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Title: Summary of previous lesson


1
Summary of previous lesson
  • ASCOMYCETES, BASIDIOMYCETES, OOMYCETES
  • DISEASE TRIANGLE humans
  • Locus/ allele/ polymorphisms
  • Invasive organism
  • Genetic traits of invasive populations reduced
    genetic diversity and differentiation among new
    populations because of founder effect and lack of
    equilibrium

2
Definitions
  • Alternatively fixed alleles
  • Dominant vs. co-dominant markers
  • Genotype

3
Alternatively fixed alleles
  • Two flower species (species 1 and species 2) can
    have one of two features
  • Long (L) or short (s) leaves
  • Red ( R) or white (w) flowers
  • Ten individuals from species 1 have the following
    traits
  • LR LR LR LR LR LR LR sR sR sR
  • Ten individuals from species 2 have the following
    traits
  • sw sw sw sw sw sw sw Lw Lw Lw

4
Which one is the alternatively fixed allele?
  • Both alleles will differentiate the groups
    (frequencies are significantly different)
  • Only one will be diagnostic because alternatively
    fixed
  • It is the color of the flower all flowers in
    species 1 are R, all flowers in species 2 are w
    (all implies your sampling size is adequate!!)

5
Dominant vs. co-dominant markers
  • Flowers are red or white or yellow, DNA sequence
    is agg, agt, agc DNA fragment is 10, 12 0r 14 bp
    long (CO-DOMINANT, we know what alternative
    alleles are)
  • Flowers are red or non-red, DNA is agg or not,
    size is 10bp or not. We only see the dominant
    allele and we express it in binary code
    1(present), 0(absent)

6
Limitations of co-dominant markers
  • Not all non-red flowers are the same, but we
    assume they are (non red flowers can be orange or
    yellow)
  • If at one locus we have a dominant A allele and a
    recessive a allele, using a codominant marker we
    would say AAAa but not aa. We know in reality
    AA and Aa are quite different.

7
Genotype
  • A unique individual as defined by an array of
    genetic markers. (the more markers you have the
    less mistaken identity you will have.
  • blonde

8
  • Blonde
  • Blue-eyed

9
  • Blonde
  • Blue-eyed
  • Hairy

10
  • Blonde
  • Blue-eyed
  • Hairy
  • 6 feet tall

11
  • Blonde
  • Blue-eyed
  • Hairy
  • 6 feet tall
  • Missing two molars

12
In the case of microbes it will probably be
something like
  • Genotype A 01010101
  • Genotype B 00110101
  • Genotype C 00010101

13
Summary of third lesson
  • DNA polymorphisms can be diagnostic
  • Mutations/Sex/Barriers to mating
  • Plant Diseases can be biotic (interaction between
    host and causal agent ), or abiotic
  • Many organisms can cause plant diseases, but
    fungi are the No.1 cause
  • Diversity of fungi, but all have ideal structure
    for plant infection
  • hypha/cord/rhizomorph/infection peg/appressorium
  • Sexual vs. asexual reproduction can do both

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16
Fungi again!
  • ASCOMYCETES
  • BASIDIOMYCETES
  • OOMYCETES (fungus-like, water molds)

17
ASCOMYCETES
  • Yeasts (fermentation, human mycoses)
  • Truffles, morels
  • Penicillia (penicillin), Fusaria (potent toxins,
    damping off of seedlings), molds

18
Ascus is the sack in which the spores are
contained
19
Asci can be placed on a disk (apothecium), many
apothecia can be together in a fruitbody
Morel fruitbody
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21
Asci can be carried inside a flask (perithecium)
Nectria
22
Ploidy is mostly n
23
BASIDIOMYCETES
  • Mushrooms. mycorrhizal
  • Wood decay organisms
  • Rusts, Smuts
  • Yeasts and damping off

24
Toadstools and huitacochle are both basidiomycetes
25
Basidium means club, it carries the
basidiospores (dispersion propagules) naked
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28
Most of their life, they are nn (dikaryons),
some rare ones are diploid
29
Oomycetes
  • Belong to the kingdom Stramenopila, used to be
    called Chromista
  • Phytophthora, Pythium, Saprolegnia

H20
30
Hyphae, sporangia, and zoospores of P. ramorum
31
Most of their lifecycle they are 2n Have
cellulose in cell wall Not fungi!!, but
look like them because of convergent evolution
32
Fungi do not photosynthesize
  • Biotrophic mycorrhyzae, rusts
  • Endophites clavicipetaceae,
  • Necrotrophic most pathogens
  • Saprobes primary (involved in litter
    decomposition)

33
DISEASE!!
  • Symptoms vs. signs e.g. chlorosis vs. fruit-body
  • The disease triangle

34
Disease triangle
  • Effect of humans

35
Human activities affecting disease incidence in
forests
  • Introduction of exotic pathogens
  • Planting trees in inappropriate sites
  • Changing stand density, age structure,
    composition, fire frequency
  • Wound creation
  • Pollution, etc.

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Effects of fire exclusion
38
DISEASE plant microbe interaction
  • 1-Basic compatibility need to be present
  • 2- Chemotaxis, thighmotropy
  • 3- Avirulence in pathogen matched by resistance
    in host according to the gene for gene model
  • 4-Pathogenicity factors such as toxins and
    enzymes important in the infection process

39
1- Basic compatibility
  • Size of infectious propagules
  • Timing of susceptibility in host and production
    of infectious structures

40
2- Finding the host
  • Chemotaxis pathogen has receptor that detects
    food base in oomycetes zoospores will all swim
    towards host
  • Thigmotropy recognizing morphological structures
    that indicate presence of host prelude to
    production of infective structures such as
    infection pegs and appressoria

41
3- Infecting the host
  • Pathogen will produce array of enzymes to infect
    host cells
  • Upon identification of infection, host will
    produce array of antimicrobial compounds , or
    will kill some of its cells to halt infection
    process (hypersensitive response)

42
3- Infecting the host
  • Plant that are resistant, must be able to react
    (dominant R resistant allele)
  • Plants that cannot react (r allele) are always
    sensitive
  • Pathogens that are not noticed by plant can
    infect (recessive avirulence allele)
  • Pathogens that are noticed may be stopped
    (dominant A avurulence allele)

43
3- Infecting the host
  • RA no disease
  • Radisease
  • radisease
  • rAdisease
  • There will be a strong selection in favor of R
    alleles but R comes at a cost

44
4- Causing disease
  • Correlated to ability of pathogen to invade plant
    cell, pathogenicity is usually a dominant trait

45
Categories of wild plant diseases
  • Seed decay
  • Seedling diseases
  • Foliage diseases
  • Systemic infections
  • Parasitic plants
  • Cankers, wilts , and diebacks
  • Root and butt rots
  • Floral diseases

46
Seed diseases
  • Up to 88 mortality in tropical Uganda
  • More significant when seed production is episodic

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48
Stress cone crop
BS on DF
49
Seedling diseases
  • Specific diseases, but also diseases of adult
    trees can affect seedlings
  • Pythium, Phytophthora, Rhizoctonia, Fusarium are
    the three most important ones
  • Pre- vs. post-emergence
  • Impact up to 65 mortality in black cherry.
    These diseases build up in litter
  • Shady and moist environment is very conducive to
    these diseases

50
Foliar diseases
  • In general they reduce photosynthetic ability by
    reducing leaf area. At times this reduction is
    actually beneficial
  • Problem is accentuated in the case of small
    plants and in the case other health issues are
    superimposed
  • Often, e.g. with anthracnose,needle cast and
    rust diseases leaves are point of entry for twig
    and branch infection with permanent damage
    inflicted

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53
Systemic infections
  • Viral?
  • Phytoplasmas
  • Peronospora and smuts can lead to over 50
    mortality
  • Endophytism usually considered beneficial

54
Grass endophytes
  • Clavicipetaceae and grasses, e.g. tall fescue
  • Mutualism antiherbivory, protection from
    drought, increased productivity
  • Classic example of coevolutionary development
    Epichloe infects flowers of sexually
    reproducing fescue, Neotyphodium is vertically
    transmitted in species whose sexual reproductive
    ability has been aborted

55
Parasitic plants
  • True (Phoradendron) and dwarf mistletoe
    (Arceuthobium)
  • Effects
  • Up to 65 reduction in growth (Douglas-fir)
  • 3-4 fold mortality rate increase
  • Reduced seed and cone production
  • Problem accentuated in multistoried uneven aged
    forests

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60
Cankers, wilts, and die-backs
  • Includes extremely aggressive, often easy to
    import tree diseases pine pitch canker, Dutch
    elm disease, Chestnut blight, White pine blister
    rust
  • Lethal in most cases, generally narrow host range
    with the exception of Sudden Oak Death

61
Root diseases
  • Extremely common, probably represent the most
    economically damaging type of diseases
  • Effects tree mortality (direct and indirect),
    cull, effect on forest structure, effect on
    composition, stand density, growth rate
  • Heterobasidion, Armillaria, Phellinus weirii,
    Phytophthora cinnamomi

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66
Removing food base causes infection of roots of
other trees
Hyphae in plant tissue or soil (short-lived)
Melanin-covered rhizomorphs will allow for fungus
to move to new food Sources (Armillaria mellea)
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70
Effects of fire exclusion
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72
Floral diseases
  • Pollinator vectored smut on silene offers an
    example of well known dynamic interaction in
    which pathogen drives genetic variability of
    hosts and is affected by environmental condition
  • Puccinia monoica produces pseudoflowers that
    mimic real flowers. Effects reduction in seed
    production, reduction in pollinators visits

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74
Density-dependence
  • Most diseases show positive density dependence
  • Negative dependence likely to be linked to
    limited inoculum e.g. vectors limited
  • If pathogen is host-specific overall density may
    not be best parameter, but density of susceptible
    host/race
  • In some cases opposite may be true especially if
    alternate hosts are taken into account

75
Counterweights to numerical effects
  • Compensatory response of survival can exceed
    negative effect of pathogen
  • carry over effects?
  • NEGATIVE progeny of infected individuals less
    fit
  • POSITIVE progeny more resistant (shown with
    herbivory)

76
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

77
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
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