Definitions

• Propagule= structure used by an organism to spread or survive

• Locus= a physical portion of a chromosome,a gene

• Intron= a portion of DNA , a locus that does not code for a protein

• Exon= a coding gene

Definitions-2

• Alleles= different DNA sequences at the same locus

• If a locus has variation in sequence it is polymorphic (many forms)

• Polymorphisms are differences in DNA among organisms, the more polymorphisms the easier it is to differentiate organisms

• There are more polymorphisms in introns

Definitions-3• Invasive organisms: exotic organism that reproduces and

occupies progressively a larger area:– Fast reproductive cycle– Vectored– Hardy– Occupy unoccupied niches– Different drain on natural resources– Make environment favorable for itself and other invaders– Linked to disturbances– If pathogen , more changes because top of pyramid– May hybridize with native species: new taxon is created

• MICROBIAL INVASIONS OF NATURAL ECOSYSTEMS:– Cannot be eradicated

– Problematic because not noticeable for decades

– Can cause limited problems

– Can cause major alterations:

Because of lack of coevolution between host and pathogen

Because they are where similar organisms were not before

Introduced organisms

• Have a smaller genetic variation than original population

• Strong founder effects

• Each founder can create a significantly different population if not in equilibrium

• Mating will homogenize variation

• Mating barriers will increase difference

How does DNA help

• Identify microbe

• Determine whether equally named organism from elsewhere is the same or not

• Determine how it is reproducing

• Quantify organism

• Determine whether it is hybridizing or not

Definitions

• Phylogeny

• Phylogeography

• Gene geneaology

DISEASES AND TREES

• What exactly is a disease? It is the outcome of an interaction between a plant and the environment, resulting in an altered physiology of the host

• Sustained interaction=biotic• Single event= abiotic

What is a pathogen?

• Strictly speaking a pathogen is the causal agent of disease• Bacteria• Viruses• Nematodes• Stramenopiles• Algae• Phytoplasmas• Higher plants

Nematodes

And of course… fungi

• Fungi: saprophytic, symbionts, and pathogens

• Polyphyletic group in evolutionary terms– Basidiomycetes

Ascomycetes

Zygomycets

Animals

Plants

Red algae

Brown algae

Myxomycetes

Diversity of fungi, but all have ideal structure for plant infection:– hypha/cord/rhizomorph/infection peg/appressorium– Sexual vs. asexual reproduction: can do both– Do not photosinthesize– Chitin in cell wall– Exogenous digestion– Indefinite growth– Phenotypic plasticity and pleomorphisms

Septa

Pores

Pores

CELLS

Fungi… again!

• ASCOASCOMYCETES

• BASIDIOBASIDIOMYCETES

• OOMYCETES (fungus-like, water molds)

ASCOASCOMYCETES

• Yeasts (fermentation, human mycoses)Yeasts (fermentation, human mycoses)

• Truffles, morelsTruffles, morels

• Penicillia (penicillin), Fusaria (potent toxins, damping off of seedlings), molds

Ascus is the sack in which the spores are contained

Asci can be placed on a disk (apothecium), many apothecia can be together in a fruitbody

Morel fruitbody

Asci can be carried inside a flask (perithecium)

Nectria

Ploidy is mostly

n

BASIDIOBASIDIOMYCETES

• Mushrooms. mycorrhizal Mushrooms. mycorrhizal

• Wood decay organismsWood decay organisms

• Rusts, Smuts

• Yeasts and damping off

Toadstools and huitacochle are both basidiomycetes

Basidium means “club”, it carries the basidiospores (dispersion

propagules) naked

Most of their life, they aren+n (dikaryons), some rareones are diploid

Oomycetes

• Belong to the kingdom Stramenopila, used to be called Chromista

• Phytophthora, Pythium, Saprolegnia

H20

Oomycetes are not fungi

• Cellulose in cell wall• Ploidy is 2n• Result of sexual activity is oospore

(2n)• Meiosis, somatogamy, caryogamy

all occur at the same time

• Water adapted biology, flagellate phase

• No septa, holocoenocytic hyphae

• Chitin in cell wall• Ploidy is n, or n+n• Result of sexual activity is a spore

n• Meiosis, somatogamy,caryogamy

are usually interupted by vegetative (somatic phase)

• Better adapted for aerial transmission

• Septate hyphae

PhytophthoraPhytophthora

• Some important plant pathogens, with very well known history– Phytophthora infestans and the Irish potato

famine– Phytopthora cinnamomi and the Jarrah dieback

in Australia

The Irish Potato FamineThe Irish Potato Famine

• From 1845 to 1850• Phytophthora

infestans• Resulted in the death

of 750,000 • Emigration of over 2

million, mainly to the United States.

Phytophthora: “Phytophthora: “plant plant destructor”destructor”

• Best known pathogen whose long-distance transport linked to agriculture. – Infected root-stocks – Infested soil– Infected plants

70 species of 70 species of PhytophthoraPhytophthora

• 60 until a few years ago, research accelerated, especially by molecular analyses

• Differentiated on basis of:– Type of sexual intercourse– Type of sexual activity– Number of hosts– Ideal temperature– Type of biology– Evolutionary history (Waterhouse-Cooke)

Hyphae, sporangia, and zoospores of Hyphae, sporangia, and zoospores of P. ramorumP. ramorum

Zoospore

Hyphae, sporangia, and zoospores of Hyphae, sporangia, and zoospores of P. ramorumP. ramorum

Most of their lifecyclethey are 2n

Have cellulose in cellwall

Not fungi!!, but looklike them because of convergent evolution

Fungi do not photosynthesize

• Biotrophic: mycorrhyzae, rusts

• Endophites: clavicipetaceae,

• Necrotrophic; most pathogens

• Saprobes: primary (involved in litter decomposition)

DISEASE!!

• Symptoms vs. signs; e.g. chlorosis vs. fruit-body

• The disease triangle

host-pathogen-environment

• Susceptibility of individuals or of portions of individuals

• Genetic variability• Basic compatibility (susceptibility) between

host and pathogen• Ability to withstand physiological

alterations

Genetic resistance in host Genetic resistance in host

Length of lesion (mm)

Proportion of stem girdled (%)

Nicasio\ 42.5a 0.71a

China Camp 40.5a 0.74a

San Diego 27.8b 0.41b

Ojai 25.0b 0.47b

Interior live oak (Maricopa)

14.1b 0.33b

Cankers byCankers by P. ramorum P. ramorum at 3 monthsat 3 monthsfrom time of inoculation on two coastfrom time of inoculation on two coastlive oakslive oaks

host-pathogen-environment

• Basic compatibility with host (virulence)• Ability to maintain diversity: sex vs. no sex• Size of genetic pool• Agressiveness (pathogenicity) towards

hosts• Ability to survive without host

Chlamydospores of Chlamydospores of P. ramorumP. ramorum

Pr75 Qa MontereyPr75 Qa Monterey Pr87 Am MarinPr87 Am Marin Pr86b Am MarinPr86b Am Marin Pr86a Am MarinPr86a Am Marin Pr84 Soil MarinPr84 Soil Marin Pr82 Vo MarinPr82 Vo Marin Pr80 Vo MarinPr80 Vo Marin Pr72 Rh AlamedaPr72 Rh Alameda Pr65 Qp Santa CruzPr65 Qp Santa Cruz Pr58 Vo MarinPr58 Vo Marin Pr50 Qa SonomaPr50 Qa Sonoma Pr201b Rh Santa CruzPr201b Rh Santa Cruz Pr201a Rh Santa CruzPr201a Rh Santa Cruz Pr47b Qa SonomaPr47b Qa Sonoma Pr47a Qa SonomaPr47a Qa Sonoma Pr35 Qa SonomaPr35 Qa Sonoma Pr28 Ld SonomaPr28 Ld Sonoma Pr24 Qa SonomaPr24 Qa Sonoma Pr22 Qa SonomaPr22 Qa Sonoma Pr20 Qa SonomaPr20 Qa Sonoma Pr19 Qa NapaPr19 Qa Napa Pr16 Qa Santa CruzPr16 Qa Santa Cruz Pr13 Qa Santa CruzPr13 Qa Santa Cruz Pr11b Qa MontereyPr11b Qa Monterey Pr11a Qa MontereyPr11a Qa Monterey Pr10 Ld MontereyPr10 Ld Monterey Pr08 Qa NapaPr08 Qa Napa Pr06 Qa MarinPr06 Qa Marin Pr05 Ld MarinPr05 Ld Marin Pr04 Qk MarinPr04 Qk Marin Pr03 Ld MarinPr03 Ld Marin Pr88 Uc SonomaPr88 Uc Sonoma Pr89 Uc SonomaPr89 Uc Sonoma Pr90 Qa MarinPr90 Qa Marin Pr91 Uc SonomaPr91 Uc Sonoma Pr97 Qa NapaPr97 Qa Napa Pr102 Qa MarinPr102 Qa Marin Pr103 Ld MarinPr103 Ld Marin Pr104 Ld MarinPr104 Ld Marin Pr107 Uc SonomaPr107 Uc Sonoma Pr110 Uc MarinPr110 Uc Marin Pr112 Uc MarinPr112 Uc Marin Pr113 Uc MarinPr113 Uc Marin Pr114 Uc MarinPr114 Uc Marin Pr115 Uc MarinPr115 Uc Marin Pr116 Uc MarinPr116 Uc Marin Pr136 Uc MarinPr136 Uc Marin Pr156 Ld OregonPr156 Ld Oregon Pr157 Ld OregonPr157 Ld Oregon Pr158 Ld OregonPr158 Ld Oregon PrJL3.1 Ss SonomaPrJL3.1 Ss Sonoma PrSDC21.6 Ss SonomaPrSDC21.6 Ss Sonoma

Pr36 Qa SonomaPr36 Qa Sonoma Pr27 Qa MarinPr27 Qa Marin

Pr57 Ld Santa ClaraPr57 Ld Santa Clara Pr70 Vo MarinPr70 Vo Marin Pr159 Ld OregonPr159 Ld Oregon

Pr52a Rh Santa CruzPr52a Rh Santa Cruz Pr52b Rh Santa CruzPr52b Rh Santa Cruz PrCoen Rh Santa CruzPrCoen Rh Santa Cruz

PrJL3.5.3 Ss SonomaPrJL3.5.3 Ss Sonoma Pr106 Uc SonomaPr106 Uc Sonoma

Pr71 Qa SonomaPr71 Qa Sonoma Pr01 Qa MarinPr01 Qa Marin

PrE9/95 Rh GermanyPrE9/95 Rh Germany PrE16/99 Vb GermanyPrE16/99 Vb Germany

PrE12/98 Rh GermanyPrE12/98 Rh Germany PrE104 Water GermanyPrE104 Water Germany

PrE69082 Rh GermanyPrE69082 Rh Germany PrE9/3 Water GermanyPrE9/3 Water Germany

PrE14/98-a Rh GermanyPrE14/98-a Rh Germany Pl33 Cl Del Norte

Pl16 Soil Josephine Pl27 Tb Del Norte0.1

Clone groupClone group

European groupEuropean group

P. lateralisP. lateralis (outgroup)(outgroup)

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host-pathogen-environment

• Temperatures• Shading• Relative humidity• Free standing water• pH and any potentially predisposing factors• Nutrient status

Colo

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Colo

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Presence of free water

Between 6 and 12 hours requiredBetween 6 and 12 hours requiredfor infection of bay leavesfor infection of bay leaves

Some pathogen roles in natural plant communities

• Selection of individuals best suited for the site• Maintenance of genetic diversity and stability in

host plant populations• Establishment or maintenance of host geographic

ranges• Natural succession• Regulation of stand density, structure, and

composition

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.

Effects of fire exclusion

DISEASE: plant microbe interaction

• Basic compatibility need to be present• Chemotaxis, thighmotropy• Avirulence in pathogen matched by

resistance in host according to the gene for gene model

• Pathogenicity factors such as toxins and enzymes important in the infection process

Effects of diseases on host mortality, growth and reproduction

• Young plants killed before reaching reproductive age

• Affect reproductive output

• Directly affect flowers and fruits

WGR

Complexity of forest diseases

• At the individual tree level: 3 dimensional

• At the landscape level” host diversity, microclimates, etc.

• At the temporal level

Definitions

• Alternatively fixed alleles

• Dominant vs. co-dominant markers

• Genotype

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?

• 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

• 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

• 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.

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

• Blonde

• Blue-eyed

• Blonde

• Blue-eyed

• Hairy

• Blonde

• Blue-eyed

• Hairy

• 6 feet tall

• Blonde

• Blue-eyed

• Hairy

• 6 feet tall

• Missing two molars

In the case of microbes it will probably be something like

• Genotype A= 01010101

• Genotype B= 00110101

• Genotype C= 00010101

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

Progression of cankersProgression of cankers

Older canker with dry seepOlder canker with dry seep

HypoxylonHypoxylon, a secondary , a secondary sapwood decayer will appearsapwood decayer will appear

Stem cankerStem cankeron coast live oakon coast live oak

Root disease center in true fir caused by Root disease center in true fir caused by H. annosumH. annosum

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

• Up to 88% mortality in tropical Uganda

• More significant when seed production is episodic

Stress cone crop BS on DF

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

• 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

• Viral?

• Phytoplasmas

• Peronospora and smuts can lead to over 50% mortality

• Endophytism: usually considered beneficial

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

• 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

• 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

• 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)

Melanin-covered rhizomorphs willallow for fungus to move to new food Sources (Armillaria mellea)

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

POPULATION DYNAMICS

Species interactions and diversity

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

• 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

• 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

Diseases and succession

• Soil feedbacks; normally it’s 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

Janzen-Connol

• Regeneration near parents more at riak 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

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

Frequency-, or density dependent, or balancing selection

• New alleles, if beneficial because linked to a trait linked to fitness will be positively selected for.– Example: two races of pathogen are present, but

only one resistant host variety, suggests second pathogen race has arrived recently

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

• 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