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Summary of previous lesson

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

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Summary of previous lesson

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  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 AA=Aa 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

  14. Fungi… again! • ASCOMYCETES • BASIDIOMYCETES • OOMYCETES (fungus-like, water molds)

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

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

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

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

  19. Ploidy is mostly n

  20. BASIDIOMYCETES • Mushrooms. mycorrhizal • Wood decay organisms • Rusts, Smuts • Yeasts and damping off

  21. Toadstools and huitacochle are both basidiomycetes

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

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

  24. Oomycetes • Belong to the kingdom Stramenopila, used to be called Chromista • Phytophthora, Pythium, Saprolegnia H20

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

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

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

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

  29. Disease triangle Effect of humans

  30. 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.

  31. Effects of fire exclusion

  32. 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

  33. 1- Basic compatibility • Size of infectious propagules • Timing of susceptibility in host and production of infectious structures

  34. 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

  35. 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)

  36. 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)

  37. 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

  38. 4- Causing disease • Correlated to ability of pathogen to invade plant cell, pathogenicity is usually a dominant trait

  39. 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

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

  41. Stress cone crop BS on DF

  42. 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

  43. 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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