Publikation: Mechanisms by which pathenogenic fungi recognize and attack their host plants: 3. Fungal morphogenesis and enzyme secretion during pathogenesis
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Fungi represent a highly diverse evolutionary group of eukaryotic, heterotrophic organisms which share a common cellular organisation. The fungal thallus or mycelium consists of hyphae, tubular structures which may be divided into cellular units by septa. Growth of fungal hyphae occurs at the tip and is mediated by continuous synthesis and secretion of cell wall material to the apex. Hyphal tip growth allows the mycelium to rapidly spread over, and feed on, a variety of substrata. While many fungi are feeding saprophytically on dead organic matter, several fungal groups are able to exploit other organisms as nutrient sources during symbiotic or parasitic stages. Plant parasitic fungi have developed a variety of refined mechanisms to invade their hosts and to live at their expense. So-called necrotrophic (perthotrophic) fungi rapidly kill the infected host by secretion of toxins (Chapter 4) and wall-mazerating enzymes. In contrast, biotrophic fungi are able to absorb nutrients from living host cells while maintaining host integrity and viability for an extended period of time. Intermediate relationships are called hemibiotrophic, because an initial biotrophic phase is followed by tissue destruction and colonization of the dead host tissue. In fact, it has become evident that many of the necrotrophic fungi are going through a short initial infection phase without affecting host cell viability (Rodriguez-Gálvez + Mendgen 1995). Successful infection depends on correct recognition of, and adaptation to, the host and is often accompanied by a high degree of cytological and molecular differentiation of the fungus. Fungal pathogenicity and plant susceptibility or resistance are meehanistically inseparable from each other, and only a combined understanding of both aspects will give a comprehensive perspective of the parasite-host relationship. This applies in particular to those fungal-plant interactions determined by gene-for-gene relationships, which are now beginning to he understood on a molecular level (see Chapters 8 and 10). We expect that this knowledge will expand our potential to develop novel strategies for plant protection, e.g. by interfering with specific steps of pathogen development.
In this Chapter, we will describe the various stages of fungal infection and discuss properties and functions of specialized hyphae (infection structures) in this process. The morphogenetic differentiation of the invading fungus is accompanied by a regulated expression of genes, such as those encoding cuticle- and wall-degrading enzymes. Our present knowledge of their properties
and their particular role during pathogenesis will also be discussed.
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HAHN, Matthias, Holger DEISING, Christine STRUCK, Kurt MENDGEN, 1997. Mechanisms by which pathenogenic fungi recognize and attack their host plants: 3. Fungal morphogenesis and enzyme secretion during pathogenesis. In: H. HARTLEB …, , ed.. Resistance of Crop Plants against Fungi. Jena: G. Fischer, 1997, pp. 33-57BibTex
@incollection{Hahn1997Mecha-7015, year={1997}, title={Mechanisms by which pathenogenic fungi recognize and attack their host plants: 3. Fungal morphogenesis and enzyme secretion during pathogenesis}, publisher={G. Fischer}, address={Jena}, booktitle={Resistance of Crop Plants against Fungi}, pages={33--57}, editor={H. Hartleb …}, author={Hahn, Matthias and Deising, Holger and Struck, Christine and Mendgen, Kurt} }
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Hyphal tip growth allows the mycelium to rapidly spread over, and feed on, a variety of substrata. While many fungi are feeding saprophytically on dead organic matter, several fungal groups are able to exploit other organisms as nutrient sources during symbiotic or parasitic stages. Plant parasitic fungi have developed a variety of refined mechanisms to invade their hosts and to live at their expense. So-called necrotrophic (perthotrophic) fungi rapidly kill the infected host by secretion of toxins (Chapter 4) and wall-mazerating enzymes. In contrast, biotrophic fungi are able to absorb nutrients from living host cells while maintaining host integrity and viability for an extended period of time. Intermediate relationships are called hemibiotrophic, because an initial biotrophic phase is followed by tissue destruction and colonization of the dead host tissue. In fact, it has become evident that many of the necrotrophic fungi are going through a short initial infection phase without affecting host cell viability (Rodriguez-Gálvez + Mendgen 1995). Successful infection depends on correct recognition of, and adaptation to, the host and is often accompanied by a high degree of cytological and molecular differentiation of the fungus. Fungal pathogenicity and plant susceptibility or resistance are meehanistically inseparable from each other, and only a combined understanding of both aspects will give a comprehensive perspective of the parasite-host relationship. This applies in particular to those fungal-plant interactions determined by gene-for-gene relationships, which are now beginning to he understood on a molecular level (see Chapters 8 and 10). We expect that this knowledge will expand our potential to develop novel strategies for plant protection, e.g. by interfering with specific steps of pathogen development.<br />In this Chapter, we will describe the various stages of fungal infection and discuss properties and functions of specialized hyphae (infection structures) in this process. The morphogenetic differentiation of the invading fungus is accompanied by a regulated expression of genes, such as those encoding cuticle- and wall-degrading enzymes. Our present knowledge of their properties<br />and their particular role during pathogenesis will also be discussed.</dcterms:abstract> <dspace:isPartOfCollection rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/> <dc:rights>Attribution-NonCommercial-NoDerivs 2.0 Generic</dc:rights> <dcterms:title>Mechanisms by which pathenogenic fungi recognize and attack their host plants: 3. 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