diseases and trees - College of Natural Resources

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Transcript diseases and trees - College of Natural Resources

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:
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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?
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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:
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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!
• ASCOMYCETES
• BASIDIOMYCETES
• OOMYCETES (fungus-like, water molds)
ASCOMYCETES
• Yeasts (fermentation, human mycoses)
• Truffles, 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
BASIDIOMYCETES
• Mushrooms. mycorrhizal
• Wood 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 are
n+n (dikaryons), some rare
ones are diploid
Oomycetes
• Belong to the kingdom Stramenopila, used
to be called Chromista
• Phytophthora, Pythium, Saprolegnia
H20
Oomycetes are not fungi
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Cellulose in cell wall
Ploidy is 2n
Result of sexual activity is oospore
(2n)
Meiosis, somatogamy, caryogamy
all occur at the same time
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Water adapted biology, flagellate
phase
No septa, holocoenocytic hyphae
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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
Phytophthora
• 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 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: “plant
destructor”
• Best known pathogen whose long-distance
transport linked to agriculture.
– Infected root-stocks
– Infested soil
– Infected plants
70 species of Phytophthora
• 60 until a few years ago, research accelerated, especially
by molecular analyses
• Differentiated on basis of:
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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 P. ramorum
Zoospore
Hyphae, sporangia, and zoospores of P. ramorum
Most of their lifecycle
they are 2n
Have cellulose in cell
wall
Not fungi!!, but look
like them because of
convergent evolution
Fungi do not photosynthesize
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Biotrophic: mycorrhyzae, rusts
Endophites: clavicipetaceae,
Necrotrophic; most pathogens
Saprobes: primary (involved in litter
decomposition)
DISEASE!!
• Symptoms vs. signs; e.g. chlorosis vs. fruitbody
• 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
Length of lesion Proportion of stem
(mm)
girdled (%)
Nicasio\
China Camp
42.5a
40.5a
0.71a
0.74a
San Diego
27.8b
0.41b
Ojai
Interior live
oak
(Maricopa)
25.0b
14.1b
0.47b
0.33b
Cankers by P. ramorum at 3 months
from time of inoculation on two coast
live oaks
host-pathogen-environment
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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 P. ramorum
93
100
0.1
Pr75 Qa Monterey
Pr87 Am Marin
Pr86b Am Marin
Pr86a Am Marin
Pr84 Soil Marin
Pr82 Vo Marin
Pr80 Vo Marin
Pr72 Rh Alameda
Pr65 Qp Santa Cruz
Pr58 Vo Marin
Pr50 Qa Sonoma
Pr201b Rh Santa Cruz
Pr201a Rh Santa Cruz
Pr47b Qa Sonoma
Pr47a Qa Sonoma
Pr35 Qa Sonoma
Pr28 Ld Sonoma
Pr24 Qa Sonoma
Pr22 Qa Sonoma
Pr20 Qa Sonoma
Pr19 Qa Napa
Pr16 Qa Santa Cruz
Pr13 Qa Santa Cruz
Clone group
Pr11b Qa Monterey
Pr11a Qa Monterey
Pr10 Ld Monterey
Pr08 Qa Napa
Pr06 Qa Marin
Pr05 Ld Marin
Pr04 Qk Marin
Pr03 Ld Marin
Pr88 Uc Sonoma
Pr89 Uc Sonoma
Pr90 Qa Marin
Pr91 Uc Sonoma
Pr97 Qa Napa
Pr102 Qa Marin
Pr103 Ld Marin
Pr104 Ld Marin
Pr107 Uc Sonoma
Pr110 Uc Marin
Pr112 Uc Marin
Pr113 Uc Marin
Pr114 Uc Marin
Pr115 Uc Marin
Pr116 Uc Marin
Pr136 Uc Marin
Pr156 Ld Oregon
Pr157 Ld Oregon
Pr158 Ld Oregon
PrJL3.1 Ss Sonoma
PrSDC21.6 Ss Sonoma
Pr36 Qa Sonoma
Pr27 Qa Marin
Pr57 Ld Santa Clara
Pr70 Vo Marin
Pr159 Ld Oregon
Pr52a Rh Santa Cruz
67
Pr52b Rh Santa Cruz
89
PrCoen Rh Santa Cruz
PrJL3.5.3 Ss Sonoma
96
Pr106 Uc Sonoma
Pr71 Qa Sonoma
Pr01 Qa Marin
PrE9/95 Rh Germany
PrE16/99 Vb Germany
PrE12/98 Rh Germany
PrE104 Water Germany
European group
PrE69082 Rh Germany
PrE9/3 Water Germany
PrE14/98-a Rh Germany
Pl33 Cl Del Norte
Pl16 Soil Josephine
P. lateralis
Pl27 Tb Del Norte
(outgroup)
host-pathogen-environment
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Temperatures
Shading
Relative humidity
Free standing water
pH and any potentially predisposing factors
Nutrient status
Colony diameter (mm) at 13 days
Presence of free water
Between 6 and 12 hours required
for 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
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Blonde
Blue-eyed
Hairy
6 feet tall
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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 cankers
Older canker with dry seep
Hypoxylon, a secondary
sapwood decayer will appear
Stem canker
on coast live oak
Root disease center in true fir caused by H. annosum
Categories of wild plant diseases
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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
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 (shortlived)
Melanin-covered rhizomorphs will
allow 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:
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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