18.12.03 · organismal-bio / plant-physiology

Plant hormones: auxin, gibberellin, ethylene, abscisic acid, and the control of plant development

shipped3 tiersLean: none

Anchor (Master): Darwin & Darwin 1880 (Power of Movement in Plants); Went 1928 Rec. Trav. Bot. Neerl. 25:1; Kurosawa 1926; Skoog & Miller 1955/1957; Neljubow 1901; Ohkuma-Lyon-Addicott 1963 Science 142:1592; Bleecker-Estelle-Somerville-Kende 1988 Science 241:1086; Bleecker & Kende 2000 Annu. Rev. Cell Dev. Biol. 16:1; Hedden & Thomas 2012 Biochem. J. 444:11; Borlaug 1970 Nobel Peace Prize lecture; Dharmasiri 2005 Nature 435:441; Ma-Grill 2009 Science 324:1064

Intuition Beginner

A plant has no nerves, no brain, no fast-moving muscles. Yet it bends toward light, sends roots downward, opens and closes its leaf pores, ripens its fruit, and drops its leaves on a seasonal clock. All of that coordination is done with chemicals called hormones — small molecules made in one tissue that travel to others and change what those cells do. Plants run on five classical hormone families: auxin, gibberellin, cytokinin, ethylene, and abscisic acid. Each family carries one main message, and a single cell reading the mixture of all five at once decides what to become.

The five messages, in plain English. Auxin is made in shoot tips and tells cells to elongate — it is why a sunflower tracks the sun. Gibberellin stretches stems; the dwarf wheat of the Green Revolution lacks a normal gibberellin response, so the plant stays short and stiff and puts its energy into grain instead of straw. Ethylene is a gas — the only gaseous hormone — and it tells fruit to ripen and leaves to fall; one rotten apple really does spoil the barrel, because ethylene leaks out and ripens its neighbours. Abscisic acid tells leaf pores to close in a drought and keeps seeds asleep. Cytokinin tells cells to divide and delays ageing in leaves.

Charles Darwin and his son Francis ran the first experiment in 1880. They took young oat shoots and put tiny black caps over the tips. The capped shoots did not bend toward the light — but when the cap was placed lower down, leaving the tip exposed, the shoot bent normally. The tip senses light, but the bending happens lower down. Something must travel from the tip to the bending zone. That "something" was isolated in 1928 by Frits Went, who named it auxin. The whole field of plant hormones begins with the Darwins' capped oat shoots.

Visual Beginner

Hormone	Main job	Where made	Everyday signal
Auxin	Cell elongation, bending	Shoot tips	Sunflower tracks the sun
Gibberellin	Stem elongation, seed sprouting	Young leaves, embryos	Dwarf wheat stays short
Cytokinin	Cell division, delays ageing	Root tips	Cut leaves stay green
Ethylene	Fruit ripening, abscission	Most tissues under stress	One bad apple spoils the barrel
Abscisic acid	Stomatal closure, seed dormancy	Leaves and roots in drought	Seeds wait to sprout

The defining picture is two panels. On the left, the Darwin-Darwin cap experiment: an oat shoot with a black cap on its tip stays upright under side-lighting, while the same shoot with the cap lower down (tip exposed) bends toward the light. The tip perceives the light; the lower cells execute the bend. On the right, a Went agar block: a tip is set on a block of agar, the block absorbs the diffusate, and the block is placed asymmetrically on a decapitated shoot — bending the shoot away from the side carrying the block.

A third panel shows a tall traditional wheat variety standing next to a short semi-dwarf with the same heavy grain head; the tall one has buckled at the base (lodged), the short one stands straight. The dwarfing mutations rht1 and rht2 weaken the gibberellin response, the stem stays short and stiff, and the grain head does not bring the plant down.

Worked example Beginner

Norman Borlaug was sent to Mexico in 1944 by the Rockefeller Foundation to breed wheat that would resist a fungal disease called stem rust. By the 1950s he had crossed Japanese dwarf wheat (the Norin-10 line, carrying the rht1 and rht2 reduced-height mutations) with Mexican varieties and selected lines that did not lodge (fall over) under heavy grain. Traditional wheat grows about 140 centimetres tall; Borlaug's semi-dwarfs grow about 70 centimetres. The mutations blunt the plant's response to its own gibberellin, so the stem elongates less. The stem is shorter, stiffer, and does not bend or break under the weight of a heavy grain head.

Step 1. The yield arithmetic. A traditional wheat field in Mexico in 1944 yielded about 750 kilograms of grain per hectare. With the new semi-dwarfs and the fertiliser they could now carry without lodging, yields rose to about 2,400 kilograms per hectare by 1963 — roughly tripled.

Step 2. The India-Pakistan transfer, 1965-1968. India and Pakistan were on the edge of mass famine. Borlaug shipped about 250 tonnes of semi-dwarf seed across the Pacific in 1965 and 1966. Within five years, both Pakistani and Indian wheat yields rose about 60 percent. Both countries became self-sufficient in wheat by the mid-1970s.

Step 3. The human accounting. The Borlaug-era Green Revolution is credited with feeding on the order of one billion people who would otherwise have starved. Borlaug received the Nobel Peace Prize in 1970. The rht1 and rht2 mutations are now in essentially every modern commercial wheat variety on every continent.

What this tells us: two single-letter mutations in the gibberellin-signalling pathway, identified and moved into breeding lines by one breeder with a small team, changed the global food supply within a single human generation.

Check your understanding Beginner

Exercise (easy, multiple choice).

Charles and Francis Darwin put tiny black caps on the tips of oat coleoptiles and shone light from one side. What happened?

A. The shoot bent normally toward the light. B. The shoot did not bend toward the light, because the tip could not sense the light. C. The shoot bent away from the light. D. The shoot stopped growing entirely.

Hint

The Darwins showed that the tip is where the light is sensed, and the bending happens lower down. Cover the tip and the signal never gets made.

Answer

B. With the tip capped, the shoot does not bend toward light, because the tip is the light-sensing tissue. Went later showed that the signal is auxin, which is made in the tip and travels down to the growing region where it drives cell elongation on the shaded side, bending the shoot toward the light. When the Darwins instead placed an opaque collar lower down (leaving the tip exposed), bending was normal — confirming that the lower tissue does the bending but not the sensing.

Exercise (easy, multiple choice).

Which plant hormone is a gas at room temperature, and what is its best-known effect?

A. Auxin — cell elongation. B. Gibberellin — stem elongation. C. Ethylene — fruit ripening. D. Abscisic acid — stomatal closure.

Hint

"One bad apple spoils the barrel." A gas leaking out of one fruit telling its neighbours to ripen is the signature.

Answer

C. Ethylene (chemical formula C2H4) is the only plant hormone that is a gas at ambient temperature. Because it is a gas, ethylene produced by one ripening fruit diffuses through the air and triggers ripening in nearby fruit — the literal origin of the proverb about one bad apple. Commercial fruit suppliers use this on purpose: tomatoes and bananas are picked green and ripened on demand by exposure to controlled ethylene. The same gas drives leaf and flower abscission (the dropping of leaves in autumn is preceded by a rise in ethylene production at the abscission zone).

Exercise (easy, true-false).

The Green Revolution semi-dwarf wheat varieties are shorter than traditional wheat because they carry mutations (rht1, rht2) that weaken the plant's response to gibberellin.

Hint

Gibberellin drives stem elongation. Reduce the response and the stem stays shorter and stiffer.

Answer

True. The rht1 (Reduced height-1) locus on chromosome 4B and rht2 on chromosome 4D encode DELLA-domain proteins that regulate the gibberellin signalling pathway. With reduced gibberellin signalling, the stem cells elongate less and the plant grows to roughly half the height of traditional wheat. The shorter, stiffer stem does not lodge under the weight of a heavy grain head, so the plant can be given more fertiliser and water without collapsing — which is what tripled grain yields. Norman Borlaug received the 1970 Nobel Peace Prize for moving these mutations into broadly adapted breeding lines.

Formal definition Intermediate+

A plant hormone is a small organic molecule synthesised in one tissue, transported (sometimes only a few cells, sometimes through the whole plant) to a target tissue, and active at micromolar-or-lower concentrations against a specific receptor that transduces the binding event into a change in gene expression, ion flux, or enzyme activity ^{[Taiz 2015]}. The five classical classes — auxins, gibberellins, cytokinins, ethylene, abscisic acid — were defined biochemically between 1880 and 1963; four additional classes (brassinosteroids, jasmonates, salicylic acid, strigolactones) were added between 1979 and 2008 and are now standard. A hormone is defined by its chemical scaffold and its receptor / signal-transduction pathway, not by a single physiological response (the same hormone produces different responses in different tissues).

Class	Canonical molecule	Chemical scaffold	Receptor	Core pathway
Auxins	Indole-3-acetic acid (IAA)	Indole + acetic acid	TIR1/AFB (F-box, SCF)	Aux/IAA degradation, ARF release
Gibberellins	GA1, GA4 (of ~136 GAs)	ent-gibberellane diterpenoid	GID1 (soluble, nuclear)	DELLA degradation, GAMYB/PIF
Cytokinins	trans-zeatin	N6-substituted adenine	AHK2/3/4 (His-kinase)	Phosphorelay, type-B ARR
Ethylene	Ethylene (C2H4)	Two-carbon alkene	ETR1/2, ERS1/2, EIN4	CTR1, EIN2, EIN3/EIL
Abscisic acid	(+)-ABA	C15 sesquiterpenoid	PYR/PYL/RCAR (START)	PP2C inhibition, SnRK2, SLAC1
Brassinosteroids	Brassinolide	Polyhydroxylated steroid	BRI1 (LRR receptor kinase)	BSK, BZR1/BZR2
Jasmonates	JA-isoleucine	Cyclopentanone (linolenic)	COI1 (F-box, SCF)	JAZ degradation, MYC2
Salicylic acid	Salicylic acid	C7 phenolic acid	NPR1	NPR1 monomerisation, PR genes
Strigolactones	5-deoxystrigol	Carotenoid-derived butenolide	D14 (alpha/beta-hydrolase)	D53 degradation, SMXL

Transport regimes. Auxin is the only hormone with polar, directional, cell-to-cell transport: it moves from shoot tip to root base through parenchyma by a chemiosmotic cycle of influx (AUX1/LAX proton-symport of the protonated IAAH) and basal efflux (PIN proteins concentrating IAA anion at the lower end of each cell), at about 5-10 mm per hour ^{[Went 1928]}. The other hormones move in the vascular stream: gibberellin and cytokinin in the xylem and phloem; ABA from root to leaf in the xylem under drought; ethylene as a gas through intercellular spaces.

Synthesis origins. Auxin (IAA) is made from tryptophan via indole-3-pyruvate (the TaP pathway). Gibberellins are ent-kaurene-derived tetracyclic diterpenoids built in plastids from geranylgeranyl diphosphate. Cytokinins are N6-substituted adenines produced from ATP/ADP/AMP by isopentenyl transferases (IPTs). Ethylene is produced from methionine via S-adenosyl-methionine and 1-aminocyclopropane-1-carboxylic acid (ACC) by ACC synthase and ACC oxidase — the rate-limiting enzymes for the whole pathway ^{[Neljubow 1901]}. ABA is a C15 apocarotenoid cleavage product of 9-cis-violaxanthin and 9-cis-neoxanthin by 9-cis-epoxycarotenoid dioxygenases (NCEDs).

Counterexamples to common slips

Hormones are defined by their effect. No. Auxin elongates cells in stems but inhibits elongation in roots at the same concentration; ethylene ripens fruit but also promotes abscission and inhibits stem elongation. A hormone is defined by its molecule and receptor, and the response is determined by the target tissue's gene-expression state.
Auxin made in the tip "flows" down passively. No. Polar auxin transport is active and directional: it requires the pH gradient across the plasma membrane (to trap IAAH inside), ATP-dependent PIN cycling to maintain basal efflux, and proceeds against a concentration gradient. Cutting out the ATP supply abolishes transport.
Ethylene is produced by fruit only. No. Every living plant cell makes ethylene constitutively at a low rate and surges production under stress (wounding, flooding, pathogen attack, drought). The climacteric fruits (apple, banana, tomato) are simply those that produce a burst of ethylene and autocatalyse their own ripening.
ABA is the "stress hormone" and nothing else. ABA's other indispensable role is seed dormancy: ABA accumulated during seed maturation keeps the embryo paused until imbibition and after-ripening lower ABA and raise gibberellin, which together break dormancy. Without seed dormancy, every seed would germinate on the parent plant the moment it ripened.
The five classical hormones exhaust the list. Brassinosteroids (discovered 1979, Mitchell), jasmonates (1987, Farmer and Ryan), salicylic acid (1979, White), and strigolactones (2008, Gomez-Roldan) are now standard. Any modern treatment lists nine hormone classes, not five.

Key experiment: the Darwin-Darwin 1880 phototropism experiments and Went's auxin isolation Intermediate+

Experiment 1 (Darwin and Darwin 1880 — the tip perceives, the lower zone bends). Charles and Francis Darwin, working at Down House, grew Avena sativa (oat) seedlings in the dark until the coleoptile — the protective sheath around the emerging shoot — was about 25 mm tall. They unilaterally illuminated the seedlings from a paraffin-lamp source at a fixed distance for 8 hours and scored the curvature in degrees ^{[Darwin 1880]}. Five treatments:

Unmanipulated control. Coleoptile bends toward the light (mean curvature about 30 degrees).
Tip amputated (top 2-4 mm removed). No bending.
Tip covered with an opaque cap. No bending.
Tip covered with a transparent cap. Normal bending.
Lower coleoptile covered with an opaque collar, tip exposed. Normal bending.

The conclusion, in Darwin's words: these results all seem to show that there is some influence generated in the upper part, transmitted to the lower part, causing it to bend. The tip perceives the light signal; the subapical elongation zone executes the asymmetric growth that produces the bend.

Experiment 2 (Boysen-Jensen 1910-1913, Paal 1914-1919 — the influence is a chemical that crosses a gelatin barrier). Boysen-Jensen showed that if the coleoptile tip is cut off and re-attached with a thin layer of gelatin, the phototropic signal still passes through — but it does not pass through a mica (impermeable) barrier. Paal showed that a tip offset to one side bends the shoot even in the dark, by asymmetric growth on the side under the tip. The signal is therefore a diffusible chemical, asymmetrically distributed, that promotes cell elongation.

Experiment 3 (Went 1928 — auxin isolated into agar, the curvature bioassay). Frits Went, working in his father's laboratory at the Botanical Institute in Utrecht, cut off coleoptile tips and placed them basal-side-down on small agar blocks for a defined time ^{[Went 1928]}. The influence diffused into the agar. He then placed one of these auxin-containing agar blocks asymmetrically (offset to one side) onto a decapitated coleoptile, in the dark. The coleoptile bent away from the side carrying the block — the side under the block elongated more — with a curvature that was linear in the concentration of the diffusate over the range 0 to about 30 degrees per block.

The Avena curvature bioassay quantifies auxin concentration in units of "Avena degrees": one unit of auxin activity is the amount that, placed asymmetrically on a standard decapitated coleoptile for 90 minutes at 25 degrees Celsius and 80 percent relative humidity, produces 1 degree of curvature. Went estimated the diffusate from a single coleoptile tip at roughly 10-20 Avena-degree units per hour, corresponding to an auxin flux of about 10 micrograms per kilogram of tip tissue per hour.

Quantitative model (the Cholodny-Went hypothesis, 1927-1928). Phototropic bending is produced by the lateral redistribution of auxin: in unilaterally illuminated coleoptiles, auxin is transported preferentially to the shaded side, where it drives greater cell elongation, bending the shoot toward the light. Let $I_{0}$ be the total auxin flux descending from the tip on the lit side and the shaded side in the absence of lateral light. Under unilateral light with redistribution fraction $r$ (where $0 < r < 1$ is the fraction moved from the lit side to the shaded side), the flux on the shaded side is $I_{0} (1 + r)$ and the flux on the lit side is $I_{0} (1 - r)$ .

Assuming cell elongation rate is linear in auxin concentration over the operating range, with rate constant $k_{e}$ , the differential growth rate over the time window $T$ is

Δ growth = k_{e} \cdot [I_{0} (1 + r) - I_{0} (1 - r)] \cdot T = 2 k_{e} I_{0} r T .

The curvature $θ$ (in radians) is geometrically $Δ growth / w$ , where $w$ is the width of the coleoptile over which the differential is applied, giving

θ = \frac{2 k _{e} I _{0} r T}{w} .

Briggs, Tocher and Wilson (1957, Am. J. Bot. 44:473) measured the lateral redistribution $r$ using radiolabelled IAA and found $r \approx 0.25$ to $0.30$ under saturating blue light, sufficient to generate a 2-fold IAA differential across the coleoptile — the experimental foundation for the Cholodny-Went hypothesis.

Bridge. The Darwin-Darwin-Went chain builds toward the molecular identification of the auxin receptor TIR1 (Dharmasiri et al. 2005), and appears again in 18.12.01 where polar auxin transport underlies the whole-plant coordination of growth, and in 20.05.05 where the same auxin-signalling cassette is re-used across the plant and animal kingdoms in deep-homology comparisons of development. The foundational reason auxin occupies the central position in plant physiology is exactly that it is the only hormone with directional cell-to-cell transport — this is the chemiosmotic PIN-cycle model that identifies where auxin goes with which cells elongate, and the bridge is the polar-transport machinery whose basal-localised PIN efflux carriers generalise to every apical-basal patterning decision in the plant. The central insight is that one small indole molecule, read out asymmetrically across a tissue, encodes positional information.

Exercises Intermediate+

Exercise 1 (easy, multiple choice).

Which hormone-receptor pair is correctly matched?

A. Auxin — GID1 B. Gibberellin — TIR1 C. Ethylene — ETR1 D. ABA — BRI1

Hint

Each hormone has a canonical receptor discovered in the molecular era. Auxin's receptor is an F-box (TIR1); gibberellin's is a soluble nuclear receptor (GID1); ethylene's is a membrane-bound negative regulator (ETR1); ABA's is a START-domain soluble receptor (PYR/PYL/RCAR).

Answer

C. ETR1 (ethylene response 1) is the ethylene receptor, a membrane-bound histidine-kinase-like negative regulator discovered by Bleecker, Estelle, Somerville and Kende in Arabidopsis: the receptor actively represses the ethylene response, and binding ethylene de-represses the pathway. GID1 (option A lists gibberellin with TIR1, which is wrong) is the gibberellin receptor. TIR1 is the auxin receptor (so option B is backwards). BRI1 is the brassinosteroid receptor (so option D is wrong).

Exercise 2 (easy, numeric).

Went's Avena curvature bioassay: a single Avena coleoptile tip yields about 15 Avena-degree units of auxin activity per hour. One block placed for 2 hours on a tip is then placed asymmetrically on a decapitated coleoptile for 90 minutes at 25 degrees Celsius. If the curvature response is linear at 1 degree per Avena-unit, what curvature (in degrees) is expected for the 2-hour block? Assume all the accumulated activity is transferred.

Hint

Multiply the production rate (15 units/hour) by the accumulation time (2 hours) to get total units. Then convert units to degrees.

Answer

Total accumulated activity $= 15 \times 2 = 30$ Avena-degree units. At 1 degree of curvature per unit, the expected curvature is 30 degrees. Real Avena bioassays are linear only up to about 30 degrees, above which the coleoptile saturates; Went's quantitative work was carefully designed to stay within this linear range, and the assay became the standard for measuring auxin concentration until it was replaced by mass spectrometry and anti-IAA immunoassays in the 1970s.

Exercise 3 (medium, numeric).

Polar auxin transport in an oat coleoptile moves at about 7 mm per hour. If you apply a small droplet of radiolabelled IAA to a point on the stem and measure radioactivity at a point 14 mm basal to the application site, what is the expected arrival time for the first detectable signal, in hours? Give the transport rate in centimetres per hour as well.

Hint

time = distance / rate. Convert millimetres to centimetres if needed.

Answer

time $= 14 mm /7 mm/hr = 2$ hours. The first detectable signal arrives about 2 hours after application. In centimetres per hour, the rate is $0.7$ cm/hr. Polar auxin transport is among the slowest intercellular signalling modes in biology — much slower than nerve conduction (metres per second) or even phloem transport (about 1 m/hr). The slow rate reflects the chemiosmotic cycle: each IAA molecule must diffuse across the cell, be pumped out basally by PIN, be protonated in the acidic apoplast, re-enter the next cell via AUX1, and repeat. This slow-but-directional transport is what makes auxin a morphogen — it builds spatial patterns over hours, not seconds.

Exercise 4 (medium, symbolic).

The Cholodny-Went model of phototropism predicts that under unilateral light, auxin redistributes laterally with fraction $r$ from the lit side to the shaded side. Write the predicted ratio of auxin concentration on the shaded side ( $C_{shade}$ ) to that on the lit side ( $C_{lit}$ ) in terms of $r$ . If Briggs's measurements give $r = 0.27$ under saturating blue light, compute the predicted ratio and confirm it falls in the experimental range of 1.5- to 2-fold.

Hint

The starting flux is $I_{0}$ on each side. With redistribution, $C_{shade} = I_{0} (1 + r)$ and $C_{lit} = I_{0} (1 - r)$ . The ratio is $(1 + r) / (1 - r)$ .

Answer

The ratio is

\frac{C _{shade}}{C _{lit}} = \frac{I _{0} ( 1 + r )}{I _{0} ( 1 - r )} = \frac{1 + r}{1 - r} .

For $r = 0.27$ :

\frac{1 + 0.27}{1 - 0.27} = \frac{1.27}{0.73} \approx 1.74.

So the shaded side has about 1.74 times the auxin concentration of the lit side, well within the experimental range of 1.5- to 2-fold reported by Briggs and subsequently confirmed by radiolabelled-IAA measurements. This ratio drives the differential elongation that bends the coleoptile: with the growth rate approximately linear in auxin in the sub-saturating regime, the shaded side elongates about 74 percent faster than the lit side over the response window, producing the curvature.

Exercise 5 (medium, multiple choice).

Which statement about the Green Revolution semi-dwarf wheat is correct?

A. The rht1 and rht2 mutations increase gibberellin synthesis, making the plant grow faster. B. The rht1 and rht2 mutations are in DELLA-domain repressors that reduce gibberellin signalling, shortening the stem. C. The dwarfing is caused by an ethylene receptor mutation that prevents stem elongation. D. The dwarfing is caused by loss of auxin transport, preventing apical dominance.

Hint

Gibberellin normally promotes stem elongation by triggering removal of DELLA repressors. A mutation that makes the repressor resist gibberellin-driven degradation keeps stems short.

Answer

B. The rht1 locus on chromosome 4B and rht2 on chromosome 4D encode DELLA-domain proteins (the wheat orthologues of Arabidopsis GAI/RGA). The wild-type DELLA repressor is degraded upon gibberellin binding to GID1, allowing growth. The rht1 and rht2 mutations alter the DELLA domain so the repressor resists gibberellin-induced degradation; signalling stays partly off, and stem internodes elongate less. Hedden and Thomas (2012, J. Exp. Bot. 63:433) showed that the rht alleles reduce gibberellin responsiveness rather than gibberellin synthesis — the plant still makes GA1, but the cells cannot fully respond. The shorter, stiffer stem does not lodge under heavy grain or high fertiliser input.

Exercise 6 (medium, symbolic).

The ABA-mediated stomatal closure pathway proceeds: ABA binds PYR/PYL/RCAR receptors, which sequesters the PP2C phosphatase (ABI1/ABI2), releasing SnRK2 kinases (OST1) from dephosphorylation; active SnRK2 phosphorylates the SLAC1 anion channel, which opens and releases anions from the guard cell, depolarising the membrane and driving K+ efflux through GORK channels; water follows, turgor drops, and the stomatal pore closes. Write this as a sign-consistent cascade and identify the rate-limiting step under moderate drought. For each level, state whether doubling ABA concentration increases (+) or decreases (-) the activity.

Hint

ABA binding to PYR/PYL/RCAR sequesters PP2C (the negative regulator). Removing the negative regulator frees SnRK2 to phosphorylate SLAC1.

Answer

Cascade, doubling ABA:

Step	ABA up, effect	Sign
PP2C activity (free, active on SnRK2)	down (sequestered by ABA-bound PYR/PYL)	-
SnRK2 activity	up (less dephosphorylation)	+
SLAC1 channel open probability	up (phosphorylated by SnRK2)	+
Anion and K+ efflux from guard cell	up	+
Guard-cell turgor	down	-
Stomatal aperture	down	-

The rate-limiting step under moderate drought is ABA biosynthesis in the root vasculature via NCED3 (the 9-cis-epoxycarotenoid dioxygenase). Root-sourced ABA is then transported in the xylem to the leaf, where it acts on guard cells. Under drought severe enough to trigger leaf-local ABA biosynthesis, the rate-limiting step shifts to ABA perception (PYR/PYL receptor abundance). The chemical logic of the cascade — receptor, then inhibitor-of-inhibitor, then kinase, then channel, then ion flux, then turgor — is what makes the closure response fast (minutes) despite operating on gene-expression timescales for the ABA-synthesis side.

Exercise 7 (hard, symbolic).

Polar auxin transport via the chemiosmotic PIN cycle. The basal-localised PIN efflux carrier cycles between the plasma membrane and endosomes with first-order exocytosis rate $k_{on}$ and endocytosis rate $k_{off}$ . At steady state, the plasma-membrane PIN fraction is $f = k_{on} / (k_{on} + k_{off})$ . The net cell-to-cell polar transport velocity $v = γ f$ where $γ$ bundles the IAAH-influx and IAA-anion-efflux rate constants.

(a) Show that the PIN-endocytosis inhibitor TIBA (2,3,5-triiodobenzoic acid, which lowers $k_{on}$ ) reduces polar transport velocity, and compute the sensitivity $d v / d k_{on}$ at the wild-type operating point $k_{on} = k_{off}$ .

(b) Brefeldin A (BFA) at 10 micromolar reduces $f$ from 0.8 (wild-type) to 0.2. By what factor does polar auxin transport velocity change, and what is the predicted new velocity if wild-type is 7 mm/hr?

(c) Explain why the basal polarity of PIN localisation — rather than simply the abundance of PIN at the membrane — is what makes transport directional. What would happen if PIN were uniformly distributed on all faces of the cell?

Hint

For (a), express $v$ in terms of $f$ and note that $f$ is monotone in $k_{on}$ . For (b), take the ratio $v_{BFA} / v_{WT} = f_{BFA} / f_{WT}$ . For (c), think about what symmetric efflux would do to the net apical-to-basal flux.

Answer

(a) $v = γ f = γ k_{on} / (k_{on} + k_{off})$ , which is monotone increasing in $k_{on}$ . Lowering $k_{on}$ (TIBA's effect) therefore lowers $v$ . The sensitivity is $d v / d k_{on} = γ k_{off} / (k_{on} + k_{off})^{2}$ . At $k_{on} = k_{off}$ : $d v / d k_{on} = γ / (4 k_{on})$ , which is positive, confirming the monotonicity. For a 10 percent reduction in $k_{on}$ near this operating point, $v$ drops by about 2.5 percent — a modest but measurable effect, consistent with TIBA requiring concentrations in the tens of micromolar to substantially inhibit transport.

(b) $v_{BFA} / v_{WT} = f_{BFA} / f_{WT} = 0.2/0.8 = 0.25$ . The transport velocity drops to 25 percent of wild-type: $7 \times 0.25 \approx 1.75$ mm/hr. Steinmann, Geldner and colleagues (1999) and Petrasek and colleagues (2006) showed that BFA at this concentration collapses PIN into intracellular aggregates and abolishes nearly all polar auxin transport in root assays, matching the 4-fold prediction.

(c) Directional transport requires that PIN be localised predominantly to the basal face of each cell. If PIN were uniformly distributed on all faces, auxin would efflux symmetrically from every face, each cell would act as an omnidirectional source, and no net polar (apical-to-basal) flux would build up across a file of cells. The basal localisation — established and maintained by the GNOM ARF-GEF-dependent exocytosis pathway — is what converts a chemiosmotic pump into a directional transporter. This is the reason auxin, uniquely among plant hormones, functions as a morphogen: its directional transport encodes positional information along the whole plant axis.

Exercise 8 (hard, symbolic).

The acid-growth hypothesis (Rayle and Cleland 1970; Hager 1971): auxin activates plasma-membrane H+-ATPases, acidifying the cell wall (apoplast); the lower pH activates wall-loosening enzymes called expansins that break load-bearing bonds, reducing the cell-wall yield threshold and permitting cell elongation. The Lockhart equation for cell expansion (Lockhart 1965) is $(1/ L) (d L / d t) = m (Ψ_{p} - Y)$ when $Ψ_{p} > Y$ , and zero otherwise, where $m$ is wall extensibility, $Ψ_{p}$ is turgor pressure, and $Y$ is the wall yield threshold. Let $Y = Y_{0} - α E$ with $α > 0$ , and let $E = E (A)$ be an increasing function of H+-ATPase activity $A$ , which is itself activated by auxin. Show that auxin-induced H+-ATPase activation increases elongation rate via the expansin term, and predict what happens to auxin-driven growth in an expansin-knockdown mutant ( $α \to 0$ ).

Hint

Substitute $Y = Y_{0} - α E$ into the Lockhart equation. Argue that auxin monotonically increases $A$ , which increases $E$ , which decreases $Y$ , which increases $d L / d t$ . Then examine the limit $α \to 0$ .

Answer

Substituting $Y = Y_{0} - α E (A)$ into the Lockhart equation:

\frac{1}{L} \frac{d L}{d t} = m [Ψ_{p} - Y_{0} + α E (A (auxin))] .

This is monotone increasing in auxin concentration (in the regime $Ψ_{p} > Y$ , i.e. when the bracket is positive). The auxin effect is mediated entirely through the $α E$ term: increasing auxin raises $A$ (H+-ATPase phosphorylation at Thr-947 via the TIR1-Aux/IAA-SAUR cascade), which raises $E$ (expansin activation by apoplastic acidification), which lowers $Y$ (the yield threshold), which raises the growth rate.

In an expansin-knockdown mutant ( $α \to 0$ ), the equation reduces to

\frac{1}{L} \frac{d L}{d t} = m (Ψ_{p} - Y_{0}),

which is independent of auxin. The cell elongates at its basal rate, set by turgor and the unmodified yield threshold. If $Ψ_{p}$ is only marginally above $Y_{0}$ (the usual case in growing tissue), the basal rate is small and auxin-driven growth is lost. Cosgrove and colleagues (Cosgrove 2000, Nature 407:321; Cosgrove 2016) confirmed this prediction by isolating the alpha-expansin and beta-expansin families and showing that antibodies against expansins block auxin-induced growth. The acid-growth mechanism is the molecular link between auxin signalling and the biophysics of cell expansion, and it generalises to every organ whose shape is set by turgor-driven cell expansion (root hairs, pollen tubes, xylem vessels).

Advanced results Master

Theorem 1 (Darwin and Darwin 1880 — the coleoptile tip perceives unilateral light; a diffusible signal mediates the bending). In The Power of Movement in Plants (John Murray, London, 1880), Charles and Francis Darwin reported that decapitating or capping the tip of the Avena coleoptile abolishes phototropic bending, while illuminating the tip alone (with the lower coleoptile darkened) gives normal bending ^{[Darwin 1880]}. The conclusion — that some influence generated in the upper part is transmitted to the lower part — opened the field of chemical signalling in plants. The Darwin experiments established, fifty years before the molecule was named, the conceptual framework for the hormone: a substance made in one tissue, transported a short distance, and active on a different tissue.

Theorem 2 (Went 1928 — auxin isolated by agar-block diffusion; the Avena curvature bioassay quantifies hormone concentration). Frits Went in Utrecht placed decapitated Avena coleoptile tips on agar blocks, collected the diffusate, and applied the block asymmetrically to a decapitated coleoptile in the dark ^{[Went 1928]}. The curvature obtained was proportional to the number of tips and the duration of diffusion — establishing that the signal was a chemical that could be collected, diluted, and dosed. Went named the substance auxin (from the Greek auxein, to grow). The active principle was identified as indole-3-acetic acid (IAA) by Kogl, Haagen-Smit and Erxleben in 1934 (Hoppe-Seyler's Z. 228:90). The Avena bioassay — one degree of curvature per unit — was the quantitative foundation of auxin research for forty years.

Theorem 3 (Kurosawa 1926 — gibberellin discovered as a fungal metabolite causing bakanae disease in rice). Eiichi Kurosawa in Japan showed that the "foolish seedling" disease of rice (elongated, spindly, etiolated seedlings) was caused by a substance secreted by the fungus Gibberella fujikuroi (anamorph Fusarium fujikuroi) into the culture medium ^{[Kurosawa 1926]}. Yabuta and Sumiki isolated the active compounds — the gibberellins — in 1938 (J. Agric. Chem. Soc. Japan 14:1526). The crop-genetics cross-reference: Borlaug's dwarf wheat (1944-1970) exploits reduced gibberellin signalling. Hedden and Thomas (2012, J. Exp. Bot. 63:433) showed that the rht1 and rht2 mutations of bread wheat are in DELLA-domain repressor genes (orthologues of Arabidopsis GAI/RGA) that resist gibberellin-induced degradation, reducing stem responsiveness to GA1 — the molecular basis of the Green Revolution.

Theorem 4 (Skoog and Miller 1955 — kinetin and the cytokinin-auxin ratio controls morphogenesis in tobacco callus). Folke Skoog and Carlos Miller at Wisconsin, working with tobacco-pith tissue cultures, showed that the adenine derivative kinetin (6-furfurylaminopurine, isolated from autoclaved herring-sperm DNA) promotes cell division ^{[Skoog-Miller 1955]}. The ratio of auxin to cytokinin determines the developmental fate of the callus: high cytokinin-to-auxin gives shoots, high auxin-to-cytokinin gives roots, and intermediate ratios give undifferentiated callus. Skoog and Miller (1957, Symp. Soc. Exp. Biol. 11:118) codified the full ratio-morphogenesis map. The discovery founded the field of plant tissue culture and is the technological basis of modern plant regeneration from single cells, including the Agrobacterium-mediated transformation pipeline used for every transgenic crop.

Theorem 5 (Neljubow 1901 — ethylene identified as the active component of illuminating gas that causes the triple response in pea seedlings). Dimitry Neljubow in St Petersburg showed that the growth response of dark-grown pea seedlings in laboratory air contaminated with coal gas — epinastic bending of the plumular hook, radial swelling of the hypocotyl, and horizontal growth — was caused by ethylene (C2H4), a trace component of illuminating gas ^{[Neljubow 1901]}. Gane (1934, Nature 134:1008) demonstrated that plants themselves produce ethylene. The climacteric fruits (apple, banana, tomato, avocado) were shown by Kidd and West in the 1930s to produce a burst of ethylene at the onset of ripening. The Burg and Burg gas-chromatography method (1965, Biochim. Biophys. Acta) brought ethylene measurement to physiologically relevant concentrations and enabled the quantitative physiology era.

Theorem 6 (Addicott 1963 — abscisic acid isolated as the hormone of abscission and dormancy). Frederick Addicott and colleagues at UC Davis isolated a substance that accelerates cotton-fruit abscission — naming it "abscisin II" — and a separate group led by Philip Wareing in Aberystwyth isolated a substance promoting birch bud dormancy, called "dormin" ^{[Addicott 1963]}. The two proved to be the same molecule, (S)-(+)-abscisic acid (ABA), a C15 sesquiterpenoid apocarotenoid. Ohkuma, Lyon and Addicott (1963, Science 142:1592) and Cornforth, Milborrow and Ryback (1965, Nature 205:1269) established the absolute configuration. ABA's role in stomatal closure under drought was established by Mittelheuser and Van Steveninck (1969, Nature); the molecular mechanism — PYR/PYL/RCAR receptor family releasing PP2C from SnRK2 — was resolved by Cutler, McCourt, Grill and colleagues in 2009 (Ma et al., Science 324:1068; Park et al., Science 324:1068).

Theorem 7 (Bleecker, Estelle, Kende and Somerville 1988 — the ethylene receptor ETR1 and the Arabidopsis mutant-screen paradigm). The isolation of the ethylene-insensitive Arabidopsis mutant etr1 by Bleecker, Estelle, Somerville and Kende (1988, Science 241:1086) identified ETR1 as a membrane-bound receptor that is a negative regulator of the ethylene response ^{[Bleecker-Kende 2000]}. Ethylene binding to ETR1 de-represses the pathway: in air, ETR1 actively suppresses ethylene responses via the CTR1 kinase (Kieber, Ecker and colleagues 1993, Cell 72:427); binding ethylene inactivates ETR1, releases CTR1, and allows the EIN2-EIN3 cascade to drive ethylene-responsive gene expression. The Arabidopsis framework — genetic screen for insensitive mutants, clone the gene, identify the receptor, reconstruct the signalling pathway — was then applied to every other hormone: TIR1 (auxin, Dharmasiri 2005), GID1 (gibberellin, Ueguchi-Tanaka 2005), PYR1 (ABA, Ma and Park 2009), BRI1 (brassinosteroid, Li and Chory 1997). The 2000 publication of the Arabidopsis genome (AGI, Nature 408:796) enabled the systematic reverse-genetics era.

Theorem 8 (Borlaug 1944-1970 — the Green Revolution: reduced-height wheat and the integration of plant hormone biology into global agriculture). Norman Borlaug, working for the Rockefeller Foundation in Mexico from 1944, crossed the Japanese Norin-10 dwarf wheat (carrying rht1 and rht2) with Mexican rust-resistant varieties, selected for day-length insensitivity, and developed semi-dwarf lines that yielded two to three times more grain per hectare than traditional tall varieties under intensive fertiliser ^{[Borlaug 1970]}. The introduction of these lines into India and Pakistan in 1965-1968 averted mass famine in both countries; Borlaug received the 1970 Nobel Peace Prize. The rht1 and rht2 alleles are in DELLA-domain gibberellin-signalling repressors and reduce stem elongation responsiveness to endogenous GA1 (Hedden and Thomas 2012) — the molecular-genetic foundation of the Green Revolution. The semi-dwarf trait has since been engineered into rice (sd1, a gibberellin-biosynthesis mutation, IR8 1966) and is now in essentially every commercial small-grain cultivar worldwide.

Synthesis. The seven theorems trace the canonical arc of plant-hormone biology from 1880 to 2009, and the foundational reason the field resolved so completely is the convergence of three forces: the Darwin-Went experimental tradition of diffusible-chemical signalling, the Arabidopsis molecular-genetics era that assigned every hormone a named receptor, and the Borlaug crop-genetics tradition that converted hormone biology into food supply. The central insight is that a small number of small molecules (IAA, GA1, trans-zeatin, ethylene, ABA) carry the entire developmental programme of a sessile organism that cannot move to escape its environment — putting these together identifies plant development with a chemical-readout problem in which the same hormone is re-used across organs and across the life cycle, and the bridge is the receptor-signalling cassette (TIR1, GID1, AHK, ETR1, PYR/PYL) that converts a small-molecule input into a transcriptional output.

This pattern generalises: every plant hormone receptor discovered since 1988 has followed the Arabidopsis mutant-screen paradigm, and the pattern recurs in the modern hormone additions (brassinosteroids via BRI1, Li and Chory 1997; strigolactones via D14, Umehara 2008; jasmonate via COI1, Xie 1998). The nine-hormone framework appears again in 20.05.05 evo-devo where the auxin-patterning cassette is deeply homologous across the plant and animal kingdoms, and the same chemical-signalling logic builds toward 18.12.02 where stomatal aperture is the central control variable of the photosynthesis-transpiration compromise. The bridge is the conserved architecture of hormone signalling — a small molecule, a specific receptor, a transcriptional output, and a tissue-context-dependent interpretation — and the foundational reason plant hormones are the cleanest system in all of developmental biology is exactly that the inputs and outputs are molecularly enumerable.

Full proof set Master

Proposition 1 (the chemiosmotic basis of polar auxin transport — Rubery and Sheldrake 1974, Raven 1975). The pH-partition mechanism combined with basal localisation of the PIN efflux carrier is sufficient to produce directional, cell-to-cell transport of indole-3-acetic acid against a concentration gradient. Let the cytoplasmic pH be $pH_{c} \approx 7.0$ and the apoplastic pH be $pH_{a} \approx 5.5$ . IAA has $p K_{a} \approx 4.7$ , so the ratio of protonated (membrane-permeant) IAAH to anionic (membrane-impermeant) IAA anion at pH $p$ is $[IAAH] / [IAA^{-}] = 1 0^{p K_{a} - p}$ . The intracellular fraction of IAAH is $1 0^{4.7 - 7.0} \approx 0.002$ ; the apoplastic fraction is $1 0^{4.7 - 5.5} \approx 0.16$ . Polar transport arises from four constraints acting in concert.

Proof. The four-step argument:

(i) Influx by protonation. In the apoplast at pH 5.5, about 16 percent of total IAA is in the protonated, membrane-permeant IAAH form. IAAH diffuses passively across the plasma membrane into the cytoplasm at pH 7.0, where only about 0.2 percent is protonated. The proton gradient therefore traps IAA anion inside the cell — the same chemiosmotic logic that powers bacterial lactose uptake and mitochondrial ATP synthesis. The AUX1/LAX family of H+-IAA symporters augments this passive route in tissues requiring high auxin influx.

(ii) Dissipation is anion-flux limited. Once inside, the IAA anion cannot passively cross back. Efflux requires the PIN family of transporters (PIN1 through PIN8 in Arabidopsis), which carry the IAA anion across the plasma membrane.

(iii) Basal polarity of PIN. PIN proteins recycle between endosomal compartments and the plasma membrane via the BFA-sensitive ARF-GEF GNOM. At steady state, in auxin-transporting cells, PIN is localised predominantly to the basal membrane (the membrane facing the root). This basal polarity is the directional bias.

(iv) Net polar transport. Combining (i) through (iii): IAA enters from the apoplast preferentially at the apical face (where apoplastic IAAH is delivered from the cell above), is trapped as IAA anion, and effluxes via basal PIN to the apoplast below. The cell acts as a one-way valve. Over a file of $N$ cells, the bulk flux is strictly basal (shoot-to-root).

The net velocity is limited by PIN recycling dynamics (Steinmann, Geldner, Grebe and colleagues, Nature 1999; Petrasek and colleagues, Science 2006), and the system transports IAA against a concentration gradient because the energy input — the plasma-membrane H+-ATPase maintaining the pH gradient — is continuously supplied. TIBA and NPA (1-N-naphthylphthalamic acid) inhibit the pathway by interfering with PIN cycling (Noh and Murphy, Plant Cell 2001). $□$

The chemiosmotic model is the foundational reason auxin is the only plant hormone with directional, cell-to-cell transport, and the central insight explaining why auxin functions as a morphogen — a molecule whose spatial distribution encodes positional information — a role no other plant hormone fulfils.

Proposition 2 (the ABA-PYR/PYL-PP2C-SnRK2-SLAC1 stomatal-closure cascade — Cutler, McCourt, Grill 2009). In the guard cell, ABA binds a PYR/PYL/RCAR receptor, which binds and inactivates the PP2C phosphatase ABI1/ABI2; active SnRK2 kinases (OST1 in Arabidopsis), freed from PP2C-mediated dephosphorylation, phosphorylate the SLAC1 anion channel; SLAC1 opens and releases chloride and malate dianion from the guard cell, depolarising the membrane; outward-rectifying K+ channels (GORK) open; water follows osmotically; turgor drops; the stomatal pore closes.

Proof. The logic of the pathway is an inhibitor-of-an-inhibitor-of-an-activator:

Level	Without ABA	With ABA bound
PYR/PYL/RCAR	unbound, open conformation	bound, closed — PP2C-binding competent
PP2C (ABI1/ABI2)	active, dephosphorylates SnRK2	sequestered by PYR/PYL, inactive
SnRK2 (OST1)	dephosphorylated, inactive	autophosphorylated, active
SLAC1 channel	closed	phosphorylated, open
Anion flux (chloride, malate)	minimal	efflux, depolarisation
K+ flux (GORK)	minimal	efflux
Turgor	high	low
Pore	open	closed

The molecular-kinetic argument: ABA affinity for PYR/PYL is sub-micromolar ( $K_{d} \approx 0.5$ to $1 μ M$ ); the root xylem delivers ABA at concentrations of $0.1$ to $10 μ M$ under moderate-to-severe drought. PYR/PYL-PP2C binding follows mass action with 2:1 stoichiometry (two PYL dimers to one PP2C), creating a sensitive switch rather than a graded response. SnRK2/OST1 phosphorylation of SLAC1 follows Michaelis-Menten kinetics; once a fraction of SLAC1 is phosphorylated, the anion efflux depolarises the membrane past the GORK activation threshold, producing a rapid K+ efflux and a near-binary drop in turgor. Closure is complete within 10-20 minutes of ABA application to a guard cell — fast enough to limit water loss within the time scale of midday vapour-pressure deficit changes. Sirichandra, Turk, and colleagues (2009, Plant Cell) and Brandt, Pozzer and Schroeder (2022, Nat. Plants) provide the full kinetic accounting. $□$

The ABA cascade is the molecular basis of the stomatal drought response introduced in 18.12.01, and the inhibitor-of-inhibitor architecture — receptor, then phosphatase, then kinase, then channel — generalises to several other plant signalling pathways, including the immune-response cascades triggered by pattern-recognition receptors.

Connections Master

Plant physiology — transport, photosynthesis, hormones, and stress 18.12.01. The chapter survey introduces the integrated-physiology framework: water and sugar transport, photosynthesis, abiotic and biotic stress. The current unit deepens that framework at the level of the signalling molecules that coordinate every organ-level decision — auxin for vascular patterning and apical dominance, ABA for stomatal drought response, ethylene for ripening and abscission. The peer's stomatal-turgor treatment is the substrate on which the ABA cascade acts; the current unit supplies the receptor-to-channel pathway.
Photosynthesis pathways (C3/C4/CAM) and plant water relations 18.12.02. Stomatal aperture is the single control variable that mediates the photosynthesis-transpiration trade-off, and ABA is the hormone that closes stomata. The downstream specialisation in 18.12.02 treats the Cowan-Farquhar optimisation of stomatal conductance; the current unit provides the molecular mechanism that executes the optimiser's decision. Cross-reference flows both ways — water-stress physiology defines the input, and the ABA-SLAC1 cascade is the actuator.
Evo-devo: evolutionary developmental biology, deep homology, and the genetic tool-kit 20.05.05. Plant and animal developmental biology share a deeper chemical-signalling logic than was appreciated until the genomic era: auxin patterning of the plant axis and Wnt patterning of the animal axis both use a concentration gradient to encode positional information. The cross-domain comparison in 20.05.05 places the auxin-TIR1 system in the broader context of the developmental-genetic tool-kit that is deeply conserved across eukaryotes. The current unit provides the molecular detail that the evo-devo survey references.
Nutrition: macronutrients, micronutrients, and diet 35.04.01. The Green Revolution sits at the intersection of plant hormone biology and human nutrition. The crop yields that feed the global population depend on rht1/rht2 gibberellin-signalling mutations; the iodine, selenium, zinc, and iron micronutrients surveyed in 35.04.01 are the substrates whose dietary sufficiency is enabled by adequate grain supply. Biofortification (Golden Rice provitamin-A engineering, IRRI high-zinc rice) extends the same plant-hormone-driven yield platform into micronutrient-delivery vehicles.

Historical & philosophical context Master

The field of plant hormones begins with Charles and Francis Darwin's 1880 monograph The Power of Movement in Plants (John Murray, London), where the capped-coleoptile experiments on Avena sativa established that the tip of the seedling shoot perceives light and transmits a signal to the lower zone where bending occurs ^{[Darwin 1880]}. The Darwins themselves did not name the substance — they wrote only of an influence generated in the upper part and transmitted to the lower part — but the conceptual framework (signal made in one tissue, transported to another, active at a distance) is theirs. Boysen-Jensen (1910, 1913) and Paal (1914, 1919) extended the work by showing that the signal crosses gelatin but not mica barriers and is asymmetrically distributed.

Frits Went, working in his father F. A. F. C. Went's laboratory in Utrecht, isolated the signal into agar blocks in 1926-1928 and named it auxin ^{[Went 1928]}. Kogl, Haagen-Smit and Erxleben identified the active molecule as indole-3-acetic acid (IAA) in 1934. The Avena curvature bioassay — one degree of curvature per unit of auxin activity — was the quantitative foundation of auxin research for forty years and was the prototype for every subsequent hormone bioassay. The other four classical hormones followed: Kurosawa's 1926 identification of fungal gibberellin from Gibberella fujikuroi (Yabuta and Sumiki 1938 isolated the pure compounds); Skoog and Miller's 1955 identification of kinetin from autoclaved herring-sperm DNA and the codification of the auxin-cytokinin morphogenesis map; Neljubow's 1901 attribution of the pea-seedling triple response to ethylene in illuminating gas (Gane 1934 confirmed plants produce ethylene endogenously); Addicott's 1963 isolation of abscisin II, which proved identical to Wareing's dormin and was renamed abscisic acid.

The applied lineage converges on Norman Borlaug's 1944-1970 programme in Mexico. Crossing the Japanese Norin-10 dwarf wheat with Mexican varieties and selecting for photoperiod insensitivity, Borlaug built semi-dwarf lines whose stems did not lodge under heavy grain or fertiliser — the rht1 and rht2 alleles, identified by Hedden, Thomas and colleagues in 2012 as DELLA-domain gibberellin-signalling mutations, were the molecular basis ^{[Borlaug 1970]}. The introduction of Borlaug's varieties into India and Pakistan in 1965-1968 averted mass famine; Borlaug received the 1970 Nobel Peace Prize. The parallel IR8 rice (1966, IRRI), carrying the sd1 gibberellin-biosynthesis mutation, did the same for rice.

The molecular-receptor era opened with Bleecker, Estelle, Kende and Somerville's 1988 isolation of the ethylene-insensitive etr1 mutant in Arabidopsis, which established ETR1 as a negative-regulator ethylene receptor ^{[Bleecker-Kende 2000]} and the Arabidopsis mutant-screen paradigm that was then applied to every other hormone: TIR1 for auxin (Dharmasiri 2005), GID1 for gibberellin (Ueguchi-Tanaka 2005), PYR/PYL/RCAR for ABA (Cutler-McCourt-Grill 2009), BRI1 for brassinosteroid (Li and Chory 1997), COI1 for jasmonate (Xie 1998), and D14 for strigolactones (Umehara 2008). The 2000 publication of the Arabidopsis genome (AGI, Nature 408:796) enabled the systematic reverse-genetics era.

Bibliography Master

Primary literature.

@book{DarwinDarwin1880,
  author = {Darwin, Charles and Darwin, Francis},
  title = {The Power of Movement in Plants},
  publisher = {John Murray},
  address = {London},
  year = {1880},
}

@article{Went1928,
  author = {Went, F. W.},
  title = {Wuchsstoff und Wachstum},
  journal = {Rec. Trav. Bot. N\'eerl.},
  volume = {25},
  year = {1928},
  pages = {1--116},
}

@article{Kurosawa1926,
  author = {Kurosawa, E.},
  title = {Experimental studies on the nature of the substance secreted by the ``bakanae'' fungus},
  journal = {Trans. Nat. Hist. Soc. Formosa},
  volume = {16},
  year = {1926},
  pages = {213--227},
}

@article{Neljubow1901,
  author = {Neljubow, D.},
  title = {Ueber die horizontale Nutation der Stengel von {Pisum sativum} und einiger anderen Pflanzen},
  journal = {Beih. Bot. Centralbl.},
  volume = {10},
  year = {1901},
  pages = {128--139},
}

@article{SkoogMiller1957,
  author = {Skoog, F. and Miller, C. O.},
  title = {Chemical regulation of growth and organ formation in plant tissues cultured {in vitro}},
  journal = {Symp. Soc. Exp. Biol.},
  volume = {11},
  year = {1957},
  pages = {118--131},
}

@article{Miller1955,
  author = {Miller, C. O. and Skoog, F. and Okumura, F. S. and von Saltza, M. H. and Strong, F. M.},
  title = {Structure and synthesis of kinetin},
  journal = {J. Am. Chem. Soc.},
  volume = {77},
  year = {1955},
  pages = {2662--2663},
}

@article{OhkumaAddicott1963,
  author = {Ohkuma, K. and Lyon, J. L. and Addicott, F. T. and Smith, O. E.},
  title = {Abscisin {II}, an abscission-accelerating substance from young cotton fruit},
  journal = {Science},
  volume = {142},
  year = {1963},
  pages = {1592--1593},
}

@article{BleeckerKende1988,
  author = {Bleecker, A. B. and Estelle, M. A. and Somerville, C. and Kende, H.},
  title = {Insensitivity to ethylene conferred by a dominant mutation in {Arabidopsis thaliana}},
  journal = {Science},
  volume = {241},
  year = {1988},
  pages = {1086--1089},
}

@article{BleeckerKende2000,
  author = {Bleecker, A. B. and Kende, H.},
  title = {Ethylene: a gaseous signal molecule in plants},
  journal = {Annu. Rev. Cell Dev. Biol.},
  volume = {16},
  year = {2000},
  pages = {1--18},
}

@article{HeddenThomas2012,
  author = {Hedden, P. and Thomas, S. G.},
  title = {Gibberellin biosynthesis and its regulation},
  journal = {Biochem. J.},
  volume = {444},
  year = {2012},
  pages = {11--25},
}

@article{Dharmasiri2005,
  author = {Dharmasiri, N. and Dharmasiri, S. and Estelle, M.},
  title = {The {F-box} protein {TIR1} is an auxin receptor},
  journal = {Nature},
  volume = {435},
  year = {2005},
  pages = {441--445},
}

@article{Ma2009,
  author = {Ma, Y. and Szostkiewicz, I. and Korte, A. and Moes, D. and Yang, Y. and Christmann, A. and Grill, E.},
  title = {Regulators of {PP2C} phosphatase activity function as abscisic acid sensors},
  journal = {Science},
  volume = {324},
  year = {2009},
  pages = {1064--1068},
}

@article{Petrasek2006,
  author = {Petr\'asek, J. and Mravec, J. and Bouchard, R. and Blakeslee, J. J. and Abas, M. and Seifertov\'a, D. and Wisniewska, J. and Tadele, Z. and Kube\v{s}, M. and Covanov\'a, M. and others},
  title = {{PIN} proteins perform a rate-limiting function in cellular auxin efflux},
  journal = {Science},
  volume = {312},
  year = {2006},
  pages = {914--918},
}

@misc{Borlaug1970,
  author = {Borlaug, N. E.},
  title = {The Green Revolution, Peace and Humanity},
  howpublished = {Nobel Peace Prize lecture, Oslo, 11 December 1970},
  year = {1970},
}

Textbook and monograph.

@book{TaizZeiger2015,
  author = {Taiz, L. and Zeiger, E. and M{\o}ller, I. M. and Murphy, A.},
  title = {Plant Physiology and Development},
  edition = {6th},
  publisher = {Sinauer Associates},
  year = {2015},
}

@book{HopkinsHuner2009,
  author = {Hopkins, W. G. and H{\"u}ner, N. P. A.},
  title = {Introduction to Plant Physiology},
  edition = {4th},
  publisher = {Wiley},
  year = {2009},
}

@book{RavenEvertEichhorn2005,
  author = {Raven, P. H. and Evert, R. F. and Eichhorn, S. E.},
  title = {Biology of Plants},
  edition = {7th},
  publisher = {W. H. Freeman},
  year = {2005},
}

Prerequisites

18.12.01

Tier anchors

beginner: Raven P, Evert R, Eichhorn S 2005 Biology of Plants (Freeman) Ch. 37 'Regulation of Plant Growth'; Taiz, Zeiger, Moller & Murphy, Plant Physiology and Development 6e Ch. 23 introductory sections
intermediate: Taiz, Zeiger, Moller & Murphy, Plant Physiology and Development, 6th ed. (Sinauer, 2015), Ch. 23-26; Hopkins & Huner, Introduction to Plant Physiology 4e (Wiley, 2009), Ch. 17-19
master: Darwin & Darwin 1880 (Power of Movement in Plants); Went 1928 Rec. Trav. Bot. Neerl. 25:1; Kurosawa 1926; Skoog & Miller 1955/1957; Neljubow 1901; Ohkuma-Lyon-Addicott 1963 Science 142:1592; Bleecker-Estelle-Somerville-Kende 1988 Science 241:1086; Bleecker & Kende 2000 Annu. Rev. Cell Dev. Biol. 16:1; Hedden & Thomas 2012 Biochem. J. 444:11; Borlaug 1970 Nobel Peace Prize lecture; Dharmasiri 2005 Nature 435:441; Ma-Grill 2009 Science 324:1064

References

Darwin C. & Darwin F. - The Power of Movement in Plants · John Murray, London, 1880; coleoptile phototropism experiments, pp. 7-20, 472-479; first identification that the shoot tip senses light but the bending response occurs at a distance
Went F. W. - Wuchsstoff und Wachstum · Rec. Trav. Bot. Neerl. 25 (1928) 1-116; isolation of auxin by diffusion into agar blocks from Avena sativa coleoptile tips, and the Avena curvature bioassay
Kurosawa E. - Experimental studies on the nature of the substance secreted by the bakanae fungus · Trans. Nat. Hist. Soc. Formosa 16 (1926) 213-227; gibberellin from Gibberella fujikuroi causing foolish-seedling disease in rice
Skoog F. & Miller C. O. - Chemical regulation of growth and organ formation in plant tissues cultured in vitro · Symp. Soc. Exp. Biol. 11 (1957) 118-131; the auxin-cytokinin ratio determines organogenesis in tobacco callus
Neljubow D. - Ueber die horizontale Nutation der Stengel von Pisum sativum · Beih. Bot. Centralbl. 10 (1901) 128-139; ethylene identified as the active component of illuminating gas causing the triple response
Ohkuma K., Lyon J. L., Addicott F. T. & Smith O. E. - Abscisin II, an abscission-accelerating substance from young cotton fruit · Science 142 (1963) 1592-1593; isolation of abscisic acid
Bleecker A. B. & Kende H. - Ethylene: a gaseous signal molecule in plants · Annu. Rev. Cell Dev. Biol. 16 (2000) 1-18; the ETR1 receptor and the ethylene signal-transduction framework
Borlaug N. E. - The Green Revolution, Peace and Humanity · Nobel Peace Prize lecture, Oslo, 11 December 1970; the semi-dwarf wheat programme in Mexico 1944-1970
Taiz L., Zeiger E., Moller I. M. & Murphy A. - Plant Physiology and Development, 6th ed. · Sinauer, 2015, Ch. 23-26 (Hormones and signal transduction); canonical graduate reference for hormone chemistry, receptors, and developmental physiology
Hopkins W. G. & Huner N. P. A. - Introduction to Plant Physiology, 4th ed. · Wiley, 2009, Ch. 17-19 (Hormones and growth regulators); quantitative worked examples on the Avena bioassay, polar auxin transport, and GA signalling

Estimated time

beginner: 20m
intermediate: 45m
master: 85m