Plant Growth Regulators
Plants respond to the environment by:
Sending signals between different parts of the plant.
Tracking the time of day and the time of year.
Senseing and responding to gravity and direction of light, etc.
Responding to environmental cues by adjusting their growth
pattern and development.
These control systems evolved through interactions with the environment.
I. Hormones and Their Actions
A. Hormone - An organic compound produced by one part of an
organism that is translocated to other parts where in low
concentrations it triggers a response in target cells and
tissues.
B. Hormones control plant growth and development by affecting
division, elongation, and differentiation of cells.
1. Effects depend on site of action, stage of plant growth
and hormone concentration.
2. Reaction to hormones depends on hormonal balance (relative
concentration of one hormone compared with others).
3. The hormonal signal is amplified, perhaps by affecting
gene expression, enzyme activity, or membrane
properties.
C. The concept of differential target cell sensitivity to
hormones
1. Anthony Trewayas in the early 1980’s proposed that target
cell sensitivity was more important in determining
the effects of a hormone than it’s concentration within
the target cell.
2. Since that time it is now excepted that both target cell
sensitivity and hormone concentration are important in
the action of a hormone.
3. There are three parts of a hormonal response system:
a. The hormone must be present in sufficient quantities in
the target cells.
b. The hormone must be recognized by and bound tightly to
the target cells that respond to the hormone. This
action occurs through hormone-binding receptor
proteins in the membranes of the plant cell. It
appears that the plasma membrane is most important,
but the tonoplast and endoplasmic reticulum also have
been noted to have hormone-binding receptor
proteins.
c. The receptor protein must cause other metabolic changes
that lead to amplification of the hormonal signal.
These receptor proteins function by changing their
conformation after they are activated by the hormone.
The altered conformation then allows the receptor
proteins to activate other proteins or nucleic acids
(DNA or RNA)
D. It has been found that hormones effect gene activity.
1. This gene activation can result in a large degree of
amplification of the hormonal signal.
2. There are various controls points at which a hormone could
affect the expression of a gene:
a. Transcription: DNA to RNA
b. Translation: RNA to Protein
c. Post-translational modification of proteins.
E. Sites of hormonal activity usually involve membranes:
1. Hormones act first in the plasma membrane where receptor
proteins are located.
2. In animals there are two such receptor protein process
that have been identified. Each one involves a second-
messenger.
a. Cyclic-AMP (cAMP): involves the enzyme Adenylate
cyclase. Adenylate cyclase uses ATP to form cAMP.
cAMP is then involved in activation of protein
kinases. Protein kinases function by activating or
inactivating other enzymes by a process of
phosphorylation. Thus far, the cyclic-AMP process has
not been found to be important in plants.
b. Inositol Triphosphate (IP3): involves the binding of
the hormone to a receptor protein in the plasma
membrane of the target cell. The bound hormone-
receptor complex then activates phospholipase c (PLC).
Phospholipase c hydrolyzes phosphoinositol (a
nonabundant membrane phospholipid) into inositol-
1,4,5-trisphosphate (IP3) and diacylglycerol (DAG).
Both of these compound that cause a cascade effect.
(1) IP3 is water-soluble and moves to the vacuole and
causes the release of Ca2+ into the cytosol.
[NOTE: in animals IP3 stimulates Ca2+ release from
the endoplasmic reticulum.] These increased Ca2+
levels in the cytosol causes activation of enzymes,
including several different kinds of protein
kinases. When Ca2+ concentration rise in the
cytosol, four Ca2+ combine to form a chelate with
calmodulin. This Ca-calmodulin complex can
activate other enzymes. such as protein kinases,
NAD+ kinase. One enzyme that is activated is
ATPase which functions to transfer excess Ca2+ out
of the cell.
(2) DAG is not water-soluble, so it functions within the
plasma membrane where it activates Protein Kinase c
(PKC). This kinase uses ATP to phosphorylate other
enzymes that regulate metabolism.
F. So far, five classes of plant hormones have been identified.
1. Auxin (such as IAA)
2. Gibberellins (such as GA,)
3. Cytokinins (such as kinetin)
4. Abscisic acid
5. Ethylene
II. Auxin
A. Auxin = A hormone that promotes elongation of young
developing stems or coleoptiles.
1. The term "Auxin" comes from the Greek auxin with means
"to increase". This terms was coined by Frits Went in
1926. Frits Went had been working as a graduate
student on the phototropic responses of coleoptiles in
response to auxin application.
2. Phototropism = Growth toward or away from light (e.g.
growth of a shoot toward light).
a. Results form differential growth of cells in opposite
sides of a shoot or, in the case of a grass seedling,
coleoptile.
b. Cells on the darker side elongate faster.
c. Experiments on phototropism led to the discovery of
auxin as a plant hormone.
3. Charles and Francis Darwin removed the tip of the
coleoptile from a grass seedling (or covered it with an
opaque cap) and it f ailed to grow toward light.
a. Concluded that the coleoptile tip was responsible for
sensing light, and, since the curvature occurs some
distance below the tip, the tip sends a signal to the
elongating region.
4. Peter Boysen-Jensen separated the tip from the remainder
of the coleoptile by a block of gelatin, preventing
cellular contact but allowing chemical diffusion.
a. Seedlings behaved normally.
b. If an impenetrable barrier was substituted, no
phototropic response occurs.
c. Demonstrated that the signal was a mobile substance.
5. F.W. Went removed the coleoptile tip, placed it on an agar
block, and then put the agar (without the tip) on
decapitated coleoptiles kept in the dark.
a. If block was placed off -center, the plant curved away
from the side with the block.
b. Concluded the agar block contained a chemical that
diffused into it from the coleoptile tip, and that
this chemical stimulated growth.
c. Went called this chemical an Auxin.
6 Auxin was purified and characterized by Kenneth Thimann.
B. Natural Auxin is a compound named indoleacetic acid (IAA).
1. There are three other compounds that are structurally
similar to IAA that also act as auxins:
a. 4-chloroindoleacetic acid (4-chloroIAA): found in young
seeds of legumes.
b. Phenylacetic acid (PAA): widespread and more abundant
than IAA.
c. Indolebutyric acid (IBA): found in corn leaves and many
dicots.
2. Auxin Precursors: indoleacetaldehyde, indoleacetonitrile,
and indole ethanol.
3. Synthetic Auxins: a-naphthalene acetic acid (NAA), 2,4-
dichlorophenoxyacetic acid (2,4-D), 2-methyl-4-
chlorophenoxyacetic acid (MCPA).
a. NAA: is used as an auxin source in tissue culture
b. 2,4-D is used as a herbicide on broadleaf (dicot) weeds
in narrowleaf (monocot) crops. It is especially
useful to eliminate broadleaf weeds in lawns.
Another related compound is 2,4,5-T. During the Viet
Nam Conflict ("WAR") 2,4-D and 2,4,5-T were the
active ingredients for Agent Orange. Since that time
the U.S. Environmental Protection Agency has forced
removal of 2,4,5-T from the market because it
contains dioxin (a mutagen and carcinogen) as a by-
product of manufacturing.
c. Other herbicides that are auxin derivatives are: MCPA,
Picloram, and Dicamba
d. The effect of these herbicides on broadleaf plants occur
by an alteration of DNA transcription and RNA
translation that disrupt enzymes needed for
coordination of plant growth. As a result plants
treated with these compounds respond by producing
twisted and deformed leaves, petioles, and stems.
C. The synthesis, concentration control, and degradation of
IAA.
1. IAA is structurally similar to tryptophan (an amino acid)
and it is indeed the precursor of IAA. The enzymes
necessary for the conversion of tryptophan to IAA are
found in young tissues such as meristems, growing leaves
and fruits. It is not surprising that auxin
concentrations are highest in these tissues.
2. Concentration control of auxin in plant tissues is achieved
by:
a. The rate of synthesis.
b. Temporary inactivation by conjugate formation, or what
has often been called bound auxin. There are
numerous IAA conjugates: peptide (indoleacetyl
aspartic acid, esters (IAA-inositol and IAA-
glucose). IAA can be released from these conjugates
by hydrolase enzymes.
c. Conjugates are storage forms of IAA, and are important
in the transport of IAA.
3. Degradation of IAA:
a. Oxidation by O2 and loss of the carboxyl group as CO2 to
form 3-methyleneoxindole. This reaction is
catalyzed by IAA oxidase. There are several IAA
oxidase isozymes which are all nearly identical to
the peroxidase that is involved in lignin synthesis.
Synthetic auxins and auxin conjugates are not
degraded by IAA oxidase.
b. Another pathway of degradation involves the oxidation of
carbon 2 in the heteroxylic ring to form oxindole-
3-acetic acid.
D. The transport of auxin in the plant.
1. IAA is translocated through parenchyma cells in contact
with vascular bundles. IAA will move through sieve
tubes if it is applied to the surface of a leaf that is
exporting sugars. But, the normal transport of IAA in
plant stems is along the petioles of the leaf to the
cells along the vascular bundles.
2. Auxin movement is slow, about 1 cm per hour. This,
however, is 10X faster than diffusion.
3. Polar Auxin transport requires metabolic energy.
a. IAA is actively transported down a stem by Auxin
carriers located on the basal ends of cells
(carriers are absent on the apical ends).
b. Even in root the transport is in an acropetal (apex-
seeking) direction.
c. Antiauxins such as 2,3,4-triiodobenzoic acid (TIBA) and
a-naphthylthalamic acid (NPA) inhibit this polar
transport.
4. Mechanism for polar transport of auxin:
a. Cells use plasma membrane ATPase to pump H+ from the
cytosol into cells walls. The lower pH of the cell
walls keeps the carboxyl group of auxin less
dissociated than in the cytosol. The noncharged auxin
moves from the cell wall into the cytosol by a
cotransport mechanism with H+.
b. Once inside the cytosol the higher pH causes the
carboxyl group on auxin to dissociate and become
negative. As the concentration of charged auxin
builds up, the outward flow becomes favored
thermodynamically.
c. Polar transport requires auxin to move out only at the
basal end of the cell. It is assumed that a carrier
transports auxin basipitally within the cell and then
transports it out into the cell wall, where the low pH
starts the cycle again.
d. Some flavonoids (quercetin, apigenin, kaempferol) have
been found to inhibitors of the basal transporter of
auxin.
e. Auxin transport is important for: (1) vascular cambium
activity in woody plants during the spring and early
summer, (2) differentiation of xylem and phloem in
leaf petioles, (3) stem cell growth, (4) lateral bud
inhibition.
E. Roots and their responses to auxins:
1. Auxin concentrations in roots are similar to other parts
of the plant.
2. Auxin inhibits root growth at low concentrations. For
many years it was thought that this was due to increased
ethylene production which is stimulated by increases in
auxin. Ethylene retards root and stem elongation. But,
recent research has shown that auxin inhibits growth of
roots by an unknown mechanism that is independent of
ethylene.
3. Roots can synthesize enough auxin for their growth. There
is probably a balance between growth of root and shoot
systems that is strongly influenced by auxin from the
stems. Auxin from the stems influences root initiation
and adventitious root development on stems.
F. Lateral-bud development and auxin effects:
1. Apical Dominance: the inhibitory influence the apical bud
exerts on the lateral (axillary) buds. This apical
dominance slows the development of the lateral buds. It
also causes lateral branches to grow horizontally. This
horizontal growth reduces shading of the lower branches
and thus increases photosynthetic productivity of the
plant.
2. The IAA concentration in lateral buds increases after the
plant is decapitated. This is contrary to what would be
predicted - one would suspect that auxin concentration
would decrease when the apical bud is removed.
3. Lateral buds have been found to be deficient in
cytokinins. There may be an interaction between these
two growth hormones.
4. Abscisic acid, ethylene, and gibberellins have also been
found to be important in apical dominance.
G. Auxin Mechanism of Action:
1. Growth requires water absorption, cells must maintain a
water potential more negative than that of the
surrounding solution. Cell walls of auxin-treated cells
yield more easily, so the pressure potential required
to force cell expansion is not as great as untreated
cells. Auxins cause wall loosening, the more rapidly
extensible or plastic nature of cell walls.
2. The most studied mechanism of action has been: the acid-
growth hypothesis that states that cell elongation is
due to stimulation of a proton pump which acidifies the
cell wall. Auxin treated cells pump H+ into the cell
walls, thus lowering the pH so that the wall loosens and
can grow faster.
a. Acidification activates enzymes that break the
crosslinks between the walls cellulose myofibrils.
b. This loosens the wall, allowing turgor pressure to
elongate the cell.
c. There is a difference between growth promotion of cells
caused by cytokinins and cell wall acidification.
Other growth hormones cause wall loosening and cell
expansion in some species by some unknown mechanism
3. Which cells respond to auxin?
a. Epidermal cells: these elongate in response to auxin
treatment.
b. Subepidermal cell layers (hypodermis, cortex, pith)
contain cells that are under pressure. These cells
are ready to elongate because of their internal
pressure. Elongation is restricted because
their cell wall polysaccharides are continuous with
those of the epidermal cells that are unable to
stretch. The subepidermal cell layer elongates just
enough to keep the epidermal cell walls under
tension. Auxins cause epidermal cell wall
polysaccharides to loosen and elongate. The
elongation of the epidermal cells is followed by the
elongation of the connecting subepidermal cells such
that the stem elongates in unison.
4. How do auxins control the cell responses:
a. Auxins have been found to cause rapid changes in genetic
activity.
b. Auxins change the kinds of proteins formed in the cell.
The main control seems to be at the level of
transcription.
c. Auxin works by binding to an auxin receptor protein
found mainly in the endoplasmic reticulum and to a
lesser extend in the plasma membrane. This receptor
protein is a dimer of two polypeptides of about 20 kDa
each.
III. Cytokinins
A. A Very Brief History of Cytokinin Discovery:
1913: Gottlieb Haberlandt first found a growth hormone that
stimulated cell division (cytokinesis) in plants. These
substances are now called cytokinins. In the 1940's
Johannes vanOverbeek found cytokinins in the endosperm of
immature coconuts. In the 1950's Folke Skoog and F.C.
Steward used this information about cytokinins in
endosperm in their plant tissue culture work. D.S.
Letham (1974) isolated two very active forms of
cytokinins, Zeatin and Zeatin-riboside, from the coconut
endosperm. Carlos Miller (1954) found a substance that
was named Kinetin, in aged or autoclaved herring-sperm
DNA. This work helped lead to the defining of the
structure of cytokinins.
B. Chemistry of Cytokinins:
1. Cytokinins are not found in DNA or breakdown products of
DNA, even though they are involved in cytokinesis. Some
cytokinins do occur in transfer-RNA and ribosomal-RNA.
2. Cytokinins have been found in seed plants, mosses, brown
and red algae, diatoms, fungi, bacteria, and primates.
More than 30 free and bound forms of cytokinins have
been identified. In pathogenic fungi and bacteria,
cytokinins influence the disease process. In non-
pathogenic fungi and bacteria cytokinins influence the
mutualistic relationship with plants (mycorrhizae and
root nodules).
3. Most common and physiologically active natural forms are:
zeatin, dihydrozeatin, isopentenyl adenine (IPA).
4. Synthetic cytokinins: Kinetin and benzyladenine (BA)
5. Cytokinin Structure:
a. Cytokinins can exists as free-bases or and nucleosides
or nucleotides
b. Substituted adenine compounds
C. Cytokinin metabolism:
1. Isopentenyl-AMP is the precursor of Cytokinins. It is
formed by the enzyme isopentenyl AMP synthase from
isopentenylpyrophosphate and AMP.
2. Cellular levels of cytokinins are influenced by their
degradation and conversion to inactive derivatives
(other than nucleosides and nucleotides). Cytokinins are
degraded by cytokinin oxidase. The most common
conjugates are glucose (cytokinin glucosides) or
alanine.
3. The cytokinin glucosides may be storage forms or transport
forms of cytokinins. The alanine conjugates are not
stored, but are formed irreversibly as removal products
of cytokinin. Conjugates represent physiologically
inactive cytokinins.
D. Sites of Cytokinin Synthesis and Transport:
1. Cytokinin levels are highest in young organs such as
seeds, fruits, young leaves, and root tips.
2. Roots tips are active in synthesis of cytokinins. The
cytokinins are transported from the root tips, through
the xylem, to all plant parts.
3. Shoot are also able to synthesize some of the cytokinins
they need.
4. Cytokinins are mainly transported through the xylem,
however, they have been identified in sieve tubes of the
phloem. For example, when the petiole of a mature leaf
is cut, cytokinins move to the base of the petiole
through the phloem.
E. Promotion of Cell Division and Organ Formation by
Cytokinins:
1. A high cytokinin-to-auxin ratio in tissue culture will
produce meristematic cells in callus culture. These
cells will give rise to buds, stems, and leaves. A low
cytokinin-to-auxin ratio will favor root formation.
2. Organogenesis: formation of shoots or adventitious roots
by callus culture.
Embryogenesis: formation of embryos by callus culture.
3. Agrobacterium tumefaciens (bacterium): contains the Ti
plasmids that codes for isopentenyl AMP synthase.
Infection of a plant with this bacterium will result in
tumorous outgrowths (galls) on stems called crown gall
disease.
F. Delay of senescence and increase of nutrient-sink activity
by cytokinins:
1. If a mature leaf is detached from the stem of a plant it
will lose chlorophyll, RNA, proteins, and lipids from
the chloroplast membrane system. This will cause the
leaf to turn yellow, a process associated with
senescence. If the leaf is treated with cytokinins,
this senescence process will be delayed.
2. Cytokinins maintain the integrity of the tonoplast
(vacuole) membrane. This is important since the vacuole
stores proteases that could hydrolyze proteins in the
cytoplasm and organelles, especially organelle
membranes.
3. Cytokinins are also able to protect membranes from
degradation by preventing oxidation of unsaturated fatty
acids. Cytokinins inhibit formation of or speed the
breakdown of free radicals (superoxide and hydroxy
radicals) that would normally attach the lipids in
membranes.
4. Cytokinins stimulate transport of solutes from older plant
parts to younger plant parts. Migration of solutes
occurs through the phloem. Young plant parts are able
to mobilize solutes towards themselves because they have
high cytokinin concentrations. Thus the young tissues
of a plant are "sinks" for solutes.
5. Some pathogenic fungi produce cytokinins in order to
mobilize nutrients from the plant to the fungi.
6. The ability of cytokinins to retard senescence has been
used in agriculture. Cytokinins are used to retard the
senescence of cut flowers and fresh vegetables.
Cytokinins increase the storage life of Brussels spouts
and celery (not done in the U.S.).
G. Promotion of lateral-bud development in dicots by
cytokinins:
1. Application of cytokinin to a lateral bud that is under
the control of a shoot apex will cause the lateral bud
to grow. It is not clear if this is what occurs in
nature.
H. Enhancement of cell expansion in dicot cotyledons and
leaves by cytokinins:
1. When dicot seeds germinate, they stay yellow (etiolated)
until they emerge above ground. When cotyledons are
exposed to light their growth increases as a response to
phytochrome and cytokinins. Growth is by cell expansion
caused by water uptake because the dry weight of the
cotyledons does not change.
I. The normal growth of stems and roots requires cytokinins
even though application of exogenous cytokinins sometimes
decreased elongation.
J. Promotion of chloroplast development and chlorophyll
synthesis by cytokinins:
1. Cytokinins enhance the development of etioplasts
(proplastids that eventually will form chloroplasts upon
maturation) into chloroplasts by promoting grana
formation and increasing the rate of chlorophyll
formation.
2. Cytokinins enhance the formation of one or more proteins
in the chloroplast membrane system to which chlorophyll
binds and is stabilized.
K. Mechanism of action for cytokinins:
1. It has been found that cytokinins may have a primary
effect that is followed by many secondary effects which
depend on the physiology of the target cell.
2. The hormonal signal is amplified by the cell.
3. Cytokinins promote RNA and enzyme formation.
4. Cytokinins promote cell division by decreasing the
transition time from G2 to mitosis by increasing the
rate of protein synthesis. It is well known that there
is a control point at the end of G2 which is controlled
by the stockpiling of enzymes and proteins that will be
need during mitosis. Benzyladenine (BA) may control DNA
synthesis since it causes a decrease in the length of
the S phase in the cell cycle.
5. Cytokinins also act on translation of mRNA. Cells treated
with cytokinins form large polysomes that aid in mRNA
translation.
6. Cytokinins also appear to effect mRNA levels by influences
in transcriptional control of some genes (turning on
some and turning off others). Cytokinins may also
affect the stability of mRNA.
7. Cytokinins have been reported to affect the amount of
mRNA:
a. Upregulation of chlorophyll a/b binding protein (part
of the LHCII thylakoid membrane)
b. Upregulation of small subunit or RuBisCo.
c. Downregulation of phytochrome (by cytokinins and red
light)
8. Cytokinins cause increased plasticity of cells walls. The
cell walls are loosened so that turgor pressure can
expand them faster. This is not an acidification
process in the cell walls as seen with auxin.
IV. Gibberellins
A. More than 84 different gibberellins, many naturally
occurring, have been identified.
1. First discovered in Japan in the 1930’s where it caused
a disease in rice plants called "foolish seedling".
Eventually it was found that a fungus (Gibberella
fujikuroi) caused the disease through a compound named
gibberellin. Although Gibberellin was found about the
same time as Auxin, it did not receive much publicity
in the west until after WWII.
2. All gibberellins are acidic and are derivative from the
ent-gibberellane structure. (19 or 20 carbon atoms in
four or five rings with one carboxyl group). The most
active form is GA3, which has been named gibberellic
acid.
3. Gibberellins are found in angiosperms, gymnosperms,
ferns, mosses, algae, and fungi. They have also been
reported in some bacteria.
B. Metabolism of Ginbberellins:
1. Gibberellins are isoprenoid compounds (diterpenes) that
are formed through the mevalonic acid pathway. They
are formed in the endoplasmic reticulum.
2. The 19 carbon gibberellins are more active than the 20
carbon gibberellins.
3. There are several commercial growth retardants that
inhibit stem elongation (stunting) by blocking
gibberellin synthesis: Phosphon D, Amo-1618, Cycocel,
ancymido, and paclobutrazol.
4. Conjugated gibberellins are inactive. Glucoside
conjugates are stored or translocated before they are
released at the proper time and place.
5. Many time active gibberellins can be changed into less
active forms.
6. Sites of gibberellin synthesis in the plant:
a. Most plant cells have the ability to synthesize
gibberellins
b. Immature seeds: usually contain large amounts of
gibberellins that arise from biosynthesis in the
seed itself, not from transport.
c. Young leave are major sties for gibberellin
synthesis.
d. Roots synthesize gibberellins. Root gibberellins
have little effect on root growth but it inhibits
adventitious-root (roots arising from above ground
stems) formation. There is evidence that roots
supply the stems with a large amount of gibberellin
that is translocated through the xylem.
7. Gibberellins are transported through the plant in the
xylem and phloem in a non-polar fashion.
C. Growth promotion by gibberellin in intact plants:
1. Gibberellins have been found to greatly increase the
stem growth of dwarf plants, or biennials that are in
the rosette stage.
2. Many of the gibberellin-synthesis mutants that have been
found are dwarf because one or more steps in the
synthesis of gibberellin is missing or non-functional.
3. Most plant species require GA1 for stem elongation.
Gibberellin-sensitivity mutants have sufficient
amounts of gibberellin in their tissues but cannot
respond to it. It is possible that a receptor protein
is missing or non-functional in these mutants.
D. Promotion of germination in dormant seeds and growth of
dormant buds by gibberellins.
1. Buds in temperate zone plants become dormant in late
summer or early fall. To break the dormancy of these
buds the plant must undergo a cold treatment in the
winter, or proper exposure to photoperiod.
2. Seeds often show dormancy when first shed from the
plant. These seeds must also undergo some treatment
(cold temperature, scarification, acid treatment,
exposure to sufficient moisture or proper photoperiod,
etc.) before they can germinate.
3. Breaking of bud and seed dormancy can be overcome by
gibberellin treatment. In some seeds, the elongation
of the radicle by gibberellin treatment allows it to
push through the seed coat.
E. Gibberellin affects on flowering:
1. Flowering in a plant depends on several factors: plant
age, environmental cues (freezing), and photoperiod.
Some plants will flower only under short day, some
flower only during long days, and some flower during
any length of day (day neutral).
2. Gibberellins are able to cause flowering in long-day
plants and plants that need a cold period.
F. Mobilization of food and mineral elements in storage cells
of seeds is stimulated by gibberellins.
1. After seed germination, root and shoot systems use
mineral nutrients, fats, starch, and proteins present
in seed storage cells. These reserves are used before
the seedling is able to absorb minerals from the soil
and before photosynthesis has begun.
2. Mineral nutrients are readily translocated via the phloem
into the roots and shoots. Fats, polysaccharides,
and proteins are not readily translocated. These
nutrients are metabolized into smaller, more mobile
molecules such as sucrose, amino acids, and amides.
Gibberellin is responsible for these conversions in
many seeds, especially monocots.
3. The embryo of monocots is surrounded by the endosperm.
The endosperm is a nutritive storage tissue with
little metabolic ability. the endosperm is surround
by a metabolically active layer called the aleurone.
the aleurone layer provides hydrolytic enzyme that
digest starch, proteins, phytin, RNA, and cell-wall
materials in the endosperm.
4. Gibberellin stimulates the secretion of hydrolytic
enzyme into the endosperm from the aleurone layer.
Mineral elements in reserve in the endosperm are
also made available by gibberellin activity.
5. Gibberellins are synthesized in the scutellum
(cotyledon) and parts of the embryo. The scutellum
is more important than the aleurone layer in
providing enzymes for digestion of the endosperm
tissues.
6. In breaking both seed dormancy and bud dormancy,
gibberellins act antagonistically with abscisic acid,
which inhibits plant growth.
G. Other effects of gibberellin:
1. Gibberellins cause parthenocarpy in fruits (seedless
fruit development)
a. Fruit development is controlled by both gibberellins
and auxins.
b. In some plants both must be present for fruit set.
c. Commercial application in spraying Thompson seedless
grapes.
2. Gibberellins in young leave help renew activity of the
vascular cambium in woody plants during the spring.
3. Gibberellins delay aging (senescence) in leaves and
citrus fruits
4. Gibberellins have been found to influence leaf shape,
especially in plants that show a difference between
their juvenile and adult forms (heterophylly).
5. Gibberellins have been implicated in flower petal
development.
H. The many a varied effects of gibberellins on plant growth
and development suggest that gibberellins have more than
one primary site of action.
1. Stimulation of cell division in shoot apexes:
gibberellins have been found to promote cell division
by stimulating cells in the G1 phase to enter into the
S phase. Gibberellins have also been found to shorten
the time a cell stays in the S phase.
2. Gibberellins promote cell growth by affecting enzymes
that increase hydrolysis of starch, fructans, and
sucrose.
3. Gibberellins can increase cell-wall plasticity
4. Gibberellins probably function by activating genes
responsible for enzyme that run these physiological
processes.
I. Uses of gibberellins in agriculture:
1. Prevent rind disorders in navel-oranges.
2. Promote seed production in Pinaceae seed orchards.
3. Improve the size of Thompson seedless-grapes.
4. Increase the rate of malting in breweries.
5. Increase the length and crispness of celery stalks.
6. Increase sugarcane growth and sugar yields in Hawaii.
V. Abscisic Acid (ABA)
A. Abscisic acid signals physiological stress such as: water,
salinity, cold, and frost. Abscisic acid helps in
embryogenesis, formation of seed-storage proteins, and
prevention of seed germination and bud growth. It is
universal in vascular plants, mosses, green algae, and
fungi.
B. Abscisic acid helps prepare plants for winter by
suspending both primary and secondary growth.
1. Directs leaf primordia to develop scales that protect
dormant buds.
2. Inhibits cell division in vascular cambium.
C. Effects of ABA on bud dormancy and leaf abscission:
1. ABA levels increase in leaves and buds when bud
dormancy occurs. ABA synthesis in leaves is
controlled by day length, and translocated to buds.
2. ABA probably has no direct role in leaf abscission but
acts to cause premature senescence of cells in the
leaf which in turn causes production of ethylene.
D. ABA also acts as a stress hormone, closing stomata in
times of water-stress.
1. ABA content rises when leaves are under water stress.
Roots under water stress form ABA that is transported
through xylem to the leaves where it causes stomatal
closure. ABA from water stressed roots comes mainly
from shallow roots, thus acting as an advanced signal
to the plant that water is in short supply.
2. ABA works by inhibiting the ATP-dependent proton pump in
the plasma membrane of the guard cells. ABA stops the
K+ influx into the guard cells, so K+ and water leak
out of the guard cells, reducing turgor, and closing
the stomates.
3. The water stress signals the plasma membranes to
activate certain nuclear genes that increase ABA
synthesis. The plasma membrane responds to Ca+ and
phosphoinositols (IP3), indicating that this is a
calmodulin response.
E. Abscisic acid involvement in salt and cold stress:
1. Salt stress: causes formation of different proteins
like osmotin. These proteins help protect the plant
against salt stress.
2. Cold Stress: activation of genes that control ABA in
cold and heat stress are similar to the responses
noted in water stress.
F. Effect of abscisic acid on embryo development in seeds:
1. Embryo development is divided into three stages:
a. mitosis and cell differentiation
b. cell expansion and accumulation of food reserves
(protein, fat, starch)
c. maturation: dehydration and dormancy
2. ABA is linked to normal maturation pathway in seed
development. ABA inhibits precocious germination of
developing seeds.
3. ABA stimulates storage of seed proteins that are needed
for later dehydration and dormancy.
4. The ratio of ABA:gibberellins determines whether seeds
remain dormant or germinate.
G. Abscisic acid metabolism and transport:
1. ABA is a 15-carbon sesquiterpenoid from the mevalonic
acid pathway. It is synthesized in plastids like the
chloroplasts. It has common metabolic intermediates
with gibberellins, sterols, and carotenoids. ABA is
synthesized as a degradation product of carotenoids in
plastids (chloroplasts - leaves, chromoplasts-fruits,
leucoplast-roots, proplastids-seeds).
2. ABA is inactivated by attachment to glucose. ABA-
glucose esters are restricted to vacuole. Also, ABA
is inactivated by oxidation with oxygen to form
phaseic acid and dihydrophaseic acid.
3. ABA is transported in the xylem and phloem. Transport
has also been found in parenchyma outside the vascular
system. There is no polarity in ABA transport.
4. ABA has three major effects on plant tissues:
a. effects plasma membrane of roots: root membranes are
positively charged probably due to the inhibition of
a plasma membrane ATPase. There is probably an
interaction with auxin-induced acid growth.
b. inhibition of protein synthesis: results in effects
on growth and development such as control of seed
and bud dormancy.
c. specific activation and deactivation of genes.
VI. Ethylene
A. A gaseous hormone that diffuses through air spaces between
plant cells. High auxin concentrations induce release of
ethylene, which acts as a growth inhibitor.
1. During fruit ripening, ethylene triggers senescence, and
then the aging cells release more ethylene. The
signal to ripen spreads from fruit to fruit since
ethylene is a gas.
2. Fruit ripening phenomenon has been know for a long time.
Ancient Chinese knew that burning incense would ripen
fruit. The Jamaican Agricultural Department knew in
1910 that oranges could not be stored with bananas on
ships because the oranges would cause the bananas to
overripen. Bonfires where used to help ripen
pineapples in Hawaii and Puerto Rico, and mangos in
the Philippines.
3. Ethylene released by soil fungi promotes seed
germination, controls seedling growth, and retards
disease caused by soil-borne organisms.
B. Synthesis of ethylene in plants:
1. All parts of the seed plant can produce ethylene. Stems
produce large amounts of ethylene when they are laid
horizontally. Roots do not produce much ethylene.
Leaf ethylene production increases gradually over the
growing period, until they senesce and abscise.
Flowers synthesize ethylene just before they fade and
wither. Fruits produce ethylene just before the
respiratory climacteric (a large increase in cellular
respiration just before the fruit ripens). In non-
respiratory climacteric fruits (citrus fruits,
cherries, grapes), ethylene has little effect on fruit
ripening. However, ethylene is used in the citrus
industry to de-green oranges and lemons.
2. Stress will also cause a plant to produce ethylene.
This can come from mechanical stress such as rubbing
(wind) or, pressure (trees leaning on each other),
pathogens (fungi, bacteria, virus, insects),
environmental stress (waterlogging or drought). Figs
can be ripened by slashing the fruit.
3. Ethylene is synthesized form methionine. Its direct
precursor is 1-amino-cyclopropane-1-carboxylic acid
(ACC).
4. Inhibitors of ethylene production:
aminoethoxyvinylglycine (AVG) and aminooxyacetic acid
(AOA). Both block the synthesis pathway from
methionine to ethylene.
5. Control of ethylene synthesis:
a. Auxin promotes ethylene production
b. Auxin promotes ACC formation, which is the direct
precursor of ethylene.
6. Ethylene stimulates its own formation in senescing
organs (autocatalytic). Thus there is some truth to
the saying that "One rotten apple can spoil the whole
bunch." Diffusion of ethylene through intercellular
spaces in a fruit coordinates ripening.
7. Light inhibits ethylene production in leaves while
carbon dioxide promotes ethylene synthesis.
C. Leaf abscission is an adaptation that prevents deciduous
trees from desiccating during winter when roots cannot
absorb water from the frozen ground.
1. Before abscission, the leaf’s essential elements are
shunted to storage tissues in the stem.
2. Environmental stimuli are shortening days and cooler
temperatures.
3. When a leaf falls, the breakpoint is an abscission zone
near the petiole base.
a. Weak area since the small parenchyma cells have very
thin walls and there are no fiber cells around the
vascular tissue.
b. Mechanics of abscission controlled by a change in the
balance of ethylene and Auxin.
c. Auxin decrease initiates changes in the abscission
layer. Cells then produce ethylene.
d. Ethylene induces synthesis of enzymes that digest the
polysaccharides in the cell walls, further
weakening the abscission zone.
e. Wind and weight cause the leaf to f all.
4. Even before the leaf falls, a layer of cork forms a
protective scar on the twig's side of the abscission
layer.
D. Ethylene effects on plants in waterlogged soils and
submerged plants.
1. Waterlogged roots produce less ethylene since
waterlogged soils are hypoxic. Ethylene synthesis is
inhibited because oxygen is required to convert ACC to
ethylene.
2. The ethylene that is synthesized is trapped in the root
because the ethylene cannot escape readily though
water.
3. Ethylene causes cortical cells to synthesize cellulase
which hydrolyzes cellulose. The cortical cells lose
their protoplast, forming air-filled aerenchyma
tissue.
4. As ACC accumulates it is transported in the xylem to the
shoots where it is metabolized into ethylene.
5. Leaf epinasty occurs because the parenchyma cells on the
upper surface of the petioles elongate in the presence
of ethylene relative to the lower surface. Ethylene
also retards stem elongation, increases radial
expansion, causes leaf senescence, and promotes
adventitious root formation.
E. Effect of ethylene on stem and root elongation:
1. Ethylene inhibits elongation of stems and roots and
subsequently causes them to become thicker by
increasing radial expansion. This is caused by the
cellulose microfibrils being laid down in a more
longitudinal orientation.
2. Important response of dicot seedlings emerging from
soil. The hook in the epicotyl or hypocotyl is formed
as a response to ethylene. The hook allows the
seedling to push through the soil without damaging the
meristematic tissue at the tip. The ethylene causes
the seedling to increase in thickness so that it is
stronger.
3. This increased thickening is also found in the
mesocotyls of monocots.
4. Ethylene causes loss of gravitropic response in
seedlings, which allows them to bend around
obstructions in the soil as they are growing.
5. Aquatic plants respond to ethylene production by causing
elongation of their stems and roots. This allows
aquatic plants to have their leaves kept above the
water line.
F. Ethylene effects on flowering:
1. Normally, ethylene inhibits flowering in plants.
However, in mangos and bromeliads (example:
pineapple), ethylene induces flowering.
2. Commercially: Ethrel (ethephon) is used to promote
flowering in Hawaiian pineapple fields which
facilitates a single mechanical harvesting. Ethrel
also used in late season on tomatoes to cause uniform
ripening and enable mechanical harvesting.
G. Other ethylene effects:
1. Ethylene causes flower senescence, probably because
after pollination there is an increase in the rate of
ethylene production in flowers.
2. Ethylene promotes adventitious-root formation, also an
effect of auxin.
3. Ethylene causes changes in the expression of flower sex.
Ethylene promotes formation of female flowers.
4. Ethylene helps break seed dormancy. Found as a function
of some soil fungi.
H. Relation of ethylene to auxin effects:
1. Auxin increases ethylene production. Raises the
question of whether some plant responses to auxin are
merely responses to ethylene.
2. Some ethylene responses that relate to auxin production:
leaf epinasty, inhibition of stem and leaf elongation,
flower induction (bromeliads and mangos), inhibition
of hook opening in dicot seedlings, female flower
production, senesces of flowers.
3. Some ethylene responses that relate to other hormones
(auxin, cytokinins, abscisic acid): abscission of
leaves, flowers, and fruits.
I. Antagonists of ethylene action:
1. High concentrations of carbon dioxide inhibits ethylene
responses in the plant. High carbon dioxide
concentrations are often used in fruit packing houses
to prevent overripening of fruits and vegetables.
2. Silver ion (Ag+) also inhibits the action of ethylene.
Silver ions in the form of silver nitrate (AgNO3)
inhibit abscission of leaves, flowers, and fruits in
plants.
3. Synthetic antagonists of ethylene are: volatile olefin,
transcycloctene, 2,5-norbornadiene.
J. Ethylene mode of action:
1. Ethylene causes an increase in synthesis of enzymes in
different target tissues. For example ethylene
stimulates cellulase and other cell wall degrading
enzymes in the leaf abscission. Different enzymes are
produced that aid in fruit ripening and flower
senescence in the presence of ethylene. During
wounding, presence of ethylene is related to
synthesis of phenylalanine ammonia lyase, an enzyme
active in phenolic compound synthesis needed for
healing. In cells infected with fungi, ethylene
stimulates the production of b-1,3-glucanase and
chitinase which degrade fungal cell walls.
2. Ethylene appears to stimulate mRNA transcription.
3. Ethylene binds one or more membrane receptor proteins
that contain copper at their active sites.
VII. Other plant growth substances (not necessarily hormones):
triacontanol, brassins, salicylic acid, turgorin, and polyamines
A. Triacontanol: 30-carbon, saturated primary alcohol.
Found to increase growth of several agricultural plants.
B. Brassins and Brassinosteroids: growth promoters. Act by
increasing sensitivity to auxins.
C. Salicylic Acid: Active ingredient in aspirin. Promotes
cyanide-resistant respiration that causes heat
production and volatilization of compounds in Arum lilies
which attract insect pollinators. Important in causing
resistance to certain plant pathogens (tobacco necrosis
virus, and fungi)
D. Turgorin: act on the turgor pressure in the pulvinus cells
of plants that have nastic movements.
E. Polyamines: polyvalent cations containing two or more
amino groups. Examples are: putrescine, cadaverine,
spermidine, spermine. Involved in promoting cell
division, stabilizing membranes and protoplasts,
promoting development of fruit, reducing water stress,
and delaying leaf senescence. The positively charged
amino groups allow them to combine to the phosphates in
DNA and RNA, thus controlling transcription and
translation.
VIII. Other inhibitory plant growth regulators:
A. Lunularic acid: found in the gemmae of liverworts as well
as many species of lower plants, but not algae. Prevents
germination of the gemmae and growth of the thallus as a
response to day length. Long days: lunularic acid
concentrations are high and growth is slow. Short days:
lunularic acid concentrations are low and growth is
rapid.
B. Batasins: found in yams where it causes dormancy in
bulbils (vegetative reproductive structures).
C. Jasmonic acid: found in oil of jasmine. Inhibits the
growth of plant parts and promotes leaf senescence.
IX. Some Unanswered Questions About Plant Hormones
A. So much is unknown about internal chemical signals of
plants that some argue it is premature to call these
growth regulators hormones.
B. For example, an increase in Auxin concentration in the
zone of elongation has not been detected.
C. According to one hypothesis, responses to these growth
regulators is due more to changes in the sensitivity of
local cells to regulators already present than to the
arrival of these regulators from other parts of the
plant.