plant pajtology exam 3

Mycotoxin

Toxic fungal secondary metabolite; harmful to humans and animals at ppm or ppb levels

Aflatoxin: crop and effect

Aspergillus flavus; maize and peanut; liver disease and liver cancer

Fumonisin: crop and effect

Fusarium verticillioides; maize; neural tube defects, equine neurological disease

Ochratoxin: crop and effect

Cereal grains, coffee, grapes; kidney and liver damage, cancer

Trichothecenes (DON): crop and effect

Fusarium graminearum; wheat, oat, barley; GI distress in livestock (vomiting, feed refusal)

Zearalenone: crop and effect

Fusarium graminearum; maize and small grains; reproductive abnormalities (estrogenic)

Factors that influence mycotoxin production

Warm humid wet weather, drought stress, insect damage, plant stress, late harvest, wet grain, poor storage; also light, nutrients, pH

Nematode

Non-segmented roundworm (phylum Nematoda); most numerous multicellular animal on Earth; needs water; not an earthworm

Plant-parasitic nematode life cycle

Egg, J1, J2, J3, J4, adult; parasitism begins when the J2 (second-stage juvenile) hatches and penetrates the root

Role of the stylet

Needle-like mouthpart: penetrates plant tissue, probes, secretes effectors, ingests cell contents

Ectoparasitic nematode

Feeds from outside the plant with its stylet; mostly migratory; e.g., ring nematode (Criconemoides), dagger nematode (Xiphinema)

Endoparasitic nematode

Enters the plant and feeds from inside; e.g., root-knot, cyst (sedentary), root lesion (migratory)

Migratory vs sedentary feeding

Migratory: keeps moving and killing cells, causes necrosis. Sedentary: induces a permanent feeding site (giant cell or syncytium) and stays there

Giant cell

Enlarged multinucleate cell (nuclear division without cell division); induced by root-knot nematode (Meloidogyne)

Syncytium

Feeding site formed when cell walls between neighboring cells dissolve; induced by cyst nematodes (Heterodera, Globodera)

Above-ground nematode symptoms

Look like nutrient deficiency: wilting, stunting, yellowing, patchy hot spots

Below-ground nematode symptoms

Galls, cysts, necrotic lesions, stubby roots, forked roots, fibrous root proliferation

How nematodes are diagnosed in the field

Symptoms are not specific, so take soil and root samples from several spots, then extract, identify, and count nematodes

Foliar nematode disease

Aphelenchoides; enters leaves through stomata; V-shaped lesions between veins (chrysanthemum); white tip of rice

Tree nematode disease

Pine wilt: pinewood nematode (Bursaphelenchus xylophilus), spread by beetles, blocks xylem, kills tree fast

Nematode disease complexes

Nematodes plus fungi: Fusarium-nematode wilt; also Verticillium, Pythium, Phytophthora, Rhizoctonia

3 most important plant-parasitic nematodes

Root-knot (Meloidogyne), cyst (Heterodera, Globodera), root lesion (Pratylenchus)

Root-knot nematode key facts

Sedentary endoparasite; induces giant cells and root galls; swollen females; wide host range; mostly parthenogenetic; most crop loss of any nematode

Cyst nematode key facts

Sedentary endoparasite; induces syncytium; female body becomes a cyst protecting eggs for 8 to 20+ years; sexual; host specific

What distinguishes root lesion nematode?

Migratory, not sedentary; no feeding site; stays worm-shaped (no swollen females); causes brown necrotic lesions

Nematode survival mechanisms

Cryptobiosis/diapause, cysts, eggs in soil, weed and perennial hosts, infected plant parts

Nematode management

Prevention (sanitation, clean material, quarantine), crop rotation, solarization/flooding/fallow, nematicides, biocontrol, resistant cultivars (best)

Environmental factors for nematicide use

Not selective, so kills beneficial nematodes; consider soil type, moisture/rainfall (leaching), temperature, persistence

GM technology against nematodes

Transgenic Bt soybean against soybean cyst nematode

Incubation period

Time from penetration to symptoms

Latent period

Time from penetration to production of secondary inoculum

Incubation or latent period: which predicts epidemics better?

Latent period; it sets how fast new infection cycles start

Lignin

Rigid phenolic polymer that strengthens woody cell walls; hard to degrade

Hemicellulose

Branched sugar polymer that cross-links cellulose

Cellulose

Glucose chains forming microfibrils; main structural polymer of the cell wall

Passive vs active defenses

Passive: always present (constitutive). Active: induced only after the pathogen is detected

Passive structural defenses

Waxy cuticle, stomata shape, trichomes, suberized cells, lignified tissue

Passive chemical defenses

Secondary metabolites: terpenoids, phenolics, alkaloids; e.g., avenacin in oat roots

Leaf abscission

Active structural defense: plant drops the infected leaf

Tyloses

Active structural defense: xylem parenchyma outgrowths that plug vessels

Lignin cell wall reinforcement

Active structural defense: lignin deposited in walls at the infection site

Callose cell wall reinforcement

Active structural defense: callose (glucose polymer) deposited in walls

Papillae

Active structural defense: deposits between cell wall and plasma membrane at the infection site

Phytoalexins

Active chemical defense: low molecular weight antimicrobials made after infection

Oxidative burst

Active chemical defense: rapid release of reactive oxygen (superoxide, H2O2) toxic to pathogen and host

MAMPs

Microbe-associated molecular patterns (chitin, flagellin, lipopolysaccharide, viral coat protein); detected by receptors to trigger PTI

Jones and Dangl zigzag model

PAMPs trigger PTI; effectors suppress it (ETS); R proteins detect effectors (ETI, often HR); repeats as pathogen and plant co-evolve

PTI

Pattern-triggered immunity: first defense layer, triggered by MAMPs/PAMPs

ETS

Effector-triggered susceptibility: pathogen effectors suppress PTI, causing disease

ETI

Effector-triggered immunity: R protein recognizes an effector; strong defense, often HR

Pathogenicity genes

Genes required for a pathogen to cause disease

Virulence genes

Genes that increase disease severity

Effector delivery by bacteria

Type III secretion system

Effector delivery by fungi

Haustoria

Hypersensitive response

Rapid, localized death of infected and nearby cells that stops pathogen spread

Effector

Pathogen protein that alters host biology to help infection; if recognized by an R protein it acts as an avirulence protein

Systemic Acquired Resistance (SAR)

Infection at one site triggers defense throughout the plant; salicylic acid signal; PR proteins made

Induced Systemic Resistance (ISR)

Like SAR but triggered by non-pathogens (rhizobacteria); no PR proteins

General resistance

Many genes (horizontal, quantitative); works against all races. Pro: durable. Con: only partial, hard to transfer

Specific resistance

One gene (vertical, qualitative); complete resistance to one race. Pro: easy to breed. Con: new races overcome it

Boom-and-bust cycle

R-gene cultivar released, widely planted, pathogen evolves to overcome it, cultivar fails, repeat

Agrobacterium in the wild

Enters wounds; phenolics activate vir genes; T-DNA from Ti plasmid moves into plant DNA; auxin and cytokinin genes cause crown gall tumors

Agrobacterium in the lab

Remove tumor genes from T-DNA, insert gene of interest, infect plant tissue, select and regenerate transgenic plants

Gene gun

Fires DNA-coated metal particles into plant cells; used for plants Agrobacterium does not infect well (many cereals)

Top 3 GM crops and traits

Corn, soybean, cotton; mostly herbicide tolerance and insect resistance

Golden rice

Rice with a corn gene and a bacterial gene to make beta-carotene (vitamin A precursor)

Papaya RNA silencing

Rainbow papaya expresses papaya ringspot virus coat protein RNA; plant cuts it into small RNAs that destroy the virus

CRISPR/Cas9 vs older methods

Guide RNA directs Cas9 to edit an exact site in the plant genome, instead of randomly inserting foreign DNA; can be transgene-free

Epidemic

Widespread increase of disease in a geographic area over time or space

5 factors that lead to an epidemic

Favorable environment, genetically uniform host, pathogen present, cultural practices that favor disease, conditions that favor vectors

Incidence vs severity

Incidence: how many plants are infected. Severity: how much tissue on each plant is affected

Spore traps

Collect airborne spores on a sticky surface to count inoculum per volume of air

Disease progress curve and AUDPC

Disease plotted over time; AUDPC = area under that curve, one number for the whole epidemic

Monocyclic disease curve

One cycle per season; slow, roughly linear increase; depends on initial inoculum

Polycyclic disease curve

Many cycles per season; exponential (q = q0 e^kt); depends on infection rate

Polyetic disease curve

Inoculum builds over several years; e.g., Dutch elm disease

GIS in epidemiology

Maps disease with layers like soil, yield, and aerial images to find where disease is and what drives it

Seed degeneration

Pathogens build up in saved seed each generation, raising initial inoculum and disease every season

Reducing t

Planting dates, short-season varieties

Reducing q0

Sanitation, vertical resistance, chemical control

Reducing k

Horizontal resistance, protectant chemicals, cultural practices

Infection period

Hours of leaf wetness at a temperature needed for infection; forecasting models use it to decide when to spray

Severity values

Accumulated infection-period scores; tell growers when to spray

False positive vs false negative forecast

False positive: predicts disease that does not happen (wasted spray). False negative: predicts no disease but it occurs (crop loss)

Cultural practices that reduce disease

Crop rotation, sanitation, soil pH/fertility, plant spacing, irrigation management, pruning

Protectant vs eradicant pesticide

Protectant: applied before infection (most common). Eradicant: kills pathogen after infection

How pesticides enter the environment

Leaching into groundwater, drift in wind, improper use and disposal

Contact vs systemic fungicide

Contact: stays on the surface where applied. Systemic: absorbed and moves through the plant

One fungicide mechanism

Strobilurins block the mitochondrial electron transport chain (cytochrome bc1), stopping respiration

FRAC codes

Group fungicides by mode of action; rotate codes to prevent resistance

Gene pyramiding

Stacking multiple resistance genes in one cultivar for more durable resistance

Biocontrol agents

Organisms that suppress pathogens; rarely used because results are inconsistent in variable field conditions

Antibiosis

Biocontrol agent produces antimicrobial compounds

Parasitism (biocontrol)

Biocontrol agent directly attacks and feeds on the pathogen

Niche competition

Biocontrol agent outcompetes the pathogen for space or nutrients

Growth promotion

Biocontrol agent boosts plant growth and can induce resistance

4 types of biological control

Introduction (classical), conservation, augmentation, habitat manipulation

Disease suppressive soils

Soils where disease stays low even in favorable conditions, due to antagonistic microbes

4 components of IPM

Monitor and identify; survey and set thresholds; prevention; control (pesticides only past threshold)