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Summary of previous lesson. ASCOMYCETES, BASIDIOMYCETES, OOMYCETES DISEASE TRIANGLE+ humans Locus/ allele/ polymorphisms Invasive organism

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summary of previous lesson
Summary of previous lesson
  • 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
  • Alternatively fixed alleles
  • Dominant vs. co-dominant markers
  • Genotype
alternatively fixed alleles
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
which one is the alternatively fixed allele
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!!)
dominant vs co dominant markers
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)
limitations of co dominant markers
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 AA=Aa but not aa. We know in reality AA and Aa are quite different.
  • A unique individual as defined by an array of genetic markers. (the more markers you have the less mistaken identity you will have.


  • Blue-eyed
  • Blue-eyed
  • Hairy
  • Blue-eyed
  • Hairy
  • 6 feet tall
  • Blue-eyed
  • Hairy
  • 6 feet tall
  • Missing two molars
in the case of microbes it will probably be something like
In the case of microbes it will probably be something like
  • Genotype A= 01010101
  • Genotype B= 00110101
  • Genotype C= 00010101
summary of third lesson
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
fungi again
Fungi… again!
  • OOMYCETES (fungus-like, water molds)
asco mycetes
  • Yeasts (fermentation, human mycoses)
  • Truffles, morels
  • Penicillia (penicillin), Fusaria (potent toxins, damping off of seedlings), molds
asci can be placed on a disk apothecium many apothecia can be together in a fruitbody
Asci can be placed on a disk (apothecium), many apothecia can be together in a fruitbody

Morel fruitbody

basidio mycetes
  • Mushrooms. mycorrhizal
  • Wood decay organisms
  • Rusts, Smuts
  • Yeasts and damping off

Most of their life, they are

n+n (dikaryons), some rare

ones are diploid

  • Belong to the kingdom Stramenopila, used to be called Chromista
  • Phytophthora, Pythium, Saprolegnia



Most of their lifecycle

they are 2n

Have cellulose in cell


Not fungi!!, but look

like them because of

convergent evolution

fungi do not photosynthesize
Fungi do not photosynthesize
  • Biotrophic: mycorrhyzae, rusts
  • Endophites: clavicipetaceae,
  • Necrotrophic; most pathogens
  • Saprobes: primary (involved in litter decomposition)
  • Symptoms vs. signs; e.g. chlorosis vs. fruit-body
  • The disease triangle
disease triangle

Disease triangle

Effect of humans

human activities affecting disease incidence in forests
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.
disease plant microbe interaction
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
1 basic compatibility
1- Basic compatibility
  • Size of infectious propagules
  • Timing of susceptibility in host and production of infectious structures
2 finding the host
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
3 infecting the host
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)
3 infecting the host42
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)
3 infecting the host43
3- Infecting the host
  • RA= no disease
  • Ra=disease
  • ra=disease
  • rA=disease

There will be a strong selection in favor of R alleles but R comes at a cost

4 causing disease
4- Causing disease
  • Correlated to ability of pathogen to invade plant cell, pathogenicity is usually a dominant trait
categories of wild plant diseases
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
seed diseases
Seed diseases
  • Up to 88% mortality in tropical Uganda
  • More significant when seed production is episodic
seedling diseases
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
foliar diseases
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
systemic infections
Systemic infections
  • Viral?
  • Phytoplasmas
  • Peronospora and smuts can lead to over 50% mortality
  • Endophytism: usually considered beneficial
grass endophytes
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
parasitic plants
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

cankers wilts and die backs
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
root diseases
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
removing food base causes infection of roots of other trees

Hyphae in plant tissue or soil (short-lived)

Removing food base causes infection of roots of other trees

Melanin-covered rhizomorphs will

allow for fungus to move to new food

Sources (Armillaria mellea)

floral diseases
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
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
counterweights to numerical effects
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)
disease and competition
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
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