PLANT IMMUNOLOGY lecture 1.pptxkkkkkkkkkkkkkkkkkkkkkkk

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1. PLANT IMMUNOLOGY (PBT-805) 1

2. Contents Plant Immune System Recognizing self from non self Plant Resistance Mechanism Post - Infectional Structural Defense Mechanisms Plant disease Disease process History of Plant diseases Useful plant pathogens Plant pathogen as medicinal Type of Plant Disease Resistance Horizontal resistance Vertical resistance Defense Signaling in Non host resistance Role of metabolic defense 2

3. Basal Resistance (MAMP- Triggered Immunity) Pathogen Effectors Bacterial MAMP or PAMP Fungal MAMP or PAMP Suppression of PTI by Pathogen Effectors Gene for Gene Hypothesis Disease Resistance or susceptibility Pathogenicity genes in phytopathogen Virulent and avirulent gene R gene and protein Direct Interaction Model Indirect Interaction Model Guard Hypothesis Decoy Hypothesis 3

4. The Hypersensitive response Thermo Regulation Cell to cell propagation Oxidative Burst in HR Systemic Acquired Resistance Historical Perspective Characteristic of SAR SAR and SA (Salicylic acid) SAR vs ISR Induced Systemic Resistance Localized Induced resistance Systemic induced resistance Type of Localized induced resistance Properties of PGPR The Negative effects of ISR Plant-microbe Interaction Bacteria Viruses Fungi MAPK Cascades in Plant Disease Resistance Signaling 4

5. 5 Grading Midterm = 30 Final = 50 Activities + Quizzes = 10 Final Project = 10 --------------------------------------------------------------- Total = 100

6. 6 Exam Pattern Objectives (30%) Mcq’s , mind maps, Identify the mistakes, label the diagram etc. Subjective (50%) Short question, medium question and concept tester. Quiz will be taken after every two lectures. Class activity will be performed after three lecture.

7. Recommended reading, including textbooks, reference books  Molecular Biology of the Cell by Bruce Albert and Dennis Bray. Garland Publishing Inc , New York and London. Handbook of Cell Signaling Vol 1-3, by Ralph Bradshaw, and Edward Dennis. Cell Signalling, by John T. Hancock, 2 nd ed. Oxford University Press. Apoptosis, Cell Signaling , and Human Diseases: Molecular Mechanisms, Volume 2 by Rakesh Srivastava. Cell Signaling and Growth Factors in Development: From Molecules to Organogenesis by Klaus Unsicker (Editor), Kerstin Krieglstein . Signal Transduction by Bastien D. Gomperts . The Biochemistry of Cell Signalling by Ernst J. M. Helmreich . 7

8. PLANT IMMUNOLOGY (PBT-805) 8 Lecture 1

9. Do Plants Have an Immune System? It Depends on How You Define “Immune System” Plants get sick. That is, they can be infected by pathogens. But after hundreds of millions of years of pathogen attacks, plants are still here. So, they must have ways to get well after being sick. Plants can defend themselves against disease-causing organisms (pathogens) such as viruses, bacteria and fungi. They do so by producing physical barriers (e.g., plant cell walls), some antibiotic compounds (e.g.,  phytoalexins ), and even enzymes that perturb pathogens. In a broad sense, these are all part of a plant’s immune response, that is, biological processes that an organism uses to defend itself against disease .

10. Do plants have an immune system similar to that in animals? One that can “remember” exposure to specific pathogens?

11. Recognizing (and Remembering) Self from Non-Self Humans, along with most other vertebrates, have a multifaceted immune system called an adaptive immune system, which is the culmination of complex interactions at the biochemical, genetic and cellular levels. Key parts of this adaptive system are the organism’s ability to biochemically distinguish between it’s own cells (self) and foreign (non-self) entities “remember” specific features of the foreigner. All pathogens – from viruses to fungi – have so-called macromolecules on their surfaces that distinguish them. Adaptive immune systems (AIS) use these macromolecules as antigens. That is, the immune system uses these characteristic surface features as a way to specifically identify foreign (non-self) entities.

12. The AIS uses the antigens to generate specific antibodies, which are used to tag the “foreigner” for destruction by specialized blood cells called lymphocytes. These specific antibodies then allow for the rapid detection of subsequent infections with a particular pathogen, which allows for relatively quick defensive responses. Although plants don’t possess such a sophisticated AIS, there are instances of self/non-self recognition in plants.

13. Plants Have an Innate (Passive) Immune System A more generic, non-specific response to infection characterizes a plant’s immune system. This type of response is called an innate immune system, in contrast to AIS. Plants don’t have antibodies or special cells that search for and destroy pathogens. Plants do, however, have cell-surface receptors to identify certain patterns characteristic of pathogens. Such receptors, when activated, trigger the production of chemical signals, such as methyl jasmonate that may elicit both local and systemic defense responses.

14. Local defensive responses included the so-called  hypersensitive response characterized by the self-destruction of the plant cells in a localized area around the site of infection. Plants also possess inducible systemic defense responses when locally infected by pathogens. That is, a single, localized infection may elicit defensive responses throughout the plant. Bottom Line:  Although plants do have the ability to defend themselves against disease-causing organisms (sort of a rudimentary immune system), plants don’t have an immune system as complex as humans.

15. P ost - Infectional Structural Defense M echanisms

16. Plant Resistance Mechanisms

17. POST INFECTIONAL DEFENSE MECHANISM (INDUCED / ACTIVE) Occurs once after the infection of a plant by a pathogen. The activation or induction of defense mechanism may be both specific and non-specific type. Several structural changes are known to be induced by a range of biotic or abiotic elicitors. These dynamic defense mechanisms prevent further colonization or spread of pathogen. Four types of induced/active structural defense mechanisms, Histological defense structures Cellular defense structures Cytoplasmic defense structures Hypersensitive/ Necrotic defense reaction

18. H istological Defense Structures Even after the establishment of infection in plant cells, the host defense system tries to create barriers for further colonization of tissues. This may be at various levels. Lignification Lignified cell wall provide effective barrier to hyphal penetration. They also act as impermeable barrier for free movement of nutrient causing starvation of pathogen. Examples: Radish: Alternaria japonica Potato: Phytophtora infestans Wheat: Septoria nodorum Cucumber: Cladosporium cucumerium Carrot: Botrytis cineria

19. Suberization In several plants the infected cells are surrounded by suberized cells. Thus, isolating them from healthy tissue. C orky layer formation is a part of natural healing system of plants. Examples : Common scab of potato

20. Abscission layers Gap between host cell layers and devices for dropping –off older leaves and mature fruits. Plant may use this for defense mechanism also. To drop-off infected or invaded plant tissue or parts, along with pathogen. Shot holes in leaves of fruit trees is a common feature. Occurred due to the infection of fungi, bacteria, and viruses.

21. Tyloses Formed by protrusion of xylem parachymatous cell walls, through pits, into xylem vessels. The size and number of tyloses physically block the vessel. The tyloses are inductively formed much ahead of infection, thus blocking the spread of pathogen. It suggests biochemical elicitors and movement of tyloses inducing factors (TIF) up the stem. Examples : Sweet potato: Fusarium oxysporum f. Sp. batatas .

22. Gum deposition The gums and vascular gels quickly accumulate and fill the intercellular spaces or within the cell surroundings the infection thread and haustoria , which may starve or die.

23. Hyphal sheathing The fungal hyphae, which penetrate the cell wall are often unsheathed by the extension of the cell wall. This delays contact between hypha and protoplasm. Later on, the hyphae penetrate the sheath and invade the lumen of the cell.

24. I nduced Cellular Defense Structures The cellular defense structures, c hanges in cell walls, have only a limited role in defense. Following types are commonly observed. Carhohydrate apposition (synthesis of secondary wall and papillae formation) Callose deposition (hyphal sheathing just outside plasma lemma around the haustorium which delays contact of pathogen ( Phytophythora infestans ) with host cells. Structural proteins Induced cytoplasmic defense that present last line of host defense and may effective against slow growing pathogens, weak parasites or some symbiotic relationship. 25

25. C ytoplasmic Defense Structures In a few cases of slowly growing , weakly pathogenic fungi that induce chronic diseases or nearly symbiotic conditions , the cytoplasm surrounds the clump of hyphae , and the nucleus is stretched to the point where it breaks in two . In some cells , the cytoplasmic reaction is overcome and the protoplast disappears while fungal growth increases . In some of the invaded cells , however , the cytoplasm and nucleus enlarge . The cytoplasm becomes granular and dense , and various particles or structures appear in it. Finally , the mycelium of the pathogen disintegrates and the invasion stops . 26

26. Hypersensitive / Necrotic Defense Reactions When the pathogen penetrates the cell wall, and establishes contact with the protoplast of the cell, the nucleus of the cell moves toward the intruding pathogen soon disintegrates forming resin-like brown granules in the cytoplasm. Firstly, all the granules are formed around the pathogen and then throughout the cytoplasm. Simultaneously the cell walls swell. As the browning of the cytoplasm continues and the necrosis is caused, the invading hypha begins to disintegrate, and the further invasion of the pathogen is stopped. Common in diseases caused by obligate fungal parasites, viruses and nematodes. 27

27. 28 Necrotic Defense Reaction