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坏死诱导蛋白(NIP)基因有助于扩展青霉在梨采后感染中的毒力。

The necrosis-inducing protein (NIP) gene contributes to Penicillium expansum virulence during postharvest pear infection.

机构信息

School of Food and Biological Engineering, Jiangsu University, Zhenjiang 212013, Jiangsu, People's Republic of China; College of Food and Drug, Luoyang Normal University, Luoyang 471934, Henan, People's Republic of China.

The University of Hong Kong, 999077, Hong Kong.

出版信息

Food Res Int. 2022 Aug;158:111562. doi: 10.1016/j.foodres.2022.111562. Epub 2022 Jun 24.

DOI:10.1016/j.foodres.2022.111562
PMID:35840251
Abstract

Penicillium expansum is the causative fungus of blue mold decay in postharvest pears resulting in substantial economic losses. Investigating P. expansum-pear fruit interactions is necessary to help develop P. expansum control strategies for effective and safe pear production. Investigating the P. expansum gene expression alterations and essential gene functions during the infection process is indispensable. Based on our results, the necrosis-inducing protein (NIP) gene was closely associated with genes related to plant cell wall degrading enzymes (CWDEs) and involved in P. expansum virulence. The NIP has high homology with other already-known fungal NIPs. To evidence the role of NIP in P. expansum virulence, NIP mutant (including knockout (ΔNIP) and complementation mutant (cNIP)) P. expansum were generated. Despite the NIP deletion did not affect the basic morphology and structure of P. expansum, it slowed down the fungal growth and hyphal production, thus reducing P. expansum's sporulation and patulin (PAT) accumulation. Furthermore, the deletion of NIP reduced the pathogenicity of P. expansum in pear. The complementation of NIP (cNIP) restored the growth, conidia production, PAT accumulation, and virulence of ΔNIP to the level of wild-type P. expansum. In addition, PAT can cause decay and aggravate the disease severity of wild-type P. expansum and ΔNIP on pears. Our results confirmed NIP plays a crucial role in P. expansum's growth, hyphal production, and pathogenicity in pears.

摘要

扩展青霉是导致采后梨果实发生青霉腐烂的病原菌,造成了巨大的经济损失。研究扩展青霉与梨果实的相互作用对于开发有效的青霉控制策略,促进安全的梨生产是必要的。研究扩展青霉在感染过程中的基因表达变化和必需基因功能是必不可少的。基于我们的结果,坏死诱导蛋白(NIP)基因与与植物细胞壁降解酶(CWDEs)相关的基因密切相关,并参与扩展青霉的毒性。NIP 与其他已知的真菌 NIP 具有高度同源性。为了证明 NIP 在扩展青霉毒力中的作用,我们生成了 NIP 突变体(包括敲除(ΔNIP)和互补突变体(cNIP))扩展青霉。尽管 NIP 的缺失并不影响扩展青霉的基本形态和结构,但它减缓了真菌的生长和菌丝的产生,从而降低了扩展青霉的产孢和棒曲霉素(PAT)积累。此外,NIP 的缺失降低了扩展青霉在梨中的致病性。NIP 的互补(cNIP)恢复了ΔNIP 的生长、分生孢子产生、PAT 积累和毒力,使其达到野生型扩展青霉的水平。此外,PAT 可以引起腐烂,加重野生型扩展青霉和ΔNIP 在梨上的疾病严重程度。我们的结果证实了 NIP 在扩展青霉的生长、菌丝产生和梨中的致病性中起着关键作用。

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