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Abstract Litchi downy blight, caused by Peronophythora litchii, is one of the most serious diseases in major litchi-producing regions worldwide. The ankyrin (ANK) repeat is one of the most common protein-protein interaction motifs found in all kingdoms of life proteins. ANK-containing proteins have been demonstrated to regulate various biological processes in animals, plants, and fungi. However, their functions in phytopathogenic oomycetes remain unknown. Here, we identified 284 non-redundant genes that encode ANK-containing proteins in P. litchii and classified them into 11 subfamilies. Among them, PlANK1 was found to be highly up-regulated in oospores and from zoospores to the infection process. Loss of PlANK1 in P. litchii resulted in impaired mycelial growth and cyst germination, accelerated zoospore encystment, and increased sensitivity to hyperosmotic stresses and Congo red. Furthermore, PlANK1 deletion mutants were defective in oospore formation and development. Inoculation assays showed that the absence of PlANK1 severely diminished the pathogen’s virulence on litchi leaf and fruit. Through transcriptome analysis and nitrogen source utilization assays, we demonstrated that PlANK1 modulates the pathogen’s nitrogen metabolism. Altogether, our findings indicate that PlANK1 is a key regulator of sexual and asexual development, and virulence in P. litchii.

Litchi downy blight, caused by Peronophythora litchii, is one of the most serious diseases in major litchi-producing regions worldwide. The ankyrin (ANK) repeat is one of the most common protein-protein interaction motifs found in all kingdoms of life proteins. ANK-containing proteins have been demonstrated to regulate various biological processes in animals, plants, and fungi. However, their functions in phytopathogenic oomycetes remain unknown. Here, we identified 284 non-redundant genes that encode ANK-containing proteins in P. litchii and classified them into 11 subfamilies. Among them, PlANK1 was found to be highly up-regulated in oospores and from zoospores to the infection process. Loss of PlANK1 in P. litchii resulted in impaired mycelial growth and cyst germination, accelerated zoospore encystment, and increased sensitivity to hyperosmotic stresses and Congo red. Furthermore, PlANK1 deletion mutants were defective in oospore formation and development. Inoculation assays showed that the absence of PlANK1 severely diminished the pathogen's virulence on litchi leaf and fruit. Through transcriptome analysis and nitrogen source utilization assays, we demonstrated that PlANK1 modulates the pathogen's nitrogen metabolism. Altogether, our findings indicate that PlANK1 is a key regulator of sexual and asexual development, and virulence in P. litchii. [ABSTRACT FROM AUTHOR]

Polydnaviruses (PDV) are viral symbionts associated with ichneumonid and braconid wasps parasitizing moth larvae, which are able to disrupt the host immune response and development, as well as a number of other physiological pathways. The immunosuppressive role of PDV has been more intensely investigated, while very little is known about the PDV-encoded factors disrupting host development. Here we address this research issue by further expanding the functional analysis of ankyrin genes encoded by the bracovirus associated with Toxoneuron nigriceps (Hymenoptera, Braconidae). In a previous study, using Drosophila melanogaster as experimental model system, we demonstrated the negative impact of TnBVank1 impairing the ecdysone biosynthesis by altering endocytic traffic in prothoracic gland cells. With a similar approach here we demonstrate that another member of the viral ank gene family, TnBVank3 , does also contribute to the disruption of ecdysone biosynthesis, but with a completely different mechanism. We show that its expression in Drosophila prothoracic gland (PG) blocks the larval-pupal transition by impairing the expression of steroidogenic genes. Furthermore, we found that TnBVank3 affects the expression of genes involved in the insulin/TOR signaling and the constitutive activation of the insulin pathway in the PG rescues the pupariation impairment. Collectively, our data demonstrate that Tn BVANK3 acts as a virulence factor by exerting a synergistic and non-overlapping function with Tn BVANK1 to disrupt the ecdysone biosynthesis. [ABSTRACT FROM AUTHOR]