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PLP 535 Lecture

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Title: PLP 535 Lecture


1
PLP 535 Lecture
  • Lee A Hadwiger

2
Lecture535jan08
  • Defense responses
  • The next two lecture periods involve signaling
    and the biochemistry and genetics of defense
    responses, primarily the nonhost resistance
    response.
  • The student will be responsible for two review
    articles and one journal article for presentation
    by the student assigned to this topic. They are
    as follows
  • Ellis J. Insights in to nonhost disease
    resistance Can they assist disease control in
    agriculture? 2006. The Plant Cell 18523-528.
  • Hadwiger, L. A. 2008. Pea/Fusarium solani
    interactions contributions of a system towards
    understanding disease resistance. Phytopathology
    (IN PRESS).
  • Student presentation article
  • Stein, M. et al. 2006 Arabidopsis PEN3/PDR8, an
    ATP binding cassette transporter, contributes to
    nonhost resistance to inappropriate pathogens
    that enter by direct penetration. Plant Cell
    128731-746.

3
  • Text of the two lecture periods
  • During evolution, a pathogen is a pathogen
    because it has found a niche on a given plant
    where it can grow and multiply. This niche can
    be destroyed or altered by a change in the host
    plant and in modern agriculture it is often
    messed up and most often by a breeding program
    that has introduced a new single dominant gene.
    The resistance expressed by this gene is
    dependent on a signal. This signal can be
    encoded by an avirulence gene, a loss of this
    gene in the pathogen again allows the pathogen to
    become virulent. In most instances this loss
    represents a loss of function. It is this loss
    of function that allows the pathogen to become
    virulent. The cloning of host R genes and
    pathogen avirulence (Avr) genes has been
    accompanied by a simplistic view of host-parasite
    interactions. Physiologically speaking, the
    appropriate match of the gene for gene
    interaction starts a process that is the straw
    that breaks the camels back. That is it is
    the apex of signaling events that occur following
    the contact between host and fungus, even though
    the match-up is the ultimate decision maker that
    determines that an incompatible reaction will
    occur.

4
Quadratic check
  • Pathogen genes
  • Host genes PP or Pp pp
  • RR or Rr Resistance Susceptible
  • rr Susceptible
    Susceptible

5
Terminology slide, spore, germ tube,
appressorium, haustorium
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Nonhost resistance(Inappropriate host)
  • You have previously been introduced to host
    resistance controlled by R genes against races of
    true pathogens (appropriate pathogens) on a given
    host. If the true pathogen challenges another
    plant, (what is now considered an inappropriate
    pathogen on a nonhost) the defense response is
    intense and in almost all cases is a plant
    defense that does not break down under field
    conditions.

8
Quadratic check in non-host resistance model
  • Fusarium Pathogens
  • Host F. solani f. sp. phas. F.s. f. sp pisi
  • Pea Resistance react. Suscept.
    Bean Suscept. react. Resist

9
NON-HOST RESISTANCE
  • Nonhost resistance responses are triggered by
    many more decision-making signals and most
    likely involving many more genes from both host
    and pathogen. There has been no demonstration of
    one gene being the key to the success or demise
    of the pathogen, however, some mutants come
    close. In Arabidopsis there is a mutant termed
    npr1 (no PR proteins) that comes close. This
    mutant hits a major function in the host
    metabolism that prevents multiple genes (PR
    genes) from being expressed

10
  • .
  • It has been established long ago, that protein
    synthesis in general is required for disease
    resistance in both nonhost and race specific
    resistance. The best demonstration coming from
    my lab. of how to break resistance was by the use
    of heat shock. Heat shock of both plants and
    animals is accompanied by a shift of protein
    synthesis from normal metabolism to activation of
    heat shock genes. When pea tissue is heat
    shocked (only one hour of 35 C temperature is
    required to this) it produces the mRNA for heat
    shock protein for about 9 hour with the
    exclusion of PR and other proteins. During this
    time the tissue is totally susceptible to
    inappropriate pathogens and unable to activate
    its PR genes to get PR proteins. After 9 hours
    the tissue returns to normal and its ability to
    resist inappropriate pathogens returns along with
    its ability to produce PR proteins.

11
RNA and Protein synthesis-for PR protein
production
  • RNA synthesis inhibitors
  • Cordycepin- blocks mRNA transport
  • Alpha- amanitin - blocks RNA polymerase
  • Protein synthesis inhibitors
  • Cycloheximide - blocks protein synthesis at the
    ribosomal level.

12
Inhibitors
  • We have also demonstrated the ability of
    specific inhibitors of enzymes controlling major
    functions in the cell to completely block disease
    resistance. There are several phosphatase
    inhibitors that work apparently by blocking major
    cell functions (phosphorylations) required for
    resistance. In early work we demonstrated that
    simply blocking total gene transcription
    (including PR genes) and translation (including
    PR proteins) it readily blocked disease
    resistance.

13
Toxins metabolic blocking and membrane damaging
  • There are some plant pathogens that bring along
    mechanisms to block aspects of the host response
    and are called toxins - and toxins come in a
    variety of chemical forms. Thus there are many
    different targets in the host plant cell for
    disruptions that can block the disease
    resistance response.

14
Quadratic check- host specific toxins
  • oat pathogen toxin corn path. Toxin
  • Host
  • Oat Susceptible react. Resist. Reaction
  • Corn Resist. Reaction Suscept. React.
  • Critical research -Scheffer E. E. Nelson

15
Time course of events in non-host resistance in
peas
  • 20 minutes - alteration of nuclear density
  • 1 hour - DNA alteration
  • 2 hours - detection of PR gene transcription
  • 2-3 hours- phosphorylation HMG-I
  • 5 hours - suppression of fungal growth
  • 6 hours - pisatin synthesis
  • 10 hours - increase in chitinase, glucanase
  • 18 hours - H.S., Cell death

16
BIOCHEMISTRY OF RESISTANCE
17
Chitosan and chitin are examples of
PAMPs or MAMPs
. Other cell
wall fragments are considered, Microb/pathoge
n
-
Chitin chitosan
Associated molec. patterns
.
Previously known as elicitors
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Pea DRR206 is on this pathway
20
PR genes for PAL, CHS, and others to Pisatin on
this pathway
21
Mutational genetics of nonhost resistance
  • The Arabidopsis researchers have used the Ti
    plasmid to mutate about every gene in this plant
    and some looked for a break-down of nonhost
    resistance.
  • Three mutant lines have been heralded as the
    major players in nonhost resistance. The genes
    are PEN1.PEN2 and PEN3.

22
Mutational genetic technology
  • The scientific approach used by many is to
    screen for a functional loss. The gene in the
    vicinity of the hit is cloned and sequenced.
    Then you go to the GenBank and see if the
    sequence of your mutated gene has a match. If it
    does, its function is called putative. You are
    then free to insert that function into a disease
    resistance model.
  • With modern gene manipulations you can also
    locate and sequence the genes promoter region.
    This will enable one to find sequences that are
    recognized by certain transcription factors.
    The promoter region can be further analyzed by
    making constructs that can contain Various
    segments of the promoter, various combinations of
    the open reading frame (ORF), attachments
    containing one of many combinations of reporter
    genes, such a green fluorescent protein, GUS etc.
    Also the open reading frame can be extended with
    a sequence that will produce a peptide that can
    be recognized by an anti-sera that is
    commercially produced.

23
Immunological technology
  • An anti-sera can be developed that will recognize
    the product of the open reading frame. Having
    the sequence of the ORF one can chose a predicted
    amino acid segment deemed to possess antigenic
    determinant properties. This segment can be
    synthesized and injected into a rabbit or other
    suitable animal to generate anti-sera specific to
    the coded protein. The entire ORF or parts of it
    can be inserted into an expression vector system
    and allow the bacterium to produce abundant gene
    product. The product can be purified and then
    injected into the rabbit to develop anti-sera.
  • With these tools there an abundance of
    techniques that will help understand the function
    of the gene detected. One of the first/best
    approaches is to over express the gene in the
    plant and determine if the greater abundance
    affects disease resistance or other functions.
    With the use of the flag peptide-antisera, the
    gene fluorescent protein (GFP) marker or the
    total gene specific antisera it is possible to
    follow the cytological location of the protein in
    a living cell.

24
PEN gene putative functions
  • PEN1 has homology with Syntaxin
  • PEN2 - has homology with glycosyl hydrolase, one
    of a large family.
  • PEN 3 encodes a putative ATP binding cassette
    (ABC) transporter PDR8. It localizes in the
    plasma membrane and may mediate targeted exports
    of toxins to the penetration site. Details of
    these mutants will be covered in the student
    lecture.
  • Bottom line each mutant enables the pathogen to
    progress some, but none enables total
    susceptibility

25
Genetic engineering
  • Systems
  • Particle gun
  • Agrobacterium tumefaciens T-I plasmid
  • Success See Punja review article

26
Engineering approaches
  • Use TI plasmid to insert the following
    constructs
  • 35S promoter- PR gene
  • 35S promoter R gene
  • 35S promoter intermediate enzyme to phytoalexin
  • 35S promoter any other vital step
  • Inducible promoter for any of the above
  • Promoter for anti-sense or siRNA sequences
  • Promoter for syntheses of or blocking receptor
    proteins
  • Unconventional constructs.
  • Promoter from DRR206 driving F. solani f. sp
    phaseoli DNase gene

27
Thought evolution of the
biochemistry of disease resistance
  • Totally chemistry
  • When J. C. Walker discovered the purple skins of
    an onion protected it from pathogens. Most
    everyone did chemical analyses of plants looking
    for resistance. Unfortunately this type of
    disease resistance was unique to onions and to
    one group of pathogens.

28
Nutrition hypothesis
  • Pathologists proposed that the reason that only
    the appropriate pathogen grew on the appropriate
    host was that the host had the right nutrients
    (biochemists were involved at that time in
    analyzing the metabolism of amino acids, sugars
    etc.) True, all pathogens need nutrition but
    most fungi could use very basic N,P,K, minor
    elements, carbon source to grow. However most
    non-obligate pathogens grew better with amino
    acid/sugar supplements but these could be found
    in and around most plants at least in low amounts
    and around germinating seeds in larger amounts.
    It was difficult to establish that nutrition was
    the basis for the appropriate pathogen growing on
    the appropriate host.

29
Phytoalexin hypothesis
  • An extension of the phenolics thinking. Plants
    ward off the inappropriate pathogens by producing
    phytoalexins (small compounds that possess
    antifungal action in vitro). Again, the
    hypothesis was true to a point. Most defense
    responses are accompanied by accumulations of
    phenolics. Often the accumulation is
    proportional to the resistance expressed.
    However there are some exceptions
  • 1. Some plants with abundant phytoalexins
    accumulations are still susceptible.
  • 2. In pea tissue the inappropriate pathogen
    growth is suppressed before there is detectable
    accumulations of phytoalexins.
  • A major benefit of phytoalexins research was the
    discovery that the accumulation of phytoalexins
    was due to the induction of genes that encode
    enzymes that are in secondary pathways.

30
Induction hypothesis
  • There was skepticism when Martin Schwochau and I
    devised the induction hypothesis to explain how
    the match ups in gene-for-gene interaction
    generated resistance that was epistatic to all
    other match-ups, even though many other genes
    were present. A man named Art Browning had
    popularized a lock and key model that was widely
    taught, was very complicated and wrong.

31
Specific inhibitors reduce skepticism
  • Much of the skepticism of the induction
    hypothesis was erased when resistance was shown
    to be blocked at three levels with specific
    inhibitors
  • Alpha amanitin blocked DNA-dependent RNA
    polymerase II.
  • Cordycepin blocked the transfer of mRNA from
    the nucleus.
  • Cycloheximide blocked the translation of mRNA
    into protein at the ribosomal level.
  • These inhibitors also worked nicely to indicate
    when each event was occurring . That is, you
    could block transcription and stop the
    development of the resistance response if it was
    applied within the first hour or so.
    Applications after 6 hours were no longer
    effective. Cordycepin applied after 3- 6 hours
    was ineffective and cycloheximide could still be
    effective at 4 hours in blocking resistance.

32
PR proteins, what do they do?
  • PR PROTEINS
  • What do PR proteins do?
  • 1. Many are associated with secondary plant
    metabolism primarily with the synthesis of
    phenolics such as flavonoids, isoflavonoids,
    salicylic acid, catechol, tannins, lignin and
    suberin.
  • Other compounds are synthesized via other
    pathways such as terpenes and alkaloids.
  • 2. Hydrolytic enzymes proteases, RNases,
    chitinases, ß-glucanases, lipases etc. The
    fragmentation products ot these enzymes can also
    signal other responses, e.g. chitin and chitosan
    oligomers.
  • 3. High Cysteine proteins (peptides).
    Defensins and other anti-fungal proteins.
  • 4. Enzymes involved in cell wall
    contruction/degradation Cellulose synthase,
    callose synthesis, etc.
  • 5. Many house keeping genes. These are picked
    up in micro array analyses and can have a variety
    of functions related to ionization, super oxide
    development transport etc.

33
Observations distinquishing the pea system from
Arabidopsis
  • 1. The pea endocarp tissue that does not have a
    cuticle barrier, can rapidly distinquish between
    the true (appropriate) pea pathogen, Fusarium
    solani f. sp. pisi and the inappropriate pathogen
    (Bean pathogen) Fusarium solani f. sp. phaseoli
    (nonhost resistance).
  • The bean pathogen growth is stopped at 6 hours
    post inoculation. The signaling between pathogen
    and host is rapid since the newly exposed pea
    endocarp tissue has no cuticle layer.
  • Note Surprisingly, plant scientists were
    reluctant until the last decade or so to believe
    that anything but small molecular compounds could
    penetrate the plant cell wall and enter the
    cytoplasm. Now they concede that compounds in
    the vicinity of 30 kD can enter without a carrier
    system.
  • 2. Other potential barriers in peas such as
    super oxides, nitric oxide, salicylic acid (SA)
    and jasmonic acid (JA) induced responses, the
    hypersensitive response (HR), programmed cell
    death (apoptosis) and phytoalexins accumulation
    are probably not initially involved in
    resistance, since they do not compromise a part
    of the pea cells response when subjected to
    an inhibitor study. Also many of these processes
    do not appear within the first 6 hours after
    inoculation, a time when the inappropriate
    pathogen is totally stopped.

34
A well studied phenolic- pisatin
  • Dr. Hans VanEtten devoted his years to the study
    of pisatin and is currently looking at the
    biosynthetic route of pisatin biosynthesis. His
    major premise was, one reason that a pathogen
    becomes an appropriate pathogen of peas is that
    it is capable of degrading pisatin the single
    phytoalexin found in peas. I will refer you to
    the assigned mini review that was reviewed by Dr.
    VanEtten for the complete story.

35
Pisatin some bottom lines
  • Some bottom lines
  • 1. Pisatin delays germination of F. solani f.
    sp. phaseoli/pisi for 24 hours.
  • 2. Pisatin accumulation is more rapid in lines
    possessing R genes.
  • 3. Pathogenic isolates of F. solani f. sp. pisi
    capable of more rapidly degrading pisatin, appear
    to be more virulent.
  • 4. Pathogens mutated to no longer produce the
    enzyme p450 (pisatin demethylase) are less
    virulent.
  • 5. A complete loss of pisatin degradation
    potential in the pathogen does not completely
    reduce virulence.
  • 6. The Fusarium solani f. sp. pisi pathogen has
    virulence traits that are located on auxiliary
    chromosomes, that have no relationship with
    pisatin degradation.

36
What does stop fungal growth on the plant surface
?
  • Much of the current literature is concentrated on
    superoxides , nitric oxide, jasmonic acid
    pathway products, salicylic acid pathway
    products, programmed cell death, callose
    accumulations, lignin accumulations, etc. which
    will be covered by other lecturers.
  • It is likely that disease resistance in
    Arabidopsis differs from that in peas and other
    legumes. Along with differences in other plant
    systems, will come differences in view-points
    based on that research. My remarks reflect my
    research on peas and the limited use of pea PR
    genes transferred to other plants.

37
Research at odds with arabidopsis
  • 1. The pea endocarp tissue that does not have a
    cuticle barrier, can rapidly distinquish between
    the true (appropriate) pea pathogen, Fusarium
    solani f. sp. pisi and the inappropriate pathogen
    (Bean pathogen) Fusarium solani f. sp. phaseoli
    (nonhost resistance).
  • The bean pathogen growth is stopped at 6 hours
    post inoculation. The signaling between pathogen
    and host is rapid since the newly exposed pea
    endocarp tissue has no cuticle layer.
  • Note Surprisingly, plant scientists were
    reluctant until the last decade or so to believe
    that anything but small molecular compounds could
    penetrate the plant cell wall and enter the
    cytoplasm. Now they concede that compounds in
    the vicinity of 30 kD can enter without a carrier
    system.

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The first cloning of a fungal Avirulence gene was
accomplished by the De Wit laboratory. Avr 9
product is a 28 amino acid residue peptide with 3
disulfide bridges. When the gene coding this
peptide in bred into a tomato plant containing
the Cf-9 R-gene, the plant dies. See page 1123
of the Biochemistry and Molecular Biol. Of Plants
Text. Figure gives 3 (p. 1128) possibilities for
how the peptide activates defense. Recently the
direct contact option is no long a possibility.
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The mlo gene controlled by a recessive trait
  • The mlo gene is the only plant resistance gene
    that has been selected for following the
    mutagenesis of a susceptible wild-type (Mlo)
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