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protein for protein concept .pptx

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This document discusses the protein-protein concept and gene-for-gene hypothesis in plant-pathogen interactions. It contains the following key points: 1. The protein-protein concept provides a biochemical explanation for the gene-for-gene hypothesis, where the mutual recognition between a host and pathogen is due to interactions between their encoded proteins, not the genes themselves. 2. In compatible/susceptible interactions, the pathogen produces a protein that can interact with and activate the host's complementary protein, inducing susceptibility. In incompatible/resistant interactions, the pathogen's protein is not recognized by the host. 3. Studies have found greater antigenic/protein similarity between hosts and pathogens leads to susceptibility, while resistance

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Protein – protein concept & immunization basis
• Protein for protein hypothesis –biochemical explanation of gene for gene hypothesis • These concepts explain how a host (plant) recognize their pathogen and suppress its further growth • (H. Flor, 1942) - For each resistance gene in the host there is a corresponding gene for avirulence in the pathogen conferring resistance and viceversa • “Avr” genes present in pathogen helps the host plant to trigger its defensive mechanisms
Recognition between host and pathogen • When a pathogen comes in contact with host cell , an early event takes place, triggers a rapid response, either allows or prevent growth of pathogen and development of disease • “Early events “ - biochemical substance, structures & pathogen elicitor molecule , these components induce specific actions or formation of specific products by other organisms
Pathogen genotype Host genotype R r A — A R + A r a + a R + a r A - pathogen with dominant a-virulent gene- produce elicitor molecule a- recessive a-virulent gene R – host with dominant resistant gene – produce receptor molecule r - host with recessive resistant gene + compatible reaction — incompatible reaction
Explanation of G-G hypothesis • Pathogen has gen: pathogencity gene & specific Avr gene A or a • A a Produce no elicitor an elicitor Host with Rgene Produce a receptor Host receptor recognize pathogen elicitor and Triggers defense reaction receptor find no elicitor ,so no defence Host resistant reaction Host AR susceptible (aR) Pathogen Host Host
Contd…….. • A a Produce no elicitor an elicitor Host with rgene Produce host with rgene no receptor Lack receptor No defence mechanism triggered Host lacks resistance to this pathogen’s virulence genes no receptor ,so no host defence mechanism triggered Host susceptible Host Ar susceptible (ar) Pathogen Host Host
Biochemical explanation for G-G concept –Protein –protein concept • There are two explanation for P-P concept • According to first specificity in gene for gene systems lies in susceptibility (Van der Plank, 1978) • whereas to other specificity lies in resistance (Ellingboe, 1981).
• According to Van der Plank (1978), specificity in gene – for- gene relationships lies in susceptibility. • He explains it with the help of interactions of five host and five pathogens attacking them specifically. • Suppose there are five host varieties with five different R genes; R1, R2, R3----------R5. • A plant with resistance gene R1 is attacked by a pathogen having virulence gene a1 and not to pathogen without this particular resistance gene irrespective of how many the virulence genes it may have.
Pathogen plant R1 R1 R2 R2 R3 R3 R4 R4 R5 R5 a1 a1 S a2 a2 S a3 a3 S a4 a4 S a5 a5 S
• Resistance is assumed to be dominant and RR can be replaced by Rr. • Virulence is assumed to be recessive. However, recessive resistance and dominant virulence are also known. R= resistant S= suscep
• Vander Plank (1978) elaborated protein for proteins hypothesis as a biochemical explanation of gene for gene interaction. • The protein for protein hypothesis states that in gene -for -gene diseases the mutual recognition of host and pathogen is not by the genes themselves but by their coded proteins.
• Vander Plank (1978) hypothesized that in susceptibility the pathogen excretes a protein (virulence for product) into the host cell which copolymerizes with a complementary host protein (resistance gene product). • This co-polymerization interferes with one auto regulation of the host gene that codes for the protein used by pathogen as a food and by so doing turns the gene on to produce more protein. • In resistance, the protein specified by the gene for avirulence in the pathogen and excreted into the host does not polymerize with the protein coded for by the gene for resistance. • It is not recognized by the host at all.
Antigenic relation b/w host and pathogen • Compatible reaction = susceptibilty , in such situations protein/ antigen pd by Path is similar to antigen pd by host • Boubly et al 1960 conducted expt. on Flax – Melamspora lini system.(rust causing path) 4 var of flax and 4 isolates if M.lini • From serological studies –titers of rust anti sera & Flax antigen / protein are similar (1:60) • Resistant reaction -1:20 less common antigens
• De vay et al 1972 - that tolerance of parasite by host increases with increasing protein / antigenic similarity , Resistance is chara by increasing disparity • antigen common to host and pathogen implies – genetic similarity & vice versa • More the matching of host genes by pathogen more susceptibilty • Eg:- Ustilago maidis shares similar antigen with oat seedlings, so that it can penetrate

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protein for protein concept .pptx

  • 1. Protein – protein concept & immunization basis
  • 2. • Protein for protein hypothesis –biochemical explanation of gene for gene hypothesis • These concepts explain how a host (plant) recognize their pathogen and suppress its further growth • (H. Flor, 1942) - For each resistance gene in the host there is a corresponding gene for avirulence in the pathogen conferring resistance and viceversa • “Avr” genes present in pathogen helps the host plant to trigger its defensive mechanisms
  • 3. Recognition between host and pathogen • When a pathogen comes in contact with host cell , an early event takes place, triggers a rapid response, either allows or prevent growth of pathogen and development of disease • “Early events “ - biochemical substance, structures & pathogen elicitor molecule , these components induce specific actions or formation of specific products by other organisms
  • 4. Pathogen genotype Host genotype R r A — A R + A r a + a R + a r A - pathogen with dominant a-virulent gene- produce elicitor molecule a- recessive a-virulent gene R – host with dominant resistant gene – produce receptor molecule r - host with recessive resistant gene + compatible reaction — incompatible reaction
  • 5. Explanation of G-G hypothesis • Pathogen has gen: pathogencity gene & specific Avr gene A or a • A a Produce no elicitor an elicitor Host with Rgene Produce a receptor Host receptor recognize pathogen elicitor and Triggers defense reaction receptor find no elicitor ,so no defence Host resistant reaction Host AR susceptible (aR) Pathogen Host Host
  • 6. Contd…….. • A a Produce no elicitor an elicitor Host with rgene Produce host with rgene no receptor Lack receptor No defence mechanism triggered Host lacks resistance to this pathogen’s virulence genes no receptor ,so no host defence mechanism triggered Host susceptible Host Ar susceptible (ar) Pathogen Host Host
  • 7. Biochemical explanation for G-G concept –Protein –protein concept • There are two explanation for P-P concept • According to first specificity in gene for gene systems lies in susceptibility (Van der Plank, 1978) • whereas to other specificity lies in resistance (Ellingboe, 1981).
  • 8. • According to Van der Plank (1978), specificity in gene – for- gene relationships lies in susceptibility. • He explains it with the help of interactions of five host and five pathogens attacking them specifically. • Suppose there are five host varieties with five different R genes; R1, R2, R3----------R5. • A plant with resistance gene R1 is attacked by a pathogen having virulence gene a1 and not to pathogen without this particular resistance gene irrespective of how many the virulence genes it may have.
  • 9. Pathogen plant R1 R1 R2 R2 R3 R3 R4 R4 R5 R5 a1 a1 S a2 a2 S a3 a3 S a4 a4 S a5 a5 S
  • 10. • Resistance is assumed to be dominant and RR can be replaced by Rr. • Virulence is assumed to be recessive. However, recessive resistance and dominant virulence are also known. R= resistant S= suscep
  • 11. • Vander Plank (1978) elaborated protein for proteins hypothesis as a biochemical explanation of gene for gene interaction. • The protein for protein hypothesis states that in gene -for -gene diseases the mutual recognition of host and pathogen is not by the genes themselves but by their coded proteins.
  • 12. • Vander Plank (1978) hypothesized that in susceptibility the pathogen excretes a protein (virulence for product) into the host cell which copolymerizes with a complementary host protein (resistance gene product). • This co-polymerization interferes with one auto regulation of the host gene that codes for the protein used by pathogen as a food and by so doing turns the gene on to produce more protein. • In resistance, the protein specified by the gene for avirulence in the pathogen and excreted into the host does not polymerize with the protein coded for by the gene for resistance. • It is not recognized by the host at all.
  • 13. Antigenic relation b/w host and pathogen • Compatible reaction = susceptibilty , in such situations protein/ antigen pd by Path is similar to antigen pd by host • Boubly et al 1960 conducted expt. on Flax – Melamspora lini system.(rust causing path) 4 var of flax and 4 isolates if M.lini • From serological studies –titers of rust anti sera & Flax antigen / protein are similar (1:60) • Resistant reaction -1:20 less common antigens
  • 14. • De vay et al 1972 - that tolerance of parasite by host increases with increasing protein / antigenic similarity , Resistance is chara by increasing disparity • antigen common to host and pathogen implies – genetic similarity & vice versa • More the matching of host genes by pathogen more susceptibilty • Eg:- Ustilago maidis shares similar antigen with oat seedlings, so that it can penetrate

Editor's Notes

  1. Av gene helps the host by giving a signal ,