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Plant Immunology

Plant Immunology. Lecture 9. Classes of plant immune responses. Basal response: transcription of genes in response to PAMP recognition. Hypersensitive response (HR); apoptosis of cells at the site of infection Systemic acquired immunity: The entire plant becomes resistant to infection

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Plant Immunology

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  1. Plant Immunology Lecture 9

  2. Classes of plant immune responses • Basal response: transcription of genes in response to PAMP recognition. • Hypersensitive response (HR); apoptosis of cells at the site of infection • Systemic acquired immunity: The entire plant becomes resistant to infection • Jasmonic acid/ethylene pathway: The entire plant and neighboring plants develop resistance to herbivores. • Non-host immunity

  3. The basal response • This is the response induced by PAMP elicited signalling. • The effectors of this response are currently being characterized.

  4. Hypersensitive response • This is a rapid apoptosis response that kills cells in the area of infection. • It can be induced by the interaction of an R gene carrying plant with an Avr carrying microbe. • In the lab one can infiltrate bacteria into the whole leaf, causing a massive cell death response but in the field the HR response is likely tiny and limits the growth of microbes to a small area on the leaf. This should stop the growth of biotrophic pathogens that require living tissue in order to survive. • Nitric oxide (NO) and hydrogen peroxide (H2O2) regulate the response. • The HR can trigger systemic acquired resistance.

  5. Systemic Acquired resistance (SAR) • Challenge a leaf with an infectious agent and distal tissues become resistant. • The distal tissues have broad resistance – not just to the original pathogen. • Can be induced by cell death; either HR or otherwise. • The effects are broad range, acting on bacteria, fungi and viruses. • A number of genes are induced by SAR but the mechanism behind the resistance in unknown. • Salicylic acid must accumulate to induce the SAR but salicylic acid is not the systemic signal; an unidentified lipid likely serves as the signal. • A SAR signal (but not salicylate) travels through the plant and increases the resistance of the plant to further infection.

  6. Basic defenses of a plant

  7. Hypersensitive responses kill small parts of the leaf

  8. Systemic acquired immunity

  9. Involves salicylate but this is not the factor acting through the plant No Salicylate wt No SAR in scion Vernooij, B. et al. 1994, Plant Cell 6: 959-965

  10. TMV plaques in scion leaves X/N N/X N/N X/X Vernooij, B. et al. 1994, Plant Cell 6: 959-965

  11. Crunchers vs suckers

  12. Jasmonic acid response (JA) • This chemical is a volatile plant hormone involved in regulating immunity. • JA synthesis is induced upon herbivory (crushing wounds). • JA induces the transcription of a number of genes that are anticipated to reduce the digestion of the herbivore. • For example, the induction of arginase in tomato plants. • This reduces the availability of arginine to the insect gut and reduces growth of the caterpillar.

  13. Pseudomonas syringae alters the immune balance of the plant

  14. PAMps (Pathogen accociated molecular patterns) • 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.

  15. Plant cells can recognize PAMPs • The Arabidopsis receptor Fls2 is a flagellin receptor • The structure comprises of the extracellular domain of the protein containing Leucine Rich Repeats. • The intracellular domain contains a serine threonine kinase • Signalingis transduced through a MAP kinase cascade and activates transcription factors in the WRKY family. • As in animals, there are many PRRs in plants that presumably can recognize microbes by more than one PAMP.

  16. Structure of the penetration peg

  17. Fls2 can be shown to have an immune function because loss of function mutations sensitized the plants to infection. Forced expression of the MAP kinases or WRKY29 will force the activation of the pathway and protect the plant from fungal and bacterial infections • This suggests that this PAMP activated pathway is required for fighting fungal as well as bacterial infections. The pathway may have originally been identified as responding to bacteria but its output can affect fungal growth as well.

  18. Bacteria have evolved methods of blocking the plant innate immune response Bacteria

  19. One example of a bacterial effector is AvrRpm1 • RIN4 is a negative regulator of PAMP elicited signaling • The presence of this protein results in increased phosphorylation of the plant protein RIN4. • AvrRpm1 interacts physically with RIN4 • Increased phosphorylation of RIN4 presumably results in decreased PAMP triggered immune defense. • The bacteria grow better because they are no longer inhibited by the PAMP triggered immune response.

  20. A second effector, AvrRpt2 is a protease that cleaves RIN4

  21. The plant has countermeasures to defend against bacterial effectors • This work developed from the study of R genes in plants. • R genes are dominant plant genes that provide resistance to pathogens carrying dominant Avr genes. • A plant carrying an R gene that is infected by a bacterium carrying an Avr gene will be immune to disease. • All other combinations will lead to disease. • Molecular analysis of R genes revealed that they form two basic classes 1. LRR containing extracellular proteins. 2. LRR containing intracellular proteins.

  22. The gene-for-gene resistance model Host Genes Microbe Genes

  23. Mi-1 is an R gene giving resistance to nematode and aphid infection Wild type: Aphid infested Carrying Mi-1 Vos, P. et al. 1998 Nature Biotechnology 16: 1365-69

  24. Arabidopsis powdery mildew Erysiphe cichoracearum Barley powdery mildew (Bgh) Blumeria graminis f.sp hordei Host infection on Barley Host infection on Arabidopsis Nonhost infection on Arabidopsis

  25. Assignment and Presentation Host resistance vs Non-host resistance Group 1 Group 2

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