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.

中文翻译：

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关键的铁同化基因ClFTR1，ClNPS6通过启动其食欲形成和毒力因子而对弯弯曲菌的毒力至关重要

铁实际上是所有生物的必需营养素，要了解铁如何促进植物致病真菌的毒性，我们在本研究中鉴定了玉米病原体弯孢弯曲菌（Cochliobolus lunatus）中的ClFTR1和ClNPS6。ClNPS6的破坏大大损害了铁载体的生物合成。ClFTR1和ClNPS6确实介导了氧化应激，但对营养生长，分生，细胞壁完整性和有性繁殖没有显着影响。孢子萌发延迟和附着胞的形成在Δ减小Clftr1与野生型（WT）CX-3进行比较。与野生型相比，ΔClftr1和ΔClnps6的转录组中负责分生孢子萌发，食欲形成，非宿主选择性毒素生物合成和细胞壁降解酶的基因也被下调。ClFTR1和ClNPS6缺失的突变株感染玉米后，其分生孢子的发育，毒素的生物合成和聚半乳糖醛酸酶的活性受到损害。在野生型中，ClFTR1和ClNPS6分别在12-24 hpi和48-120 hpi表达上调。ClFTR1积极调节分生孢子萌发，在生物营养特定阶段的粘膜形成。ClNPS6在特定于坏死性营养阶段，可正向调节非宿主选择性毒素的生物合成和细胞壁降解酶的活性。我们的结果表明，ClFTR1和ClNPS6是分生孢子发育和毒力因子已知的病原体的关键基因。