Autophagy-related protein PlATG2 regulates the vegetative growth, sporangial cleavage, autophagosome formation, and pathogenicity of peronophythora litchii

Autophagy is an intracellular degradation process that is important for the development and pathogenicity of phytopathogenic fungi and for the defence response of plants. However, the molecular mechanisms underlying autophagy in the pathogenicity of the plant pathogenic oomycete , the causal agent o...

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Veröffentlicht in:Virulence 2024-12, Vol.15 (1), p.2322183-2322183
Hauptverfasser: Lv, Lin, Yang, Chengdong, Zhang, Xue, Chen, Taixu, Luo, Manfei, Yu, Ge, Chen, Qinghe
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Sprache:eng
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Zusammenfassung:Autophagy is an intracellular degradation process that is important for the development and pathogenicity of phytopathogenic fungi and for the defence response of plants. However, the molecular mechanisms underlying autophagy in the pathogenicity of the plant pathogenic oomycete , the causal agent of litchi downy blight, have not been well characterized. In this study, the autophagy-related protein ATG2 homolog, PlATG2, was identified and characterized using a CRISPR/Cas9-mediated gene replacement strategy in . A monodansylcadaverine (MDC) staining assay indicated that deletion of abolished autophagosome formation. Infection assays demonstrated that Δ mutants showed significantly impaired pathogenicity in litchi leaves and fruits. Further studies have revealed that PlATG2 participates in radial growth and asexual/sexual development of . Moreover, zoospore release and cytoplasmic cleavage of sporangia were considerably lower in the Δ mutants than in the wild-type strain by FM4-64 staining. Taken together, our results revealed that PlATG2 plays a pivotal role in vegetative growth, sporangia and oospore production, zoospore release, sporangial cleavage, and plant infection of . This study advances our understanding of the pathogenicity mechanisms of the phytopathogenic oomycete and is conducive to the development of effective control strategies.
ISSN:2150-5594
2150-5608
DOI:10.1080/21505594.2024.2322183