Guastaferro, Valentino Maria (2024) Host sensing in the fungal pathogen fusarium oxysporum. [Tesi di dottorato]

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Tipologia del documento: Tesi di dottorato
Lingua: English
Titolo: Host sensing in the fungal pathogen fusarium oxysporum
Autori:
Autore
Email
Guastaferro, Valentino Maria
valentinomaria.guastaferro@unina.it
Data: 11 Marzo 2024
Numero di pagine: 192
Istituzione: Università degli Studi di Napoli Federico II
Dipartimento: Agraria
Dottorato: Sustainable agricultural and forestry systems and food security
Ciclo di dottorato: 36
Coordinatore del Corso di dottorato:
nome
email
MAGGIO, ALBINO
almaggio@unina.it
Tutor:
nome
email
TURRA', DAVID
[non definito]
Data: 11 Marzo 2024
Numero di pagine: 192
Parole chiave: FUSARIUM; PENETRATION; WSC1; HAM7; MID1; MECHANOSENSORS
Settori scientifico-disciplinari del MIUR: Area 07 - Scienze agrarie e veterinarie > AGR/12 - Patologia vegetale
Depositato il: 13 Mar 2024 07:49
Ultima modifica: 12 Ago 2026 05:33
URI: https://www.fedoa.unina.it/id/eprint/15438

Abstract

Fusarium oxysporum (Fo) is a soil-borne fungal pathogen that causes vascular wilt disease in susceptible tomato plants, leading to significant annual yield losses. Despite the known chemical signals that attract Fo to host roots, its penetration mechanism and inducing signals remain elusive. To colonize plant root tissues, Fo hyphae have to penetrate sub-micrometric channels, such as those encountered in the plant’s apoplast or symplast, a process likely requiring the generation of high physical pressure and the development of tiny cellular structures. The aim of this work has been to elucidate the physical and molecular mechanisms driving Fo penetration and virulence. In vitro assays showed that during the penetration process Fo hyphae are both able to penetrate pre-formed pores/channels of a fraction of a micron and to rapidly adapt to distinct osmotic environments. The latter process requires Hog1, a Mitogen-Activated Protein Kinase (MAPK) essential for osmoadaptation. We further demonstrate that hyphal compression and cell wall damage, likely outputs of fungal entrance into the host openings, trigger Fo penetration. Indeed, media supplementation with crude cell wall extracts or laminarin expedites Fo invasion in artificial membranes. Finally, we show that Ham7, Wsc1, and Mid1, putative mechanosensors and upstream components of the Mpk1 cell-wall integrity MAPK cascade, play significant roles in Fo virulence. Overall, this study unravels fundamental aspects of Fo pathogenicity, offering valuable insights for future disease management strategies.

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