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The Autophagy Protein CsATG8 is Involved in Asexual Development and Virulence in the Pepper Anthracnose Fungus Colletotrichum scovillei.


ABSTRACT: Autophagy serves as a survival mechanism and plays important role in nutrient recycling under conditions of starvation, nutrient storage, ad differentiation of plant pathogenic fungi. However, autophagy-related genes have not been investigated in Colletotrichum scovillei, a causal agent of pepper fruit anthracnose disease. ATG8 is involved in autophagosome formation and is considered a marker of autophagy. Therefore, we generated an ATG8 deletion mutant, ΔCsatg8, via homologous recombination to determine the functional roles of CsATG8 in the development and virulence of C. scovillei. Compared with the wild-type, the deletion mutant ΔCsatg8 exhibited a severe reduction in conidiation. Conidia produced by ΔCsatg8 were defective in survival, conidial germination, and appressorium formation. Moreover, conidia of ΔCsatg8 showed reduced lipid amount and PTS1 selectivity. A virulence assay showed that anthracnose development on pepper fruits was reduced in ΔCsatg8. Taken together, our results suggest that CsATG8 plays various roles in conidium production and associated development, and virulence in C. scovillei.

SUBMITTER: Lee KH 

PROVIDER: S-EPMC9848383 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature

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The Autophagy Protein CsATG8 is Involved in Asexual Development and Virulence in the Pepper Anthracnose Fungus <i>Colletotrichum scovillei</i>.

Lee Kwang Ho KH   Gumilang Adiyantara A   Fu Teng T   Kang Sung Wook SW   Kim Kyoung Su KS  

Mycobiology 20221212 6


Autophagy serves as a survival mechanism and plays important role in nutrient recycling under conditions of starvation, nutrient storage, ad differentiation of plant pathogenic fungi. However, autophagy-related genes have not been investigated in <i>Colletotrichum scovillei</i>, a causal agent of pepper fruit anthracnose disease. <i>ATG8</i> is involved in autophagosome formation and is considered a marker of autophagy. Therefore, we generated an <i>ATG8</i> deletion mutant, <i>ΔCsatg8</i>, via  ...[more]

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