Wu Pei-Ching, Chen Chia-Wen, Choo Celine Yen Ling, Chen Yu-Kun, Yago Jonar I, Chung Kuang-Ren
Department of Plant Pathology, College of Agriculture and Natural Resources, National Chung Hsing University, Taichung 40227, Taiwan.
Plant Science Department, College of Agriculture, Nueva Vizcaya State University, Bayombong, Nueva Vizcaya 3700, Philippines.
J Fungi (Basel). 2020 Oct 26;6(4):248. doi: 10.3390/jof6040248.
In addition to the production of a host-selective toxin, the tangerine pathotype of must conquer toxic reactive oxygen species (ROS) in order to colonize host plants. The roles of a peroxin 6-coding gene () implicated in protein import into peroxisomes was functionally characterized to gain a better understanding of molecular mechanisms in ROS resistance and fungal pathogenicity. The peroxisome is a vital organelle involved in metabolisms of fatty acids and hydrogen peroxide in eukaryotes. Targeted deletion of had no impacts on the biogenesis of peroxisomes and cellular resistance to ROS. The deficient mutant () reduced toxin production by 40% compared to wild type and barely induce necrotic lesions on citrus leaves. Co-inoculation of purified toxin with conidia on citrus leaves, however, failed to fully restore lesion formation, indicating that toxin only partially contributed to the loss of pathogenicity. conidia germinated poorly and formed fewer appressorium-like structures (nonmelanized enlargement of hyphal tips) than wild type. hyphae grew slowly and failed to penetrate beyond the epidermal layers. Moreover, had thinner cell walls and lower viability. All of these defects resulting from deletion of could also account for the loss of pathogenicity. Overall, our results have demonstrated that proper peroxisome functions are of vital importance to pathogenesis of the tangerine pathotype of .
除了产生寄主选择性毒素外,柑橘溃疡病菌的橘生型菌株为了在寄主植物上定殖,还必须克服有毒的活性氧(ROS)。对一个参与蛋白质导入过氧化物酶体的过氧化物酶6编码基因()的功能进行了表征,以便更好地了解ROS抗性和真菌致病性的分子机制。过氧化物酶体是真核生物中参与脂肪酸和过氧化氢代谢的重要细胞器。对的靶向缺失对过氧化物酶体的生物发生和细胞对ROS的抗性没有影响。与野生型相比,缺失的突变体()毒素产量降低了40%,并且在柑橘叶片上几乎不诱导坏死斑。然而,在柑橘叶片上用纯化毒素与分生孢子共同接种,未能完全恢复病斑形成,这表明毒素只是部分导致了致病力的丧失。与野生型相比,分生孢子萌发较差,形成的附着胞样结构(菌丝顶端非黑化膨大)较少。菌丝生长缓慢,无法穿透到表皮层之外。此外,的细胞壁更薄,活力更低。缺失导致的所有这些缺陷也可以解释致病力的丧失。总体而言,我们的结果表明,过氧化物酶体的正常功能对柑橘溃疡病菌橘生型菌株的致病性至关重要。