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Plant Immune System

Plant Immune System. Plant Physiology. Plants are resistant to most pathogens, therefore most pathogens are specialized for particular hosts. Example: APS compendium lists approximately 100 pathogens of soybean, of which only 35 are economically important.

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Plant Immune System

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  1. Plant Immune System Plant Physiology

  2. Plants are resistant to most pathogens, therefore most pathogens are specialized for particular hosts. Example: APS compendium lists approximately 100 pathogens of soybean, of which only 35 are economically important. • Some concepts regarding plant immune systems • Preformed v. induced • Gene for gene interaction • Systemic acquired resistance • Hypersensitive response

  3. Preformed resistance mechanisms • Physical barriers (cutin, cell wall….like our skin) • Preformed antimicrobial compounds How do pathogens overcome these physical barriers? enzymes (cutinases, pectinases, cellulases, etc.) Mechanical force (appresoria, binds cell wall and hyphae together) Alternate routes of entry (wounds, stomatas, etc.) Preformed antimicrobial compounds are called ‘phytoanticipins’ plants produce a diverse array of secondary metabolites, some with antimicrobial activity Phytoanticipins are unique as they are preformed, rather than being synthesized from remote precursors after pathogen infection (phytoalexins)

  4. Phytoanticipin Phytoanticipins are synthesised by the plant at a constant rate and therefore always present in the tissues of theplant, whereas phytoalexins are only produced in response to a stimulus such as a pathogenic invasion. • Constitutive:saponins (glycosylated antimicrobials) • Saponinsbind to sterols to disrupt fungal membranes • Oats: Reduced saponin levels led to reduced resistance against oat pathogens • inactive precursors processed after tissue damage • or pathogen attack (cyanogenic glycosides and • glucosinolates)

  5. Induced resistance mechanisms physical barriers (cell wall thickening, callose deposition, lignification….) induced antimicrobials (phytoalexins…) antimicrobial proteins (PR proteins, defensins…) Hypersensitive response (PCD) Host defense peptides Induced antimicrobials - Phytoalexins low molecular weight, accumulate after pathogen infection chemically diverse (ie. not all the same!) Camalexinproduction in response to Botrytis cinerea is a good example

  6. Lignification during the invasion of Phytophthora

  7. PAMP-induced MAPK cascades in the plant defense (Adapted from Pitzschke et al., 2009)

  8. Pathogen-associated molecular patterns, or PAMPs, are molecules associated with groups of pathogens, that are recognized by cells of the innate immune system. These molecules can be referred to as small molecular motifs conserved within a class of microbes. They are recognized by Toll-like receptors (TLRs) and other pattern recognition receptors (PRRs) in both plants and animals. An effector can also be a protein that is secreted from a pathogen, which alters the host organism to enable infection, e.g. by suppressing the host's immune system capabilities. Hypersensitive response: Cells surrounding the infection site die immediately depriving the pathogen of nutrients and preventing the spread. Results in ROS production (Superoxide anion, hydrogen peroxide, hydroxyl radicals.)

  9. In phase 1, plants detect microbial/pathogen-associated molecular patterns (MAMPs/PAMPs, red diamonds) via PRRs to trigger PAMP-triggered immunity (PTI). In phase 2, successful pathogens deliver effectors that interfere with PTI, or otherwise enable pathogen nutrition and dispersal, resulting in effector-triggered susceptibility (ETS). In phase 3, one effector (indicated in red) is recognized by an NB-LRR protein, activating effector-triggered immunity (ETI), an amplified version of PTI that often passes a threshold for induction of hypersensitive cell death (HR). In phase 4, pathogen isolates are selected that have lost the red effector, and perhaps gained new effectors through horizontal gene flow (in blue)—these can help pathogens to suppress ETI. Selection favours new plant NB-LRR alleles that can recognize one of the newly acquired effectors, resulting again in ETI.

  10. Tomato cell surface receptor C. fulvum PAMP A modified Zigzag Model for Cladosporium fulvum and Tomato interaction (Adapted from Thomma et al., 2011)

  11. How Cladosporium fulvum and Tomato interaction works? The C. fulvum PAMP chitin activates PTI in tomato plants, presumably upon perception by the tomato homolog of the rice cell surface receptor CEBiP. Thus far, a chitin-triggered HR has not been observed in tomato. To overcome PTI, C. fulvum employs the abundantly secreted LysM effector Ecp6 that binds chitin, thereby preventing activation of Sl-CEBiP. Since LysM effectors are widely conserved in the fungal kingdom, they qualify as PAMPs, and Ecp6-mediated PTI suppression therefore should be referred to as PAMP-triggered susceptibility (PTS). Tomato genotypes that have evolved to recognize Ecp6 develop an HR upon Ecp6 infiltration and presumably carry a cell surface receptor for this molecule, tentatively called C. fulvum resistance to Ecp6 (Cf-Ecp6), again resulting in PTI (PTI2). The question mark indicates that subsequent susceptibility can again be provoked by C. fulvum, either through mutation of the Ecp6 protein such that it still sequesters chitin fragments but is no longer recognized by Cf-Ecp6 or by producing an effector that suppresses Sl-CEBiP signaling in an alternative manner. 

  12. Gene-for-Gene Hypothesis by H.H. Flor Disease resistance in plants requires two complementary genes: an avirulence (Avr) gene in the pathogen and a matching, resistance (R) gene in the host.Suggests a receptor-ligand model in which R-protein-mediated recognition of the pathogen-derived Avr products leads to hypersensitive response (HR) in plant. Flor showed that the inheritance of both resistance in the host and parasite ability to cause disease is controlled by pairs of matching genes. One is a plant gene called the resistance (R) gene. The other is a parasite gene called the avirulence (Avr) gene. Plants producing a specific R gene product are resistant towards a pathogen that produces the corresponding Avr gene product. http://www.youtube.com/watch?v=pDwhr1mTO5s

  13. Model of innate immune signalling activated by LRR receptors in Arabidopsis, mammals and Drosophila. A putative repressor (R) could control WRKY22 and WRKY29 activity because their overexpression bypasses the requirement of elicitors. The conserved signalling pathways for innate immune responses in animals are summarized on the basis of recent reviews on mammals and Drosophila

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