Nadal M and Gold SE (2010) The autophagy genes atg8 and atg1 affect morphogenesis and pathogenicity in Ustilago maydis. Mol Plant Pathol 11(4):463-78
Abstract: Autophagy is a complex degradative process in which cytosolic material, including organelles, is randomly sequestered within double-membrane vesicles termed autophagosomes. In Saccharomyces cerevisiae, the autophagy genes ATG1 and ATG8 are crucial for autophagy induction and autophagosome assembly, respectively, and their deletion has an impact on the autophagic potential of the corresponding mutant strains. We were interested in the role of autophagy in the development and virulence of U. maydis. Using a reverse genetic approach, we showed that the U. maydis ATG8 orthologue, atg8, is associated with autophagy-dependent processes. Deletion of atg8 abolished autophagosome accumulation in the vacuoles of carbon-starved cells and drastically reduced the survival of U. maydisDeltaatg8 mutant strains during these conditions. In addition, atg8 deletion had an impact on the budding process during saprobic haploid growth. The infection of maize with compatible Deltaatg8 strains resulted in fewer galled plants, and fungal gall colonization was strongly reduced, as reflected by the very low hyphal density in these tissues. Deltaatg8 infections resulted in the formation of very few teliospores. To corroborate the role of autophagy in U. maydis development, we also deleted the ATG1 orthologue, atg1. Deletion of atg1 yielded phenotypes similar to the Deltaatg8 strains during saprobic growth, but of lower magnitude. The Deltaatg1 strains were only slightly less pathogenic than the wild-type and teliospore production was not affected. Surprisingly, atg1 deletion in the Deltaatg8 background exacerbated those phenotypes already observed in the Deltaatg8 and Deltaatg1 single-mutant strains, strongly suggesting an additive phenotype. In particular, the double mutant was completely suppressed for plant gall induction.
|Status: Published||Type: Journal Article||PubMed ID: 20618705|
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