Pex14/17, a filamentous fungus-specific peroxin, is required for the import of peroxisomal matrix proteins and full virulence of Magnaporthe oryzae
文献类型: 外文期刊
第一作者: Li, Ling
作者: Li, Ling;Wang, Jiaoyu;Chen, Haili;Chai, Rongyao;Zhang, Zhen;Mao, Xueqin;Qiu, Haiping;Jiang, Hua;Wang, Yanli;Sun, Guochang;Li, Ling
作者机构:
关键词: fungal pathogenicity;Magnaporthe oryzae;MoPEX14/17;peroxisome
期刊名称:MOLECULAR PLANT PATHOLOGY ( 影响因子:5.663; 五年影响因子:5.626 )
ISSN: 1464-6722
年卷期: 2017 年 18 卷 9 期
页码:
收录情况: SCI
摘要: Peroxisomes are ubiquitous organelles in eukaryotic cells that fulfil a variety of biochemical functions. The biogenesis of peroxisomes requires a variety of proteins, named peroxins, which are encoded by PEX genes. Pex14/17 is a putative recently identified peroxin, specifically present in filamentous fungal species. Its function in peroxisomal biogenesis is still obscure and its roles in fungal pathogenicity have not yet been documented. Here, we demonstrate the contributions of Pex14/17 in the rice blast fungus Magnaporthe oryzae (Mopex14/17) to peroxisomal biogenesis and fungal pathogenicity by targeting gene replacement strategies. Mopex14/17 has properties of both Pex14 and Pex17 with regard to its protein sequence. Mopex14/17 is distributed at the peroxisomal membrane and is essential for efficient peroxisomal targeting of proteins containing peroxisomal targeting signal 1. MoPEX19 deletion leads to the cytoplasmic distribution of Mopex14/17, indicating that the peroxisomal import of Pex14/17 is dependent on Pex19. The knockout mutants of MoPEX14/17 show reduced fatty acid utilization, reactive oxygen species (ROS) degradation and cell wall integrity. Moreover, Delta mopex14/17 mutants show delayed conidial generation and appressorial formation, and a reduction in appressorial turgor accumulation and penetration ability in host plants. These defects result in a significant reduction in the virulence of the mutant. These data indicate that MoPEX14/17 plays a crucial role in peroxisome biogenesis and contributes to fungal development and pathogenicity.
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