Aspergillus flavus Exploits Maize Kernels Using an "Orphan" Secondary Metabolite Cluster
Ludovica Antiga1, Sonia Roberta La Starza1, Cecilia Miccoli2
1Department of Environmental Biology, Sapienza University of Rome, P.le Aldo Moro 5, 00185 Roma, Italy.
International Journal of Molecular Sciences
|November 6, 2020
Summary
Aspergillus flavus uses cluster 32 to produce fungal effectors like SalOH and Npp1, which help it infect maize kernels by overcoming host defenses during the early stages of infection.
Area of Science:
- Mycology
- Plant Pathology
- Molecular Biology
Background:
- * *Aspergillus flavus* is a fungus that infects crops, producing harmful aflatoxins.
- * Aflatoxins are carcinogenic but do not significantly affect host plants like maize.
- * Previous research identified potential pathogenesis-related secondary metabolite clusters in *A. flavus*.
Purpose of the Study:
- * To investigate the role of *A. flavus* genetic cluster 32 in maize kernel infection.
- * To understand the function of fungal effectors encoded by cluster 32, including salicylate hydroxylase (SalOH) and necrosis- and ethylene-inducing proteins (Npp1).
Main Methods:
- * Creation and analysis of *A. flavus* mutants with altered cluster 32 functions (e.g., overexpression).
- * Histological and histochemical experiments to assess gene expression (SalOH, Npp1), salicylate production, and its dehydroxylated form.
- * Evaluation of mutant pathogenicity on maize kernels.
Main Results:
- * Expression of SalOH and Npp1 genes within cluster 32 significantly increased within 2 days of maize kernel infection.
- * These fungal effectors appear crucial for evading host defenses in living maize tissues like the aleurone.
- * The study observed the production of salicylate and its dehydroxylated form.
Conclusions:
- * Cluster 32 plays a significant role in the initial stages of *A. flavus* infection in maize kernels.
- * Fungal effectors SalOH and Npp1 are instrumental in colonizing maize tissues and establishing infection.
- * Understanding cluster 32's function provides insights into fungal pathogenesis mechanisms.
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