Cankers. FRST 307 Fall 2017

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Cankers FRST 307 Fall 2017

www.forestryimages.org Website maintained by the Warnell School of Forestry at the University of Georgia, USA Unlike google images, this website is curated and accurate call number in black box (usually bottom left) will take you to the image and subject page

Canker diseases of trees and other plants Results from the death of definite and relatively localized areas of bark on branches and stems Most are caused by ascomycete fungi

Infection strategy Different strategy than root pathogens Have to overcome both physical barriers (bark) and active plant defence Most of the canker pathogens need a point of entry: the physical barrier of the tree is too much for the enzymatic arsenal of fungi Attacks living cells in phloem, cambium, xylem

Natural host protection Outer surface of stems, branches and roots (but not the leaves!) are protected by periderm In response to wound or attack tree produces secondary periderm (called necrophylactic periderm) Efficacy of response depends on host vigor; complete necrophylactic periderm formation can take weeks to months

Phytoalexins antibiotics for defense Defense compounds produced by plants Similar to antiobiotics: antimicrobial activity Mode of action: puncture fungal cell wall, disrupt metabolism, prevent reproduction Often specific to a pathogen Active response during growing season https://en.wikipedia.org/wiki/phytoalexin#/media/file:capsidiol.svg

Dissemination of canker pathogen Often several spore types Ascospores Wind disseminated Result of sexual reproduction Conidia Asexual reproduction Often rain-splashed Sometimes sticky, carried by insects These spores are generally not very resistant to UV light and drying Need periods of wet conditions for release and germination on new host Generally, no tree-to-tree spread by mycelium as with the root rots and decays

Pathways to infection Usually need wounding to enter host Insect wounds Some insects create wounds and fungi use the wounds to enter Other insects are vectors and create wounds to inoculate the trees Mechanical bark wounds, including pruning wounds Natural scars Lenticels Petiole scars Dead branches or twigs Once inside the tree, pathogen still has to deal with active chemical and physical host response

Damage by canker diseases A single canker can be enough to kill a tree (if it is on the main stem) Bole deformation Reduced lumber recovery in the sawmill Stain and resin soaking of wood and bark at the canker Pulp chips contain resin-soaked bark Branch flagging Leads to a general decline, dieback Point of entry for insects, other fungi, decay Breakage

Saprophytic cankers Associated with weakened trees Can t penetrate barrier of living cells in healthy tree But in a tree that is otherwise stressed (abiotic, insects, other diseases such as root rots), tree cannot produce chemical and physical barrier to prevent the fungus from invasion Usually part of a complex that is often referred to as decline Example: Cytospora canker

Cytospora canker of aspen

Annual cankers Opportunistic fungus that rapidly infects a tree through wounds before the host has a chance to respond Not particularly specialized; few develop into large scale epidemics and are mostly related to some environmental stress Often overlooked and difficult to identify Example: Fusarium pitch canker

Fusarium Fusarium solani Fusarium subglutinans Fusarium subglutinans

Perennial cankers Invades the host when it is slow to respond Invasion often in late summer, fall, and even winter when trees have formed terminal buds or are dormant Often, fungi that are well adapted to growing in cold temperature, some can even grow at 2 C More aggressive than the annual cankers, more specialized Must tolerate some host reaction Each year, when tree growth resumes, host responds by attempting to wall off the fungus by chemical and physical barriers When tree goes dormant again, fungus resumes its slow progression in the host Canker is the symptom of this annual battle between the tree and the fungus: causes typical «target shaped cankers Examples: Nectria canker, Ceratocystis canker

Nectria spp.

Diffuse cankers Pathogen dominates the host and the host response is not fast enough or the pathogen can defeat it Rapid invasion, production of toxins by the fungus Living host tissues often destroyed in a few years and tree is girdled causing breakdown in water and nutrient transport system Since tree does not have a chance to respond or produce callus, often a large canker not visible, instead have a diffuse canker Examples: Chestnut blight, Hypoxylon canker, Scleroderris canker

Chestnut blight - Cryphonectria parasitica American chestnut Castanea dentata Extensive range in eastern NA, dominant angiosperm spp Timber, leather production, food (nuts)

Chestnut blight - Cryphonectria parasitica In late 1800 s, Chinese chestnut introduced as ornamental Castanea mollissima Chinese chestnut is resistant to endemic blight, C. parasitica Cp quickly spread though range of AC, destroying trees over ~ 2m tall Now, no AC bigger than 2m, after growing past that they die https://www.fs.fed.us/nrs/atlas/tree/niche.php?spp=421&t=4

Chestnut blight - Cryphonectria parasitica Cp destroys phloem tissues (diffuse canker), girdling trees and cutting off photosynthate transfer

Chestnut blight how do we fix this? Chinese chestnut is resistant, can we transfer that ability into American chestnut? Problems AC very difficult to clone, clones needed for testing Dr. Scott Merkle University of Georgia Somatic embryogenesis of backcrossed hybrids Hybrids are created of AC x CC These are backcrossed with AC to reduce CC morphology SE of resistant individuals to propagate resistant AC phenotypes