BIOLOGY ECOLOGY GENETICS of FOREST FUNGI

1. BIOLOGY ECOLOGY GENETICSof FOREST FUNGI • Lesson 1 of BEG Spring 2011 • Taught by Dr. Matteo Garbelotto • Matteog@berkeley.edu • Office: 338 Hilgard Hall • Office hours: WEDNESDAYS at 3 pm, THURSDAYS at 1 pm

2. Course info • One two hour lecture per week • One quiz every week on previous lecture and reading assignments • NO syllabus, but…. • Some readings will be emailed to students • Web site: www.matteolab.org • Link to UCB course • POWERPOINT LECTURES, assigned readings • Posted on Fridays

3. Course info • One final quiz (3 questions out of 9) • One short Powerpoint presentation • Possibility to improve grade by writing paper (5 pages) on same topic as oral presentation • One computer lab: use of software for genetic analyses • Participation in SOD blitz mandatory

4. GRADING • 25% class participation • 25% weekly quizzes • 25% final quiz • 25% oral presentation

5. COURSE PROGRAM-1 • What is an emergent disease ? • What do plant diseases exactly do? • How do plant and pathogens interact? • What are the evolutionary consequences of emergent diseases? • What causes plant diseases • How can we use genetic information to identify a pathogen? DNA, chromosomes and loci

6. COURSE PROGRAM-2 • DNA used to identify a species • DNA used to identify an individual within a species • Following an individual pathogen to understand infection process • Using genes to tag individuals; how far does an individual go? • Identify populations and migration among populations

7. COURSE PROGRAM-3 • Identify source of a pathogen and phylogeography • Determine whether a population is introduced or native • Rapid evolutionary changes linked to introductions • Epigenetics of disease

8. EMERGENT FOREST DISEASES: ARE THEY A THREAT TO NATIVE ECOSYSTEMS? Matteo Garbelotto U.C.Berkeley

9. “Native diseases”: • Indigenous microbes • Plant ecosystems have co-evolved to resistance • Native diseases are an important component of forest ecosystems

10. “Roles of native diseases”: • Thin natural populations of trees • Optimal allocation of resources • Selection for a genetically diverse host population • Maintain tree ranges • Succession: nutrient cycling

11. “Emergent diseases”:diseases on the rise • New introduced, exotic, organisms • Good gone bad: e.g. climate change or human activities trigger excessive pathogenicity of native organism

12. DISEASE TRIANGLE Pathogen Host Environment

13. DISEASE TRIANGLE HIGH DISEASE Pathogen Host Environment

14. Pathogen Does it need a wound to infect a host? Can it survive in the environment without a host? soil, water on alternate host How does it move around? airborne/waterborne animal vectors humans

15. Must be physically present with pathogen Must be physically compatible with pathogen Must provide window of opportunity for infection Genetic resistance? often lack of resistance if disease is introduced What type of resistance? simple= one gene complex=several genes Host

16. Environment Climatic As modified per human management Species composition Plant density

17. “Emergent diseases”:1: host • New host-pathogen combinations: exotic hosts hosts planted off site

18. Cypress canker by Seiridium cardinale • Pathogen was first described in California in the 20s. Later it was described in Italy where it started a serous epidemic of Italian cypress • Belief that pathogen is native to California: is that true and why is it then causing a significant disease in our state?

19. Conidia of Seiridium cardinale observed by optical microscope and SEM

20. Use of molecular genetics to resolve issue of origin of pathogen • Used a technique similar to the one used in human forensics • Native populations should comprise many different individuals genetically • Introduced populations should be genetically simpler because of bottleneck related to introduction events

21. RESULTS: CA vs. Europe • California population diverse genetically= native to the state • European population show no diversity=introduced

22. Fig. 3 Symptoms caused by Seiridium cardinale on Cupressus macrocarpa (above) and xCupressocyparisleylandii (right)

23. Why a disease in CA? • If pathogen is native to California, why is it causing such a serious disease? • We observed that disease incidence is variable with: • cypress species, • location,

24. Range of susceptibility • Leyland cypress, Italian, monterey are listed as most susceptible • Arizona and McKnob are regarded as more resistant

25. Range of susceptibility • 90% of Leyland are heavily infected • 10% of monterey • LEYLAND CYPRESS IS AN ORNAMENTAL CROSS, NOT NATIVE

26. Range of susceptibility • Monterey is more susceptible in inland areas where it is NOT NATIVE: we believe that colder temperatures cause more wounds that lead to infection

27. CONCLUSIONS • Cypress canker is a serious disease in Europe because pathogen was introduced • Cypress canker is a serious disease in California because hosts were introduced either through planting off range (Monterey cypress) or because host is artificial creation (Leyland cypress); extinction of LEYLAND is most likely

28. “Emergent diseases”:2: environmental changes • Forestry and intensive forest use: timber production tree felling and creation of stumps fire exclusion and increase in density oversimplified forest composition changes in forest composition changes in forest structure

29. Heterobasidion root disease • Heterobasidion (a bracket or shelf mushroom) infects trees through wounds and stumps, then it spreads through the roots to neighboring trees • With tree felling,stumps and wounds are created, suddenly exponentially increasing infection levels

30. Heterobasidion shelf fruit-body

33. Use of molecular genetics: • Differentiate Heterobasidion on fir/sequoias (H. occidentalis) from that on pine/junipers (H.irregularis) • Show that airborne meiospores are responsible for most infection of Heterobasidion • Show that in pines most infections start on stumps and that in true firs most infections on wounds

34. True firs Pines Each spore is a genetically different individual: In pines we found the same genetic individual in stumps and adjacent trees indicating direct contagion between the two In true firs and true firs/sequoias we find same individual in adjacent standing trees indicating infection not linked to stumps but to wounds on standing trees

35. CONCLUSIONS: • Logging activities increase Heterobasidion infection because of stump creation in pines and because of wounding in true firs sequoias • We have shown that in pine stumps H. irregularis and H. occidentalis can both be present and create a new hybrid entity • We have shown that in the past these hybridization events have lead to sharing of genes among these two species (Horizontal gene transfers)

36. Armillaria root diseases • Armillaria, the honey mushroom, normally infects the roots of trees. It can be a saprobe and a pathogen and is common amongst oaks • If woodland composition shifts to pine/oak, pines become the target of attacks and gaps in canopy enlarge over time. Stress (e.g. flooding) exacerbates susceptibility

37. Clusters of Armillaria

38. How Does it Infect? • Two means of dispersal to other trees: • Mycelium can grow through direct root contacts and grafts with uninfected trees. • Rhizomorphs can grow through soil to contact uninfected trees. OAK or PINE DEAD OAK SOURCE: http://www.forestpathology.org/dis_arm.html

39. What are Rhizomorphs? SOURCE: http://www.nifg.org.uk/armillaria.htm • …“conglomerations of differentiated parallel hyphae with a protective melanized black rind on the outside.” • Rhizomorphs are able to transport food and nutrients long distances which allows the fungus to grow through nutrient poor areas located between large food sources such as stumps. SOURCE: http://botit.botany.wisc.edu/toms_fungi/apr2002.html

40. Humongous Fungus It’s One of U-HAUL’s “Bizarre Roadside Attractions” http://botit.botany.wisc.edu/toms_fungi/apr2002.html

41. CONCLUSIONS Human activities shifting from oak woodlands to mixed oak-pine lead to large mortality gaps in pines around oaks if honey mushroom is present CHANGING SPECIES COMPOSITION LEADS TO SEVERE DISEASE

42. Many gaps with very little regeneration and have not closed in

43. Change in gap area 1972-1999

44. “Emergent diseases”:3: exotic pathogens • 99% of times human responsible for their introduction

45. Like the conquistadores brought diseases that were lethal to those who had never been exposed to them, so do exotic diseases cause true devastation in plant communities because of lack of coevolution between hosts and microbes

46. California invaded: 1849 A.D. Port Orford Cedar Root Disease 1950s New hybrid root pathogen 1990s Manzanita/madrone die-back Sudden Oak Death 1990s White pine blister rust 1930s Canker-stain of Sycamores 1980’s Dutch Elm Disease 1960s Pitch canker disease 1980s Oak root canker 2000

47. How can people transport pathogens • By transporting plants and plant parts • Crops, and seeds • Raw food • Ornamental plants Untreated lumber Soil Insects vectoring fungi Military activity

48. 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.

50. Is it exotic? • Our studies have indicated that California population is extremely simplified, basically two strains reproducing clonally as expected of an introduced organism • Many hosts appear to have no resistance at all • Limited geographic distribution