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Summary of previous lesson Janzen-Connol hypothesis; explanation of why diseases lead to spatial heterogeneity Diseases also lead to heterogeneity or changes through time – PowerPoint PPT presentation

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Title: Summary of previous lesson


1
Summary of previous lesson
  • Janzen-Connol hypothesis explanation of why
    diseases lead to spatial heterogeneity
  • Diseases also lead to heterogeneity or changes
    through time
  • Driving succession
  • The Red Queen Hypothesis selection pressure will
    increase number of resistant plant genotypes
  • Co-evolution pathogen increase virulence in
    short term, but in long term balance between host
    and pathogen
  • Density dependance

2
Disease and competition
  • Competition normally is conducive to increased
    rates of disease limited resources weaken hosts,
    contagion is easier
  • Pathogens can actually cryptically drive
    competition, by disproportionally affecting one
    species and favoring another

3
Janzen-Connol
  • Regeneration near parents more at risk of
    becoming infected by disease because of proximity
    to mother (Botryosphaeria, Phytophthora spp.).
    Maintains spatial heterogeneity in tropical
    forests
  • Effects are difficult to measure if there is
    little host diversity, not enough
    host-specificity on the pathogen side, and if
    periodic disturbances play an important role in
    the life of the ecosystem

4
Diseases and succession
  • Soil feedbacks normally its negative. Plants
    growing in their own soil repeatedly have higher
    mortality rate. This is the main reason for
    agricultural rotations and in natural systems
    ensures a trajectory towards maintaining
    diversity
  • Phellinus weirii takes out Douglas fir and
    hemlock leaving room for alder

5
The red queen hypothesis
  • Coevolutionary arm race
  • Dependent on
  • Generation time has a direct effect on rates of
    evolutionary change
  • Genetic variability available
  • Rates of outcrossing (Hardy-weinberg equilibrium)
  • Metapopulation structure

6
Diseases as strong forces in plant evolution
  • Selection pressure
  • Co-evolutionary processes
  • Conceptual processes potentially leading to a
    balance between different ecosystem components
  • How to measure it parallel evolution of host and
    pathogen

7
  • Rapid generation time of pathogens. Reticulated
    evolution very likely. Pathogens will be selected
    for INCREASED virulence
  • In the short/medium term with long lived trees a
    pathogen is likely to increase its virulence
  • In long term, selection pressure should result in
    widespread resistance among the host

8
More details on
  • How to differentiate linear from reticulate
    evolution comparative studies on topology of
    phylogenetic trees will show potential for
    horizontal transfers. Phylogenetic analysis
    neeeded to confirm horizontal transmission

9
Phylogenetic relationships within the
Heterobasidion complex
Fir-Spruce
Pine Europe
Pine N.Am.
10
Geneaology of S DNA insertion into P ISG
confirms horizontal transfer.Time of
cross-over uncertain
NA S
NA P
EU S
890 bp CIgt0.9
EU F
11
Complexity of forest diseases
  • At the individual tree level 3 dimensional
  • At the landscape level host diversity,
    microclimates, etc.
  • At the temporal level

12
Complexity of forest diseases
  • Primary vs. secondary
  • Introduced vs. native
  • Air-dispersed vs. splash-dispersed, vs. animal
    vectored
  • Root disease vs. stem. vs. wilt, foliar
  • Systemic or localized

13
Stem canker on coast live oak
14
Progression of cankers
Hypoxylon, a secondary sapwood decayer will
appear
Older canker with dry seep
15
Root disease center in true fir caused by H.
annosum
16
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17
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18
HOST-SPECIFICITY
  • Biological species
  • Reproductively isolated
  • Measurable differential size of structures
  • Gene-for-gene defense model
  • Sympatric speciation Heterobasidion, Armillaria,
    Sphaeropsis, Phellinus, Fusarium forma speciales

19
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20
Phylogenetic relationships within the
Heterobasidion complex
Fir-Spruce
Pine Europe
Pine N.Am.
21
Recognition of self vs. non self
  • Intersterility genes maintain species gene pool.
    Homogenic system
  • Mating genes recognition of other to allow for
    recombination. Heterogenic system
  • Somatic compatibility protection of the
    individual.

22
Recognition of self vs. non self
  • What are the chances two different individuals
    will have the same set of VC alleles?
  • Probability calculation (multiply frequency of
    each allele)
  • More powerful the larger the number of loci
  • and the larger the number of alleles per locus

23
INTERSTERILITY
  • If a species has arisen, it must have some
    adaptive advantages that should not be watered
    down by mixing with other species
  • Will allow mating to happen only if individuals
    recognized as belonging to the same species
  • Plus alleles at one of 5 loci (S P V1 V2 V3)

24
MATING
  • Two haploids need to fuse to form nn
  • Sex needs to increase diversity need different
    alleles for mating to occur
  • Selection for equal representation of many
    different mating alleles
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