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

dc.contributor.authorFélix, Carina
dc.contributor.authorMeneses, Rodrigo
dc.contributor.authorGonçalves, Micael F. M.
dc.contributor.authorDuarte, Ana S.
dc.contributor.authorJorrín-Novo, Jesus V.
dc.contributor.authorvan de Peer, Yves
dc.contributor.authorDeforce, Dieter
dc.contributor.authorNieuwerburgh, Filip Van
dc.contributor.authorAlves, Artur
dc.contributor.authorEsteves, Ana C.
dc.date.accessioned2024-04-17T15:20:56Z
dc.date.available2024-04-17T15:20:56Z
dc.date.issued2024-06-01
dc.description.abstractLasiodiplodia 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.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.doi10.1016/j.scitotenv.2024.171917pt_PT
dc.identifier.eid85189750489
dc.identifier.issn0048-9697
dc.identifier.pmid38580127
dc.identifier.urihttp://hdl.handle.net/10400.14/44657
dc.identifier.wos001227362900001
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/pt_PT
dc.subjectHuman opportunistpt_PT
dc.subjectPhytopathogenicitypt_PT
dc.subjectProteomept_PT
dc.subjectSecretomept_PT
dc.subjectTemperaturept_PT
dc.subjectTranscriptomept_PT
dc.titleHow temperature modulates the expression of pathogenesis-related molecules of the cross-kingdom pathogen Lasiodiplodia hormozganensispt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.titleScience of the Total Environmentpt_PT
oaire.citation.volume927pt_PT
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT

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