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PTS1 Peroxisomal Import Pathway Plays Shared and Distinct Roles to PTS2 Pathway in Development and Pathogenicity of Magnaporthe oryzae

文献类型: 外文期刊

作者: Wang, Jiaoyu 1 ; Zhang, Zhen 1 ; Wang, Yanli 1 ; Li, Ling 1 ; Chai, Rongyao 1 ; Mao, Xueqin 1 ; Jiang, Hua 1 ; Qiu, Haipi 1 ;

作者机构: 1.Zhejiang Acad Agr Sci, State Key Lab Breeding Base Zhejiang Sustainable, Inst Plant Protect Microbiol, Hangzhou, Zhejiang, Peoples R China

2.Zhejiang Acad Agr Sci, State Key Lab Breedin

期刊名称:PLOS ONE ( 影响因子:3.24; 五年影响因子:3.788 )

ISSN: 1932-6203

年卷期: 2013 年 8 卷 2 期

页码:

收录情况: SCI

摘要: Peroxisomes participate in various important metabolisms and are required in pathogenicity of fungal plant pathogens. Peroxisomal matrix proteins are imported from cytoplasm into peroxisomes through peroxisomal targeting signal 1 (PTS1) or peroxisomal targeting signal 2 (PTS2) import pathway. PEX5 and PEX7 genes participate in the two pathways respectively. The involvement of PEX7 mediated PTS2 import pathway in fungal pathogenicity has been documented, while that of PTS1 remains unclear. Through null mutant analysis of MoPEX5, the PEX5 homolog in Magnaporthe oryzae, we report the crucial roles of PTS1 pathway in the development and host infection in the rice blast fungus, and compared with those of PTS2. We found that MoPEX5 disruption specifically blocked the PTS1 pathway. Delta mopex5 was unable to use lipids as sole carbon source and lost pathogenicity completely. Similar as Delta mopex7, Delta mopex5 exhibited significant reduction in lipid utilization and mobilization, appressorial turgor genesis and H2O2 resistance. Additionally, Delta mopex5 presented some distinct defects which were undetected in Delta mopex7 in vegetative growth, conidial morphogenesis, appressorial morphogenesis and melanization. The results indicated that the PTS1 peroxisomal import pathway, in addition to PTS2, is required for fungal development and pathogenicity of the rice blast fungus, and also, as a main peroxisomal import pathway, played a more predominant role than PTS2.

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