-derived ROS signaling pathway and the ClM1-mediated CWI signaling pathway are involved in DHN melanin biosynthesis as a cross-linked manner.…”

“…Curvularia lunata is the pathogen that causes maize curvularia leaf spot disease. Iron assimilation gene ClFTR1 had been found to regulate the formation of appressoria [102]. Another study showed that ClM1 regulated the ClBRN1 transcriptionally and negatively regulated ClNOX2 transcriptionally, while ClNOX2 regulated the transcription of ClSCD1.…”

SreC‐dependent adaption to host iron environments regulates the transition of trophic stages and developmental processes of Curvularia lunata

“…Our previous work revealed that the RIA pathway is involved in the formation of the infection structures in the biotrophic stage and that the SIA pathway regulates the activity of virulence factors in the necrotrophic stage during C. lunata infection (Lu et al, 2020).…”

“…Transition from the asymptomatic biotrophic phase, characterized by intercellular thick primary hyphae, to the destructive necrotrophic phase, characterized by thin filamentous secondary hyphae, is referred to as the biotrophy-necrotrophy switch of hemibiotrophic fungi (Lee & Rose, 2010). Our previous study found that the transition from the biotrophic phase to necrotrophic phase at 24 h post-inoculation (hpi) matches the switch of iron assimilation pathways, which permits full virulence of C. lunata (Lu et al, 2020). Here, we show that C. lunata is exposed to drastic changes of the host iron environments during infection.…”

Curvularia lunata and Curvularia Leaf Spot of Maize in China

“…Iron is an essential nutrient for maintaining the virulence of C. lunata. Lu et al 68 demonstrated that nonribosomal peptide synthetase 6 (ClNPS6) (GenBank accession: JQ698337.1) and Fe transporter permease (ClFTR1) (GenBank accession: AHN52042.1) were involved in the iron acquisition and shown to be essential for virulence in infectious stages of C. lunata.…”