How temperature modulates the expression of pathogenesis-related molecules of the cross-kingdom pathogen Lasiodiplodia hormozganensis

Carina Félix, Rodrigo Meneses, Micael F. M. Gonçalves, Ana S. Duarte, Jesus V. Jorrín-Novo, Yves van de Peer, Dieter Deforce, Filip Van Nieuwerburgh, Artur Alves, Ana C. Esteves*

*Autor correspondente para este trabalho

Resultado de pesquisarevisão de pares

8 Transferências (Pure)

Resumo

Lasiodiplodia hormozganensis, initially recognized as a fungal plant pathogen, is recognized now acknowledged as a potential threat to humans. However, our understanding of the pathogenesis mechanisms of Lasiodiplodia species remains limited, and the impact of temperature on its pathogenicity is unclear. This study aims to elucidate the effects of temperature on the biology of L. hormozganensis, focusing on the expression of pathogenesis-related molecules and its ability to function as a cross-kingdom pathogen. We conducted experiments at two different temperatures, 25 and 37 °C, analyzing the proteome and transcriptome of L. hormozganensis. Using strain CBS339.90, initially identified as L. theobromae but confirmed through ITS and tef1-α sequence analysis to be L. hormozganensis, we aimed to understand the fungus's protein expression under varying temperature conditions. Results from the functional analysis of the secretome at 25 °C showed a noteworthy presence of proteins related to carbohydrate metabolism, catabolism, plant cell wall degradation, and pathogenesis. However, when grown at 37 °C, the fungus exhibited an increased production of stress response and pathogenesis-related proteins. Our findings identified various pathways crucial for pathogenesis in both plants and humans, suggesting that L. hormozganensis possesses the genetic foundation to infect both hosts. Specific pathogenesis-related proteins, including the phytotoxin snodprot1, aspartic protease aspergillopepsin, and virulence protein SSD1, were also identified. Concluding, we propose a possible mechanism of how L. hormozganensis adapts to different temperatures. The shift in temperature results in the expression of genes that favor human related pathogenesis molecules.

Idioma originalEnglish
Número do artigo171917
Número de páginas11
RevistaScience of the Total Environment
Volume927
DOIs
Estado da publicaçãoPublicado - 1 jun. 2024

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