R GENES

R GENES

1. GENES IN PLANTS Basavaraj kodsa pg16agr8100

2. Time Pathogen Environment Host Parasitism and Disease Development

3. How host plant defend pathogens Pathogen Defense barriers (waxy cuticle, antimicrobial compounds) Recognition of conserved structural patterns of pathogens (PAMPs) PTI Effectors Recognition of pathogens effectors by R gene proteins ETI Defense induced by pathogen recognition

4. Host-pathogen co-evolution: Central dogma of Plant Pathology Kinase NBS TIR LRR Bent and Mackey (2007) 1 2 3 4

5. Plant immune system: zig zag model PAMP Triggered Immunity (PTI) Effector Triggered Immunity(ETI) Jones and Dangl (2006)

6. Effectors can be viewed as “Product of parasite genes having phenotypic expression in host bodies” (Dawkins 1999).

7. Specialized plant pathogens can evade or suppress this MAMP triggered immunity (MTI) by secretion of virulence factors called effectors. A subset of these effectors, referred to as avirulence factors (AVRs), which can be recognized by the resistance proteins that trigger a second layer of host defense, referred to as effector triggered immunity (ETI) or R-gene mediated defense.

8. The pioneering work on genetics of plant disease resistance involving HR was done by Harold H. Flor in linseed – Melampsora lini system (Flor 1956). ‘ gene-for-gene hypothesis’

9. Martin et al. (1993) provided first evidence of direct interaction of tomato Pto gene with avrPto from Pseudomonas syringae pv . tomato. Apart from direct interaction, evidences indicate that R proteins also act as guard of a specific component of the basic defense pathway. Guard hypothesis:

10. Ex: Guard hypothesis To date, the most convincing evidence for the guard hypothesis has been found in Arabidopsis thaliana bacterial R- Avr systems where RIN4 (RPM1- interacting protein 4) was identified as a cellular protein that is required for the resistance to Pseudomonas syringae pv . tomato mediated by RPM1 and RPS2 . The RIN4 ( guardee ) is modified in various ways, depending on the Avr that it associates with, and these modifications then serve to activate the corresponding R protein (guard).

11. “AVR-R gene interaction provides the molecular basis for flor hypothesis and Receptor-Effector interaction provides the biochemical evidences for flor hypothesis”

12. Molecular recognition in gene for gene interaction

13. When induced in timely manner, the concerted response efficiently halt pathogen growth with minimal collateral damage to the plant No input is required from the farmer and no adverse environmental effects Efficient reduction of pathogen growth Minimal damage to the host plant zero input of pesticides from the farmers and Most importantly the environment friendly nature of such crops. Advantages of R gene

14. Disadvantages of R genes R genes are quickly defeated by co-evolving pathogens Many R genes recognise only a limited number of pathogen strains R genes do not provide broad spectrum resistance Introgression of R genes into a elite cultivars by convention breeding is a lengthy process

15. Classes of Plant Disease Resistance Genes Based on Structural Features Numerous R-genes identified, cloned and characterized in different plants have been categorized in eight classes (Table 1) based on their amino acid organization. ( Gururani et al. 2012).

16. Classification of R gene Based on structural feature (presence of certain Domains such as LRR, NBS, TIR, etc) Localization in the cell (Cytoplasmic, transmembrane or both) Class Function Example I Membrane associated, transcription regulating, Broad spectrum RPW8 , II Cytoplasmic, Signal transducing via Serine- Threonine protein kinase Pto III Extra cellular LRRs and Transmembrane anchor Cf2 to Cf9 IV Extracellular LRR, transmembrane receptor, has Cytoplasmic Serine- Threonine kinase (Signal transducing) Xa21 V Cytoplasmic, membrane associated, LRR, NBS and TIR domains RPP5, N 1, L6, RRPP VI Cytoplasmic, membrane associated, LRR, NBS, and a coiled coil domains RPM1, RPS2

17. Structure and classes of plant disease resistance genes

18. First R gene cloned was Hm1 in maize against race 1 of Cochliobolus carbonum in 1992 But, Hm1 was disproved to be a resistance gene………………. Because race 1 of C. carbonum produces the host specific HC toxin and this is a pathogenisity factor and essential for infection. Hm1 produce reductase enzyme which detoxifies the HC toxin and thereby confers resistance against race 1………. Therefore, logically the first R gene cloned and sequenced was Pto in tomato which recognize the avrpto protein and thereby activates the defence.

19. Plant pathogen interaction and development of disease resistance Gururani et al., 2012

20. How do R gene/protein functions Pathogen Nucleus Alters the gene expression Membrane bound receptors-Effector interaction Elicitors/effectors Elicitors recognized by R protein Activated R protein Activation of defense

21. Functions of Resistance Genes Signaling of plant stress hormones, generation of reactive oxygen species (ROS),ethylene biosynthesis, defense gene activation leading to phytoalexin biosynthesis, cell wall strengthening by the deposition of callose and hypersensitive response (Dixon et al. 2001 )

22. Fungal pathogens and interacting R-genes Gururani et al., 2012

23. Viral pathogens and interacting R-genes Gururani et al., 2012

24. Cloned nematode resistance genes Gene Resistance gene Hs1 (pro) Resistance to cyst nematode Beta procumnence Hi (tomato) Resistance to Meloidogyne incognita & Meloidogyne javanica isolated fro tomatoes Gpa2 Resistance to Globodera pallida identified In potato Hero Resistance to Globodera isolated from tomato Gro1-4 Resistance to Globodera rostochiensis

25. Nematodes and interacting R-genes

26. Evolution of R gene

27. Application of R genes RICE- BLAST ..IDENTIFIED Pi GENES PRH10-RES TO BLAST HAVING Pi54 and Piz5 WHEAT- PGT…. 96000 genes identified. SR 26, SR 29 to tackle ug99 race…

28. Conclusion.