ESPM BOOK NOTES

CHAPTER 4: Hormonal Interactions Between Plants and Animals (pgs 120-125)

• IV. Pheromonal Interactions and the Pine Bark Beetle: WESTERN PINE BEETLE, Dendroctonus brevicomis
and CALIFORNIA FIVE-SPINED IPS, Ips paraconfusus
• D. brevicomis: female attracted to volatile terpenes exuded from tree (from the oleoresins of bark). Attract males:
males release frontalin. This synergizes with females’ exo-brevicomin and tree’s myrcene. Mass aggregation!!! At
full capacity: females make (E)-verbenol, repelling females & males make verbenone and (+)-ipsdienol, repelling
males.
• Tree: myrcene. Tree altered by D. brevicomis: ipsdienol, verbenol, verbenone. D. brevicomis: exo-brevicomin,
frontalin. [alpha-pinene to verbenol and verbenone.]
• Myrcene cannot be replaced by similar structure, limonene.
• Bacterium in I. paraconfusus oxidizes alpha-pinene to verbenol; fungus in D. brevicomis oxidize verbenol to
verbenone.
• I. paraconfusus similar to D. brevicomis: uses plant terpenes. MALE absorbs myrcene, turns into ipsdienol and
ipsenol, two male pheromones.
• Certain pheromones restrict feeding of different beetle species. Ips on Dendroctonus, vice versa.
• Trees: vary oleoresin chemistry! High limonene. (beetle want low limonene, high a-pinene, myrcene. High b-
pinene okay for beetles to)

CHAPTER 5: Insect Feeding Preferences (pgs 142-146, 148)

• IV. Secondary Cmpds as Feeding Deterrents: A WINTER MOTH AND OAK LEAF TANNINS
• Plant tannins: hydrolysable and condensed. Hydrolysable: derivatives of simple phenolic acids, condensed have
higher M.W., formed by the condensation of two or more hydroxyflavanol units.
• Tannins: ability to tan animal hide to form leather. Combine with protein, often irreversibly, forming bonds with
peptides and other functional groups. Very astringent taste.
• Larvae: feed on oak leaves in spring, cease feeding in mid-June. No difference in nutritional status, environmental
parameters. [Condensed] tannin content increased.
• Lepidoptera: 110 species early-June, 65 species mid-August.
• Tree’s defense: tannin increase; toughness of leaf increase; lammas shoots to increase photosynthetic capabilities.
• Tannins not a problem of nutrition, caused lysing of gut of non adapted butterflies. (Lipids secreted in gut as
protection? P.145)
• Aphids: choose to eat lower tannin content, if forced would eat higher tannin; less offspring.
• Hydrolysable: in oak leaves toxic to farm animals… Geraniin (of Geranium) growth inhibitor of larvae of H.
virescens. (Ellagic acid released within caterpillar, chelates some essential metals.)
• C LEAF-CUTTING ANTS
• Ants feed themselves on the mycelia mat. Cut leaves attractive to other ants.
• “The choice of food plant by leaf-cutting ants is extremely catholic and few plants seem to be immune to such
attack”
• Latex production is a barrier.
• Specific terpenoids another barrier: some volatile, some not. Some singular, some combination.
• Some harm fungal food & are avoided. Plants defense against infection with side effect of protection from ants?

CHAPTER 6: Feeding Preferences of Vertebrates, Including Man (pgs 168-171)

• III. Wild Animals: typically more hardy than domestic animals.
• Desert habitats: looking for water.
• Adaptation to cardiac glycoside poisoning: hyrax and gazelle, eating oleander.
• Hyrax: hungry enough, eat furanocoumarin rich good; too much toxin, usually eat sprouts. 4 of 5 die.
• Survival is based on eating small amounts of many different plants. However: hares: snow: eat what they can.
• Desert animals: less options. Winter, wood rat only has creosote bush. Will continue to feed on even higher levels
of resin, but may lose weight and die.
 • Mountain gorilla: eats 29 species. Looks for lower condensed tannin levels, mostly adapted to alkalinity.
Develops “taste” for bitterness.
• Colobus monkeys: mostly low tannin level, one species higher than average tannin content, lower alkaloid.
• Other colobus monkeys: higher tannin in all things; eat leaves second growth vines & half of diet are seeds.

CHAPTER 7: The Co-evolutionary Arms Race: Plant Defense and Animal Response
• I. Introduction: plant: toxin 1, response: avoidance by animals. Then adaptation, then feeding attractant, Plant:
toxin 2, repeat cycles possibly with some variation.
• II. Static Plant Defense: A THE COST OF CHEMICAL DEFENSE
• Grow or defend? Note: carbon plentiful, but nitrogen not necessarily. Proteins or alkaloids?
• B EVOLUTION OF FEEDING DETERRENTS
• Affecting hormonal balance, poison, bad taste
• Every feeding deterrent has turned into a feeding stimulant for a particular insect (except condensed tannins)
• C LOCALIZATION OF TOXINS IN THE PLANT
• Frequently concentrated at or near plant surface. Glandular hairs (trichomes), leaf waxes, leaf resins, bud
exudates.
• Trichome: wild potato species: 2 types. B: alarm pheromone of aphid. A: phenolic-containing exudates
[substrate], linked to a phenolase/peroxidase enzyme [enzyme] system. Reactive!
• [insert pgs 194-201]
• IV. Animal Response: A INSECTS
• Cryptic: metabolize/excrete toxin; Aposematic: store unchanged or store metabolite; Aposematic mimic:
Metabolize/excrete toxin.
• Can switch from cryptic to aposematic; tobacco hornworm switching to Atropa belladonna & toxic afterwards.
• THC: toxin for most insects. Switching over, kills many insects; a few survive. Faced with less toxic cousin,
survival better, but given an option, chose that with THC.
• Behavioral adaptation: plant makes more toxin when bits removed; cucumber beetle cuts a circle trench around an
area of the leaf, so a few veins and pieces of lower epidermis hold the leaf in place, then it can feed safely.
• B KANGAROOS
• Resisting fluoroacetate poisoning! Converts to fluorocitrate, which blocks Krebs cycle.
• Rat kangaroo of W Aus adapted, not SE Aus (where there is not fluoroacetate in plants) MOVEMENT: W to E.
• Grey kangaroo: all adapted, MOVEMENT: W to E. E retains ability to detoxify; W will choose less toxic.
• [insert pgs 206-207]

CHAPTER 8: Animal Pheromones and Defense Substances

• I. Introduction: cAMP aggregation pheromone for mould.
• Chemicals for communication within species: pheromones, between species: allomones. (Some blurring)
• Insects: most work, for pesticide. Mammals: rats, odorant in urine of male mice has effect on female; esp
noticeable in females isolated into a group (similar to human females, synchronized menstrual cycles)
• Airborne pheromones: small M.W. v. small quantities have effect: silkworm moth: M excited by 100
molecules /ml of air.
• Aquatic pheromones: larger M.W. less volatile, water soluble. Protein: made by F. Volvox and settling barnacle
pheromones. Steroid: synchronizing m-f spawning readiness in goldfish.
• Much synthesized de novo though also used from plants as well. ANIMAL DEFENSE: allomones.
• Alkaloids: stored by moths, butterflies; synthesized by certain animals as well (frogs!)
• Terpenoids: may be both of dietary origin and the subject of direct synthesis. Quinones: bombardier beetle.
• II. Insect Pheromones: A SEX PHEROMONES
• Attract and incite to copulate.
• Most sex attractants are long chain unsaturated alcohols, acetates or carboxylic acids.
• 9-keto-2-decenoic acid: queen bee substance, attracts male drones to mate with the queen bee. 32 similar
compounds in her head.
• R-mellein: pheromone, fungal origin!
• Nepetalactone: indleg secretion of female vetch aphid; first found in plats, powerful attractant for cats: clear
example of the same molecule having quite unrelated functions in the plant, insect, mammalian kingdoms.
• Pheromones occur in very low amounts: “nearly a million virgin female moths were extracted to yield 1.5 mg”
• Any small change destroys/diminishes activity. EX: E/Z matters a lot.
• Special pheromone blend, however can be very similar between similar species (ratio may be 3:1 and 1:3 resp)
• Some unrelated compounds with similar signal: D-bornyl acetate sexual excitement of M American cockroach.
Some synthetic compounds can also cause excitement
• Plants: corn budworm, waits for host plant. Signal from plant ripening hormone gets female to deposit eggs.
• Anti-aphrodisiac pheromones (abstinones): M to F during mating; could be masking of active sex pheromones by
inactive compounds? TSETSE FLY: most def abstinone.
• Almost all sex pheromones are synthesized within the insect.
• Sex pheromones exploited by man to trap pets insects. ALSO: bolas spiders! Mimicking F pheromones.
• 2 pest controls: 1. Mimic F pheromones. 2. Release unspecific volatile chemicals which mask effect of the
pheromone and interfere with the signal.
• B TRAIL PHEROMONES
• Social insects: nest to food source. Ants, bees, termites.
• Leaf-cutting ant Atta texana highly active substance; easily detected. Formed by bacterial action in gut?
• A. texana hormonal substances: indoleacetic acid (auxin of higher plants) grow fungus. Myrmicacin prevent
growth of undesirable fungal spores. Phenylacetic acid: no bacteria.
• Trail pheromone from venom gland of 8 species red ant: same chemical signal.
• Some Lepidopteran larvae live in colonies; have steroid made from cholesterol as pheromone.
• Honey bee: from plants. Monoterpene geraniol as trail substance. Some converted to second pheromone.
• C ALARM PHEROMONES
• Mandibular or anal glands or from the sting apparatus.
• Bees and wasps: induce stinging same location; “killer bees” larger amounts of alarm pheromone.
• Labile: does not last long (aphids, reinfest same place)
• Least specific of hormones; yet ants: high degree of olfactory acuity.
• Weaver ant: 1. Alerted 2. Attracted towards scene 3. Attack 4. Short-range orientation signal
• Ant-termite: compounds termites don’t recognize. “Chemical crypsis”
• III. Mammalian Pheromones: skunk – sulfur compounds.
• Striped hyena, house shrew, black-tailed deer. Urine/feces.
• [Signal persists after a while] [insert pgs 223-227; below inserted here]
• Boar! Identified: similar to testosterone; strong musky odor. Parallel w/ civet cat, musk ox? Musky.
• IV. Defense Substances: ALKALOID: venom of ant from tobacco leaf. CYANOGENIC GLYCOSIDES:
linamarin, moths and butterflies from birdsfoot trefoil and clover. PHENOL: hydroquinone, waterbeetle from burs
of Xanthium canadense. TERPENOID: beta-selinene in lepidopteran larva from celery leaves. AMINE: barbs of
tiger moth from stinging hairs of nettle.
• B: TERPENOIDS. Volatility and powerful smell. Burning and itching too.
• Stuff in resin secreted from foregut of larvae of sawfly. (Advanced? Not making de novo)
• Termites: defense in soldiers, biting and injecting; poison-brushing; glue-squirting. Workers safe from poison by
substrate-specific reductases present in their tissues.
• Cantharidin: irritating material basis of “aphrodisiac” Spanish fly. Hazardous. Released by reflex bleeding from
the knee joints in beetle.
• Monarch butterflies and grasshoppers eat milkweed, store cardiac glycosides, only grasshoppers can spray them.
• Animal toxin related in structure to cardenolides: bufogenins, steroidal toxins act on hearts of vertebrates used by
frogs and toads (6 membered cyclolactone instead of 5)
• Some fireflies also have defensive steroids; one species feeds on the other (‘femmes fatales’) acquiring defense.
• Steroidal defense: water-beetles – fish fall into narcotic state from eating, beetle gets away.
• C ALKALOIDS. Moths eating Senecio accumulate pyrrolizidine alkaloids, highly toxic (as well as danaid
butterflies: think love dust!) [insert pg 234]
 • D PHENOLS AND QUINONES. Bombardier beetle: discharges toxin! (hot) reaction of hydroquinone with
H2O2 and enzyme catalase.Into: benzoquinone! [insert pg 236-238]

CHAPTER 9: Biochemical Interactions Between Higher Plants

• I. Introduction: allelopathy: biochemical interactions between all types of plants (adv or disadv)
• Allelopathic substances or toxins: secondary substituents, usually volatile terpenes or phenolic compounds.
Secondarily functional? For animals, became involved in plant-plant interactions.
• Auto-toxicity: between indiv of same species
• II. The Walnut Tree: at first, death range thought to be extent of root growth. Then, addition: leaching from
leaves, stems, branches of bound toxin & hydrolysis/oxidation in soil = toxin. JUGLONE: water-soluble yellow
pigment, toxic to plants (varying intensity)
• III. Desert Plants: bare patches of soil beneath canopies and around them.
• Encelia farinosa (Compositae): from leaves a toxin, released when leaves fall to ground and decompose. (Brittle
bush, tumbleweed)
• Thamnosma Montana (Rutaceae): toxic, has furanocoumarins but no allelopathic effect. Possibly turned over
quickly by micro-organisms.
• Parthenium argentatum (Compositae): growth inhibition caused by a root, rubber plant guayule. (E)-Cinnamic
acid, more toxic to itself than anything else. Must be continually produced, doesn’t persist long. (Could affect
growth of native competitors as well, though)
• IV. Allelopathy in the Californian Chaparral: A VOLATILE TERPENES AND THE FIRE CYCLE
• “Zonation of herbs around the thickets of shrubs.” Due to terpene toxins, not birds/animals.
• Terpenes: in leaves, turned over by shrubs, occur in soil, remain in soil until rain = microorganisms = degrade,
transported into plant cells, have effect on germination.
• Salvia leucophylla, sagebrush, 1,8-cineole and camphor. [hydrocarbons + natural detergent]
• Cycle: fire, annuals dominate, shrubs start, shrubs dominate, fire. (25 years)
• B WATER-SOLUBLE INHIBITORS: phenolic compounds [environment: foggy, constant drip off leaves]
• Quercus falcata: salicylic acid from leaf leachate. Inhibit undergrowth within dripline of the foliar crowns.
• Bracken: phytotoxins leached by rain from dead, standing bracken fronds – herb suppression. Autotoxic too, go
through phases of degeneration and then recolonizing.
• V. Other Allelopathic Agents: nordihydroguaiaretic acid in creosote bush. Long chain fatty acids (C14-C22)
• Sulfur compound alpha-terthienyl and phenylheptatriyne: more effective under sunlight or sources of UV light.
• Sesquiterpene lactones: possibly inhibitory / autotoxic.
• [insert pgs 256-257] note: leaving fields fallow may remain toxic & toxins may become natural herbicides.
• VII. Biochemistry of Host-Parasite Interactions: intrusive organs called haustoria: attach and feed.
• 2 chemical triggers: one for seed germination, one to induce haustorial formation, to attach to host.
• Strigol: from cotton, non-host plant. Analogue better, trigger germination of Striga so they die sans host.
• Sorgolactone: natural stimulant from Sorghum for Striga.
• Animal parasites: cyst nematode, needs hatching factor.
• Some semiparasites steal alkaloidal protection from host plant.

CHAPTER 10: Higher Plant-Lower Plant Interactions: Phytoalexins and Phytotoxins

• I. Introduction: susceptibility to disease, all too frequently apparent in cultivated plants, is the exception rather
than the rule.
• Attack: get through surface layers – waxy coating, surface hairs, thick cuticle (reduce speed of attack)
• Chemically based disease resistance: phytoalexins (“warding off” [alexos] of “disease organisms from the plant”
[phyto]) fighting off microorganisms’ secreted pathotoxins, that “poisons” the host plant.
• Pre-infectional: 1. PROHIBITINS: metabolites which reduce or completely halt the in vivo development
of micro-organisms. 2. INHIBITINS: metabolites which undergo post-infectional increase in order to
express full toxicity.
 Post-infectional: 1. POST-INHIBITINS: metabolites formed by the hydrolysis or oxidation of pre-
existing non-toxic substrates. 2. PHYTOALEXINS: metabolites formed de novo after invasion by
gene derepression or activation of a latent enzyme system.
• II. Biochemical Basis of Disease Resistance: A PREINFECTIONAL COMPOUNDS: no sharp division beause
per-infectional compounds can undergo significant post-infectional changes.
• ONE Substances inhibiting germination / growth of micro-organisms. Jackpot: heartwood of pine; “pinosylvin” –
a hydroxystilbene. (unknown, however, if compound is important to the plant)
• Onion vs. onion smudge disease: resistant species have protocatechuic acid and catechol in outer scales (highly
toxic to spores). Some relation to anthocyanin color; however, importance is if anthocyanin based on cyaniding
(ie with catechol nucleus in structure); cyaniding inhibits germination of a fungus causing apple rot.
• [insert pgs 269-270] [lupins have preinfectional compounds all the time. Isoflavone concentration in leaf surface
moisture film: bad environment for fungal development. Methylated flavones: protecting citrus leaves? Summary:
preformed fungitoxins prevent microbial invasions. Mainly phenolic, others: triterpenoids and alkaloids]
• TWO inhibitins: metabolites undergoing post-infectional increases to express their toxic potential.
• Often coumarin derivatives near site of infection.
• Blight-infected potatoes: blue fluorescent zone, protective zone between infected and healthy tissue. Fluorescent
coumarin scopolin increases 10-20X, chlorogenic acid (weaker fluorescence) increases 2-3X
• Theory: may be a symptom of the disease and not a defense? But evidence to the contrary: C. graminicola has
ability to counteract toxic effects. Produce water-soluble mucilage; glycoprotein fraction has high affinity to bind
condensed tannins and other phenols. Leachates quickly inactivated.
• B POST-INFECTIONAL COMPOUNDS: POST-INHIBITINS: present in healthy tissues as inactive glycosides,
active toxin being released by enzymic hydrolysis or oxidation following microbial invasion.
• Cyanogenic glycosides: break down to prussic acid, cyanohydrin breaks down to aldehyde/ketone and HCN.
HCN protects, except this one type which has an enzyme which can detoxify HCN.
• Glucosinolates: tissue damage releases volatile oil, allyl isothiocyanate (formed by enzymic hydrolysis of another
substance) which is highly toxic. Evidence: higher concentration of isothiocyanate in resistant varieties, in wild
populations, highest proportion of resistant seedlings: higher amounts of flavor volatiles.
• Tulips: 1-tuiliposides A and B. Rearrange to isomeric 6-tuliposides A and B, enzymic hydrolysis followed by
cyclization to yield highly fungitoxic tulipalins A and B. (complex with SH groups and inhibit enzymic activities
of attacking fungus)
• Phenolics as pre-infectional metabolites: oxidation to o-quinones highly toxic, may complex with amino
compounds making more toxic products. (“In resistant leaves, it appears that the fungitoxic o-quinone is formed
only [with damage to] cellular membranes, allowing the plant enzyme phenolase to oxidize the natural substrate.
The product of this oxidation then arrests further fungal development.”)
• Sulphur amino acids present in onion tissues: triggers germination of fungus; however, it will germinate in
presence of sulphide without host = treat soil first.
• C POST-INFECTIONAL COMPOUNDS: PHYTOALEXINS [275-285; some things skipped]
• Tenets: 1. Phytoalexin inhibits development of fungus formed/activated only when the host plants come in contact
with parasite. 2. Defense: only in living cells. 3. Inhibitory agent a product of the host cell. 4. Nonspecific in
toxicity towards fungi; fungi may be differentially sensitive 5. Response of both resistant and susceptible cells the
same: difference is speed of formation of phytoalexin 6. Defense confined to tissue colonized and immediate
neighborhood. 7. Resistant state not inherited; developed after invasion. Sensitivity of host cell dependent on
genotype.
• First: pterocarpans from legumes. [some tenets mildly altered; more sensitive system]
• TEST: drop diffusate technique. Drops (Tween-20, surface-active agent, used to prevent droplets from spreading)
with and without fungi on leaves. If phytoalexin response, push out to surface of leaf where fungal attack
occurring. Problem: diffusing out to leaf surface may leave quantitative errors.
• [I don’t really care about the TLC bit of this shit]
• Iiiiinteresting: phytoalexins may be formed when plants are subjected to stress; may occur in trace amounts in
healthy tissue… though “a completely healthy unstressed plant is difficult to define precisely.”
• All share some degree of lipid solubility.
• [Nor does it really matter all that much to me the specifics of taxonomy. Summary: more highly evolved plant,
more complex phytoalexin. BAM done.]
• Detox of phytoalexins: isoflavonoids 1. Reduce lipid solubility and increase water solubility. 2. Broken down by
aromatic-cleavage pathways to CO2.
• “Elicitors”: factors of fungal origin that elicit plant’s reaction: something on fungi outside?
Protein/glycoprotein/polysaccharide. Really anything foreign to species.
• III. Phytotoxins in Plant Disease: A THE PATHOTOXIN CONCEPT: pathotoxins = expression of the virulence
of the pathogen.
• Low m.w. pathotoxins: effect on growth/cause wilting – wilting factors. High m.w. include peptides: plant
necrosis; enzymes, tissue maceration and loss of cellular cohesion. Both may be produced from same organism.
• Dutch elm disease: necrotic lesions and wilting – proteins and 3 low m.w. phenolic metabolites.
• Symptoms directly related to toxins: chlorosis (destruction of chloroplast: accumulation of ammonia; “wild fire
toxin”: peptide – interferes with the enzyme glutamine synthetase, and ammonia accumulates), growth
abnormalities (synth of high levels of growth hormones: gibberellins in rice! Crown gall tumours in
dicotyledonous plants – genetic transfer of information via plasmids to higher plant nucleus), necrosis (dark
lesions, dryness; leathery/brittle. Blockage of primary metabolism – fire blight in apple causes evolution of
ammonia = necrosis of twigs), wilting (physical block of xylem or water stress induced by toxin).
• B PYRIDINE-BASED PATHOTOXINS
• Wilting: similar symptoms; causes death. See: Dutch elm disease.
• Low m.w.: TOMATO: lycomarasmin and fusaric acid (pyridine derivative): both chelate. Some plants can
conjugate with glycene and it will be inactive; can conjugate certain amounts though not all.
• Fusaric acid in other plants; parent compound: picolinic acid causes necrosis in rice (rice blast). Also chelates.
Can be detoxed by conversion of moiety (I believe). Second toxin in rice blast: piricularin (toxic to parasite itself,
but in vivo with protein, so only toxic to host)
• [And there’s a paragraph of name dropping that I can’t really handle right now. Pg 289]
• C HELMINTHOSPOROSIDE AND VICTORIN
• [Another side note cause I’m almost done but I don’t think this bit is all that useful. It’s cool though!]
• HS from Helminhosporium sacchari phytotoxins: binds to a single membrane protein. There are “latent” forms of
the toxin & nontoxic forms, lacking galactose units (toxoids) – these can actually be competitive inhibitors of HS.
• D MACROMOLECULAR TOXINS [pg 291] form enzymes to break down host
• E OTHER EFFECTS OF PHYTOTOXINS one my protect plant from other fungi (fungitoxic?)