Authors contributed equally.
Mitochondrial β-oxidation regulates organellar integrity and is necessary for conidial germination and invasive growth in Magnaporthe oryzae
Article first published online: 1 NOV 2012
© 2012 Blackwell Publishing Ltd
Volume 86, Issue 6, pages 1345–1363, December 2012
How to Cite
Patkar, R. N., Ramos-Pamplona, M., Gupta, A. P., Fan, Y. and Naqvi, N. I. (2012), Mitochondrial β-oxidation regulates organellar integrity and is necessary for conidial germination and invasive growth in Magnaporthe oryzae. Molecular Microbiology, 86: 1345–1363. doi: 10.1111/mmi.12060
- Issue published online: 13 DEC 2012
- Article first published online: 1 NOV 2012
- Accepted manuscript online: 8 OCT 2012 09:06AM EST
- Manuscript Accepted: 1 OCT 2012
- Temasek Life Sciences Laboratory
Fatty acids stored as triglycerides, an important source of cellular energy, are catabolized through β-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 β-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 ech1Δ failed to utilize C14 fatty acid and was partially impeded in growth on C16 and C18 fatty acids. Surprisingly, loss of β-oxidation led to significantly altered mitochondrial morphology and integrity with ech1Δ showing predominantly vesicular/punctate mitochondria in contrast to the fused tubular network in wild-type Magnaporthe. The ech1Δ appressoria were aberrant and displayed reduced melanization. Importantly, we show that the significantly reduced ability of ech1Δ 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 β-oxidation primarily contributes to conidial viability and maintenance of redox homeostasis during host colonization by Magnaporthe.