Pex13 and Pex14, the key components of the peroxisomal docking complex, are required for peroxisome formation, host infection and pathogenicity-related morphogenesis inMagnaporthe oryzae

Abstract

Peroxisomes are ubiquitous organelles in eukaryotic cells that fulfill multiple important metabolisms. Pex13 and Pex14 are key components of the peroxisomal docking complex in yeasts and mammals. In the present work, we functionally characterized the homologues of Pex13 and Pex14 (Mopex13 and Mopex14) in the rice blast fungus Magnaporthe oryzae . Mopex13 and Mopex14 were peroxisomal membrane distributed and were both essential for the maintenance of Mopex14/17 on the peroxisomal membrane. Mopex13 and Mopex14 interacted with each other, and with Mopex14/17 and peroxisomal matrix protein receptors. Disruption of Mopex13 and Mopex14 resulted in a cytoplasmic distribution of peroxisomal matrix proteins and the Woronin body protein Hex1. In the ultrastructure of Δmopex13 and Δmopex14 cells, peroxisomes were detected on fewer occasions, and the Woronin bodies and related structures were dramatically affected. The Δmopex13 and Δmopex14 mutants were reduced in vegetative growth, conidial generation and mycelial melanization, in addition, Δmopex13 showed reduced conidial germination and appressorial formation and abnomal appressorial morphology. Both Δmopex13 and Δmopex14 were deficient in appressorial turgor and nonpathogenic to their hosts. The infection failures in Δmopex13 and Δmopex14 were also due to their reduced ability to degrade fatty acids and to endure reactive oxygen species and cell wall-disrupting compounds. Additionally, Mopex13 and Mopex14 were required for the sexual reproduction of the fungus. These data indicate that Mopex13 and Mopex14, as key components of the peroxisomal docking complex, are indispensable for peroxisomal biogenesis, fungal development and pathogenicity in the rice blast fungus.

Fatty Acid Synthase Beta Dehydratase in the Lipid Biosynthesis Pathway Is Required for Conidiogenesis, Pigmentation and Appressorium Formation in Magnaporthe oryzae S6

“…The appressorium has a differentiated strong cell wall, enriched in chitin and layer of melanin formed between the cell wall and cell membrane and acts as a barrier to the efflux of glycerol during turgor pressure generation [ 75 , 76 ]. Accumulation of glycerol generates hydrostatic turgor pressure.…”

“…Studies conducted on Δ mopex13 and Δ mopex14 mutants in M. oryzae demonstrated reduced growth, lighter colored appressoria, defective melanization, appressorial glycerol accumulation and finally, its inability to infect host in pathogenicity test. Δ mopex13 and Δ mopex14 mutants were also unable to degrade fatty acids in their spore [ 75 ]. PEX13 in Colletrichum orbiculare and Aspergillus nidulans showed defective melanization and loss of ability to penetrate the cuticle of the host cells [ 19 , 75 ].…”

“…Δ mopex13 and Δ mopex14 mutants were also unable to degrade fatty acids in their spore [ 75 ]. PEX13 in Colletrichum orbiculare and Aspergillus nidulans showed defective melanization and loss of ability to penetrate the cuticle of the host cells [ 19 , 75 ]. Disruption of PEX7 blocked the PTS2 import pathway in M. oryzae that is presumed to connect lipid biosynthesis, melanin biosynthesis and interruption of lipid degradation [ 75 ].…”

“…PEX13 in Colletrichum orbiculare and Aspergillus nidulans showed defective melanization and loss of ability to penetrate the cuticle of the host cells [ 19 , 75 ]. Disruption of PEX7 blocked the PTS2 import pathway in M. oryzae that is presumed to connect lipid biosynthesis, melanin biosynthesis and interruption of lipid degradation [ 75 ]. Δpex6 mutants showed that this gene was crucial in lipid body degradation and melanization.…”

Proper Functions of Peroxisomes Are Vital for Pathogenesis of Citrus Brown Spot Disease Caused by Alternaria alternata

“…Mutation of the pex6 homolog in Colletotrichum lagenarium [ 25 ] has little or no effect on radial growth. However, mutation of pex6 or other peroxin-coding genes in the rice blast fungus Magnaporthe oryzae often results in growth retardation [ 26 , 59 , 60 ]. Deletion of the pex6 homolog in the Japanese pear pathotype of A. alternata , which produces the host-selective AK toxin, reduces radial growth by ~20% on MM containing glucose as the sole carbon source [ 16 ].…”