Fungal pathogenesis Flashcards
(6 cards)
intro - mechanisms and molecular effectors
Fungal pathogens of plants employ complex strategies to infect, colonise, and extract nutrients from their hosts. The nature of pathogenesis varies among biotrophs (which require living host cells), necrotrophs (which kill host tissue), and hemibiotrophs (which transition from biotrophy to necrotrophy), reflecting their unique interactions with host physiology.
2nd para - adhesion and penetration
The infection process begins with adhesion to the plant’s aerial surfaces, which are typically hydrophobic and chemically inert. Passive adherence occurs via hydrophobic interactions, but many pathogens actively secrete adhesive glycoproteins and polysaccharides to establish stable contact. Enzymes such as cutinases and esterases assist in breaking down the waxy cuticle, facilitating firmer anchoring. A key structure in many fungal pathogens, particularly Magnaporthe oryzae, is the appressorium, a dome-shaped cell that generates extreme turgor pressure (up to 8 MPa) through glycerol accumulation. This pressure is used to drive a penetration peg through the plant epidermis, initiating invasion.
3rd para - enzymatic degradation adn host entry
Once entry begins, fungi rely heavily on cell wall-degrading enzymes (CWDEs) to breach structural barriers and access deeper tissues. These enzymes include cutinases, pectinases, xylanases, cellulases, and ligninases, which target different components of the plant cell wall. CWDEs not only facilitate mechanical entry but also aid in nutrient acquisition by breaking down polymers into metabolically useful sugars. Necrotrophs like Botrytis cinerea produce these enzymes in large quantities, leading to rapid tissue maceration, while biotrophs deploy them more subtly to avoid activating host defences prematurely.
4th para - host manipulation and defense suppression
To maintain colonisation, fungal pathogens must actively suppress or evade host immune responses. Biotrophic fungi form haustoria, highly specialised intracellular feeding structures that extract nutrients and secrete effector proteins into host cells. These effectors manipulate plant signalling pathways and suppress immunity. For example, Ustilago maydis uses Pep1 to inhibit reactive oxygen species production, while Pit2 interferes with salicylic acid-mediated defences. Magnaporthe oryzae expresses Slp1, which binds to fungal chitin and prevents its recognition by plant pattern-recognition receptors, thereby avoiding immune activation.
5th para - toxin production and secondary metabolites
Many pathogenic fungi secrete phytotoxins to kill host cells or disrupt their physiology. Host-specific toxins (HSTs) such as T-toxin, produced by Cochliobolus heterostrophus, selectively affect susceptible maize genotypes by forming pores in mitochondrial membranes. Non-host-specific toxins (NHSTs) like tentoxin from Alternaria alternata have broader targets and inhibit chloroplast development, causing chlorosis in seedlings. Fungi may also produce gibberellic acids, plant hormone analogues that disrupt normal growth, such as in bakanae disease of rice caused by Fusarium fujikuroi. Additionally, siderophores are secreted to scavenge iron from the host environment, an essential cofactor for fungal metabolism and proliferation.
6th para - overcoming plant defenses
Plants produce phytoalexins, antimicrobial secondary metabolites that inhibit fungal growth. Successful pathogens possess mechanisms to detoxify or bypass these defences. For instance, Fusarium graminearum expresses tomatinase, which degrades tomatine, a defensive compound in tomatoes. Similarly, Fusarium solani detoxifies pisatin, a pea phytoalexin. Some fungi employ efflux transporters to actively pump toxic compounds out of their cells, further enhancing resistance to host-derived chemical defences. Maintaining cell wall integrity, via genes such as chitin synthases or MCK1 (in M. oryzae), also contributes to resistance against plant-derived stressors.
