Mitochondrial β-oxidation regulates organellar integrity and is necessary for conidial germination and invasive growth in Magnaporthe oryzae
Mitochondrial β-oxidation regulates organellar integrity and is necessary for conidial germination and invasive growth in Magnaporthe oryzae
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DOI:
10.1111/mmi.12060
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发表时间:
2012-12-01
影响因子:
3.6
通讯作者:
Naqvi, Naweed I.
中科院分区:
文献类型:
--
作者:
Patkar, Rajesh N.;Ramos-Pamplona, Marilou;Naqvi, Naweed I.
Fatty acids stored as triglycerides, an important source of cellular energy, are catabolized through beta-oxidation pathways predicted to occur both in peroxisomes and mitochondria in filamentous fungi. Here, we characterize the function of Enoyl-CoA hydratase Ech1, a mitochondrial beta-oxidation enzyme, in the model phytopathogen Magnaporthe oryzae. Ech1 was found to be essential for conidial germination and viability of older hyphae. Unlike wild-type Magnaporthe, the ech1? failed to utilize C14 fatty acid and was partially impeded in growth on C16 and C18 fatty acids. Surprisingly, loss of beta-oxidation led to significantly altered mitochondrial morphology and integrity with ech1? showing predominantly vesicular/punctate mitochondria in contrast to the fused tubular network in wild-type Magnaporthe. The ech1? appressoria were aberrant and displayed reduced melanization. Importantly, we show that the significantly reduced ability of ech1? to penetrate the host and establish therein is a direct consequence of enhanced sensitivity of the mutant to oxidative stress, as the defects could be remarkably reversed through exogenous antioxidants. Overall, our comparative analyses reveal that peroxisomal lipid catabolism is essential for appressorial function of host penetration, whereas mitochondrial beta-oxidation primarily contributes to conidial viability and maintenance of redox homeostasis during host colonization by Magnaporthe.