Liu Qiao, Long Ruhui, Zhi Cailing, Liang Zhibin, Deng Yi Zhen
Guangdong Province Key Laboratory of Microbial Signals and Disease Control, Integrative Microbiology Research Centre, College of Plant Protection, South China Agricultural University, Guangzhou, China.
Mycology. 2024 May 20;15(4):602-619. doi: 10.1080/21501203.2024.2350169. eCollection 2024.
Rice blast is one of the most devastating diseases and a serious threat to global food security. It is caused by the ascomycetous fungus . During the pathogenic development of , ferroptotic death of conidial cells is critical for appressorium formation and infection to host rice. In this study, we identified and functionally characterised orthologs of fatty acid desaturase (Fad2) and acyl-CoA synthetase long-chain family (Acsl4) in . Pathogenicity was impaired in the Δ or Δ mutant and targeted lipidomics analysis demonstrated that Fad2 and Acsl4 were involved in the production of polyunsaturated fatty acids (PUFAs)-containing phospholipids (PUFA-PLs) potentially contributing to ferroptosis. Treatment with FeCl, an oxidative agent to cause lipid peroxidation, could partially restore Δ pathogenicity. Fad2 was also found to potentially interact with proteins involved in cellular redox homoeostasis. Overall, our results elucidate the role of PUFA-PLs biosynthesis in fungal cell death and fungal pathogenicity, providing a theoretical basis for the development of specific pesticides/drugs targeting ferroptosis caused by lipid peroxidation.
稻瘟病是最具毁灭性的病害之一,对全球粮食安全构成严重威胁。它由子囊菌引起。在其致病发育过程中,分生孢子细胞的铁死亡对于附着胞形成和侵染寄主水稻至关重要。在本研究中,我们鉴定并功能表征了脂肪酸去饱和酶(Fad2)和酰基辅酶A合成酶长链家族(Acsl4)在中的直系同源物。Δ或Δ突变体的致病性受损,靶向脂质组学分析表明Fad2和Acsl4参与了含多不饱和脂肪酸(PUFAs)的磷脂(PUFA-PLs)的产生,这可能有助于铁死亡。用FeCl(一种引起脂质过氧化的氧化剂)处理可部分恢复Δ的致病性。还发现Fad2可能与参与细胞氧化还原稳态的蛋白质相互作用。总体而言,我们的结果阐明了PUFA-PLs生物合成在真菌细胞死亡和真菌致病性中的作用,为开发针对脂质过氧化引起的铁死亡的特定农药/药物提供了理论基础。