2. 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

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

4. 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

5. 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!!)

6. 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)

7. 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.

8. 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

9. Blonde Blue-eyed

10. Blonde Blue-eyed Hairy

11. Blonde Blue-eyed Hairy 6 feet tall

12. Blonde Blue-eyed Hairy 6 feet tall Missing two molars

13. In the case of microbes it will probably be something like Genotype A= 01010101 Genotype B= 00110101 Genotype C= 00010101

14. 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

17. Fungi… again! ASCOASCOMYCETES BASIDIOBASIDIOMYCETES OOMYCETES (fungus-like, water molds)

18. ASCO ASCOMYCETES Yeasts (fermentation, human mycoses)Yeasts (fermentation, human mycoses) Truffles, morelsTruffles, morels Penicillia (penicillin), Fusaria (potent toxins, damping off of seedlings), molds

19. Ascus is the sack in which the spores are contained

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

22. Asci can be carried inside a flask (perithecium) Nectria

23. Ploidy is mostly n

24. BASIDIO BASIDIOMYCETES Mushrooms. mycorrhizalMushrooms. mycorrhizal Wood decay organismsWood decay organisms Rusts, Smuts Yeasts and damping off

25. Toadstools and huitacochle are both basidiomycetes

26. Basidium means “club”, it carries the basidiospores (dispersion propagules) naked

29. Most of their life, they are n+n (dikaryons), some rare ones are diploid

30. Oomycetes Belong to the kingdom Stramenopila, used to be called Chromista Phytophthora, Pythium, Saprolegnia H20H20

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

32. Most of their lifecycle they are 2n Have cellulose in cell wall Not fungi!!, but look like them because of convergent evolution

33. Fungi do not photosynthesize Biotrophic: mycorrhyzae, rusts Endophites: clavicipetaceae, Necrotrophic; most pathogens Saprobes: primary (involved in litter decomposition)

34. DISEASE!! Symptoms vs. signs; e.g. chlorosis vs. fruit- body The disease triangle

35. Disease triangle Effect of humans

36. 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.

38. Effects of fire exclusion

39. 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

40. 1- Basic compatibility Size of infectious propagules Timing of susceptibility in host and production of infectious structures

41. 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

42. 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)

43. 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)

44. 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

45. 4- Causing disease Correlated to ability of pathogen to invade plant cell, pathogenicity is usually a dominant trait

46. 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

47. Seed diseases Up to 88% mortality in tropical Uganda More significant when seed production is episodic

49. Stress cone cropBS on DF

50. 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

51. 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

54. Systemic infections Viral? Phytoplasmas Peronospora and smuts can lead to over 50% mortality Endophytism: usually considered beneficial

55. 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

56. 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

61. 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

62. 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

67. 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)

71. Effects of fire exclusion

73. 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

75. 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

76. 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)

77. 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

78. 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