1 / 24

Topics list

Topics list. 1. Coming to a nursery near you – ‘Sudden Oak Death’ 2 . Fusarium – biocontrol in the drug wars 3 . Potato late blight – it’s back, and its not just an Irish problem 4 . No need to add nitrogen to your peas, beans or ....sugarcane?

jeanne
Download Presentation

Topics list

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Topics list 1. Coming to a nursery near you – ‘Sudden Oak Death’ 2. Fusarium – biocontrol in the drug wars 3. Potato late blight – it’s back, and its not just an Irish problem 4. No need to add nitrogen to your peas, beans or ....sugarcane? 5. ‘Black Sigatoka’:Yes, we may have no bananas! 6. ‘Fusarium head blight’: Plant pathology meets Genomics, and is there a link with‘Roundup’? 7. ‘Chestnut blight’ and hypovirulence:  can a virus save a tree? 8. BT corn - do we need to choose between butterflies and caterpillars? 9. The rice blast fungus Magnaporthe grisea: what can we learn from the genome of one of the world’s most successful fungal phytopathogens? 10. Crinipellis perniciosa: what are we going to do without chocolate? 11. Stachybotrys and sick building syndrome. 12. Lateral gene transfer – is there such a thing as a bacterial species? 13. Is bioterrorism a threat to food safety? 14. Is Ug99 a time bomb for the world’s wheat crop? 15. Golden Rice and the prevention of vitamin deficiencies

  2. How to download papers from PubMed • Go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi • Type in items (key words, author name, etc.) you are interested into find the paper(s) • Download paper in PDF format • If not available from PubMed, go to UBC ejournal site:http://www.library.ubc.ca/ejour/ • Find the journal and paper, then download.

  3. Course website: http://www.landfood.ubc.ca/undergraduate/course-listings/APBI426 Paper for Lit 1: Development of the Deleteagene knockout technology Li X, Song Y, Century K, Straight S, Ronald P, Dong X, Lassner M, Zhang Y. A fast neutron deletion mutagenesis-based reverse genetics system for plants. Plant J. 2001 Aug;27(3):235-42.

  4. Plant –pathogen interaction From Gene-for-Gene concept to the Zig-Zag model Readings: Chisholm ST, Coaker G, Day B, Staskawicz BJ. 2006. Host-microbe interactions: shaping the evolution of the plant immune response. Cell 124(4):803-14. Jones JD, Dangl JL. 2006. The plant immune system. Nature 444(7117):323-9.

  5. Disease symptoms Signs of disease

  6. Major types of microbial plant pathogens: -         Bacteria -         Fungi (>80% loss) -         Viruses -         Viroid Pathogenesis: Process of infection, colonization, and reproduction Virulence: severity of disease Plants’ defense systems:         - Preformed - Activated or induced

  7. Plants are very different from animals: • Sessile • Photosynthesis (chloroplast) • Cells have walls • No adaptive immunity • Etc. • How do they cope with environmental changes? • How do they deal with pathogens?

  8. Key Definitions 1. Hostversusnonhost resistance.

  9. a. Nonhost resistance. Most plants are resistant to most pathogens, so disease is the exception. Plants that cannot be successfully attacked by a given pathogen are called nonhosts for that pathogen, and we say that they display nonhost resistance. b. Host resistance (also called true resistance). Host resistance is seen for certain cultivars or variety of plants that normally can be infected by a given pathogen. In other words, the pathogen is capable of infecting the host species, but there are genetic variants (e.g. cultivars with different genotypes) within that plant species that are resistant.

  10. Similarly, there are genetic variants within pathogen populations that differ in their ability to successfully attack a potential host plant Disease is therefore how we describe the result of a compatible genetic interaction between host and pathogen. The pathogen is said to be virulent and the host is susceptible. Failure to cause disease is the result of an incompatible genetic interaction between host and pathogen. The pathogen is said to be avirulent and the host is resistant.

  11. Tobacco mosaic virus (TMV) and tobacco Avirulence (Avr) gene: Replicase Resistance (R) gene: N gene Incompatible (resistant) Hypersensitive response (HR) Compatible (susceptible)

  12. The Gene-for-Gene Concept

  13. The genetic analysis of pathogenic or races (physiological specialization) for fungal pathogens was first worked out in the 1940’s with two different systems: Melampsora lini (flax rust) and flax by Flor in the U.S. Ustilago tritici (loose smut of wheat) and wheat by Oort in the Netherlands.

  14. Experimental procedure: Identify two different races (race 22 and race 24) of the flax rust fungus and perform a genetic cross between these two races to look at the genetic segregation of the ability of the races to infect different flax cultivars. Note that the races are defined (distinguished) by their phenotype, which is their ability (D), or lack of ability (ND), to cause disease on the flax cultivar, Ottawa 770B (the tester line).

  15. Race 22 – causes disease on cultivar Ottawa 770B • Race 24 – fails to cause disease on Ottawa 770B • 22 X 24 •  • F1 • (all ND phenotype) •  • F2 • (3 ND phenotype : 1 D phenotype) • ND (No disease = resistant or incompatible) • D = (Disease = susceptible or compatible)

  16. Host Plant Genetics As with the fungus, it is also possible to perform crosses of the host cultivars to investigate the genetic basis of resistance in the host plant. As an example, two different flax cultivars, Ottawa 770B and Bombay, differ in their reactions when inoculated with race 24 of the rust fungus.

  17. race 24 + cultivar Ottawa 770B = ND race 24 + cultivar Bombay = D Ottawa 770B x Bombay  F1 (ND with race 24)  F2 (3 ND : 1 D)

  18. The important thing to note about this gene-for-gene interaction is that the specificity of the interaction is for recognition leading to resistance. In the absence of recognition, disease occurs. For resistance or immunity to occur, the plant must carry the dominant R gene and the pathogen must carry the dominant avirulence gene Recognition = Resistance

  19. Resistance occurs only when a dominant R gene meets a dominant Avr gene

  20. 4 5 CC: coiled coil Extracytoplasmic 1 6 3 2 RPW8 Plasma membrane Cytoplasmic

  21. PTI ETI Model for the Evolution of Bacterial Resistance in PlantsLeft to right, recognition of pathogen-associated molecular patterns (PAMP, such as bacterial flagellin) by extracellular receptor-like kinases (RLKs) promptly triggers basal immunity, which requires signaling through MAP kinase cascades and transcriptional reprogramming mediated by plant WRKY transcription factors. Pathogenic bacteria use the type III secretion system to deliver effector proteins that target multiple host proteins to suppress basal immune responses, allowing significant accumulation of bacteria in the plant apoplast. Plant resistance proteins (represented by CC-NB-LRR and TIR-NB-LRR; see text) recognize effector activity and restore resistance through effector-triggered immune responses. Limited accumulation of bacteria occurs prior to effective initiation of effector-triggered immune responses.

  22. In this scheme, the ultimate amplitude of disease resistance or susceptibility is proportional to [PTI – ETS + ETI]. 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.

  23. Effectors (Avr) L R R TIR NB L R R CC NB Non-self recognition in plants RLK apoplast plasma- membrane cytoplasm R proteins recognize effector activities • defense gene induction • SA accumulation • oxidative burst • hypersensitive response (HR) RESISTANCE PR gene expression nucleus

More Related