PLANT HORMONES (Phytohormones)




Plant hormones play pivotal roles in regulating plant development, growth, and stress responses, and the interactions (‘cross-talk’) among different hormones fine-tunes various aspects of plant physiology.


Botanists recognize eight major groups of hormones: auxins, gibberellins, ethylene, cytokinins, abscisic acid, jasmonates, brassinosteroids and strigolactones.


The concept of plant hormones originates from a classical experiment on phototropism, the bending of plants toward light, carried out by Charles Darwin and his son Francis in 1880. The Darwins were able to demonstrate that when young oat plants were exposed to a lateral light source, a transported signal originating from the plant apex promoted differential cell elongation in the lower parts of the plant that resulted in it bending toward the light source. This signal was subsequently shown to be IAA, the first identified plant hormone.


Thimann (1948) designated the plant hormones with the name ‘phytohormones’ in order to distinguish them from animal hormones. He defined a phytohormone as “an organic compound produced naturally in higher plants, controlling growth or other physiological functions at a site remote from its place of production and active in minute amounts.”


A broader definition of plant hormones was proposed by Johannes van Overbeek (1950). According to Overbeek, the plant hormones are defined as “organic compounds which regulate plant physiological process— regardless of whether these compounds are naturally occurring and/or synthetic ; stimulating and/or inhibitory ; local activators or substances which act at a distance from the place where they are formed.”


Therefore, plant hormones are produced naturally by plants and are essential for regulating growth. They act by controlling or modifying plant growth processes, such as formation of leaves and flowers, elongation of stems, development and ripening of fruit.


In modern agriculture, scientists have observed the benefits of applying plant hormones to regulate growth in plants. When natural or synthetic substances are used in this manner, they are often referred to as ‘growth regulators’ or ‘plant growth regulators’. Thus, through the application of plant hormones we are able to control certain aspects of plant growth, such as reducing stretch/stem elongation, inducing earlier budset, speeding up flowering times and increasing yields.








The term auxin is derived from the Greek word “auxein” which means to grow. Compounds are generally considered auxins if they can be characterized by their ability to induce cell elongation in stems and otherwise resemble indoleacetic acid (IAA – the first auxin isolated) in physiological activity. Auxins usually affect other processes in addition to cell elongation of stem cells but this characteristic is considered critical of all auxins and thus helps define the hormone.


Auxin transport is required for important growth and developmental processes in plants, including gravity response and lateral root growth. Thus, one of the key roles of auxins is that they stimulate adventurous root growth.[1]


Auxins play a role in maintaining apical dominance. That is, most plants have lateral (sometimes called axillary) buds located at nodes where the leaves attach to the stem. Axillary buds are embryonic meristems maintained in a dormant state. Auxin maintains this dormancy. As long as sufficient auxin is produced by the apical meristem, the lateral buds remain dormant. If the apex of the shoot is removed (i.e. if the main stem is tipped), the auxin is no longer produced. This will cause the lateral buds to break dormancy and begin to grow. In effect, the plant becomes bushier. We’ll talk more about this in a moment. For now…


Auxins also promote adventitious root initiation. For example, many cloning gels and root stimulants that are sold through the retail hydroponics industry contain the synthetic auxins in the form of NAA (1-Naphthaleneacetic acid) or IBA (indole-3-butyric acid) or the naturally occurring auxin IAA, or combinations thereof.


Auxin containing products are ideal for early growth (when the plant is first introduced into the system) to ensure adventitious root development. This helps the plant to settle in early and aids in mineral element uptake. Therefore, auxin containing root stimulants can enhance early growth rates and reduce stress when cuttings are first placed into high intensity lighting situations.


Conversely, auxins are also shown to promote gibberellin (GA) biosynthesis[2] which, in turn, can promote stretch (stem elongation) in flowering plants. We’ll discuss more about gibberellins in a moment. For now, while auxins are ideal for promoting root growth in young vegetative plants their use in flowering plants may/can prove counterproductive.



Auxins cause several responses in plants:


  • Bending toward a light source (phototropism)
  • Downward root growth in response to gravity (geotropism)
  • Stimulates cell elongation
  • Promotes (via ethylene production) femaleness in dioecious flowers
  • Stimulates growth of flower parts, fruit set and growth
  • Promotes formation of adventitious roots
  • Can induce fruit setting and growth in some plants
  • Promotes GA biosynthesis which can promote stretch in flowering plants





Cytokinins are essential for the growth of intact and isolated plant organs and tissues. Their involvement in the processes of cell division, mobilization of inorganic and organic nutrients, senescence and reduction in apical dominance are well documented. The high levels of cytokinins in developing seeds and fruits are indicative of a function of this type of hormone during periods of active cell division.[3]


Cytokinins are essential for flower bud development in grapevines and the cytokinin concentration in the phloem is critical to the induction of flowering of the long-day-plant Chenopodium murale (Nettle-leaved Goosefoot).[4]


Substantial research has shown that the exogenous application of cytokinins to various species increases bud sites, increases cell division and yields and reduces apical dominance and stretch. The level and time of application will determine outcomes; however, anecdotal evidence tends to suggest that the application of BAP-6 (6-Benzylaminopurine) via foliar at 25-50ppm during early to mid bloom, produces shorter, bushier plants with closer internodes, which join to form tighter and longer/larger flower clusters than would occur without the use of BAP-6.


Further, it has been shown that the application of BAP-6 in some species increases trichome density through (theoretically) increasing the DNA content of the nuclei in trichome cells.[5]


Additionally, various studies suggest that exogenously applied cytokin speed up flowering times.[6]


It is shown that sex expression in plants is strongly regulated by, among other things, cytokinins.[7] For example, it has been shown that the application, through the root system, of 6-benzylaminopurine to the cannabis plant at 15mg/L (15ppm) resulted in all plants being either female (pistillate flowers) or intersexes (bisexual flowers/hermaphrodites) while the application of gibberellin (25mg/L) resulted in more than 80% of the plants being male. The authors of this study concluding that the root system plays an essential role in sex expression in hemp and that this role is related to cytokinin synthesis in the roots of plants,[8]


Cytokinin Functions

A list of some of the known physiological effects caused by cytokinins are listed below. The response will vary depending on the type of cytokinin and plant species.


  • Stimulates cell division.
  • Stimulates morphogenesis (shoot initiation/bud formation) in tissue culture.
  • Stimulates the growth of lateral buds-release of apical dominance.
  • Stimulates leaf expansion resulting from cell enlargement.
  • May enhance stomatal opening in some species.
  • Promotes the conversion of etioplasts into chloroplasts via stimulation of chlorophyll synthesis.
  • Can speed up flowering times
  • Increased bud sites
  • Increased trichome density
  • Influence on sex expression


Cytokinin, Auxins and Apical Dominance


Cytokinins, in contrast to auxins, among other things, are shown to reduce apical dominance.


Cytokinins are known to overcome apical dominance by stimulating the growth of lateral and axillary buds respectively.


While the science that underpins the role of cytokinin reducing apical dominance is complex and involves an interplay of hormones including auxin, cytokinin and recently discovered strigolactone, the interaction between auxin and cytokinin in the plant’s main/primary shoot and lateral/axillary buds is pivotal in this process. To understand this (to simplify), basically IAA (auxin) accumulates in the main stem/shoot of the plant while not being present in the secondary/lateral/axillary buds. This promotes upward growth but due to lack of IAA in the axillary buds does not promote their outward/upward growth. One way of altering this and directing IAA to the axillary buds is to tip/decapitate the main shoot of the plant which results, initially, in cytokinins being directed to the axillary buds, followed by IAA being concentrated in these regions. Thus, because IAA is now concentrated in the axillary buds they begin branching and growing. I’ve actually oversimplified this to avoid discussing ‘pins’ and ‘down regulation’ (more information than the mere mortal needs to know) but hopefully you get the idea. See following image that demonstrates the interactions between IAA and cytokinins and how they affect apical dominance.



Therefore, the effects of cytokinin re apical dominance are antagonistic to those of auxin. That is, direct application of cytokinins to axillary buds promotes axillary bud outgrowth, even in non-tipped plants.[9] To date, cytokinins and sucrose (via sugar metabolism) are the only chemicals known to release axillary buds from dormancy. We’ll touch briefly on sucrose later. For now cytokin, auxin ratios are the important thing.


Skoog and Miller (1957) found that shoot formation could be induced predictably from tobacco callus using relatively low levels of auxin and a high level of cytokinin in the growth medium.[10] Since this discovery, many aspects of cellular differentiation and ‘organogenesis’ (the production and development of the organs of a plant) in tissue and organ cultures have been found to be controlled by an interaction between cytokinin and auxin concentrations.


Thus, a primary factor in the mechanism of apical dominance is a hormonal interaction between auxins and cytokinins. That is, apical dominance is antagonized by cytokinin which interferes with the abundance of IAA by increasing the naturally occurring cytokinin to auxin ratio.[11]


In research conducted by Nii et al (1986) 6-benzylamino purine (BA), was used as a foliar spray in orchard and potted plants to study its effect on branching and leaf development in peach trees, and to analyze the factors influencing its effectiveness. It was shown:


1) During the expansion of cells in peach leaves sprayed with BA, the number of chloroplasts per cell and the amount of chloroplast DNA increased with the cell size, after this phase the chloroplast number per cell continued to increase, and 2) BA-treated trees were more compact than non BA treated trees and many branches of BA-treated shoots contributed to a less open growth habit.[12]


Similarly, in research conducted by Samanthi P. Herath et al (2004) on Hibiscus cannabinus L (Kenaf) it was shown that in the control plants (non BA treated plants) neither axillary nor adventitious buds developed. The results suggested that the treatment with BA reprogrammed the developmental fate of a large number of cells in the shoot apex of kenaf. Further, it reconfirmed the ability of BA to overcome the apical dominance of shoots.[13]


Author’s note: I’ve, arguably, oversimplified the subject of auxin cytokinin interactions and apical dominance, somewhat, because very recent research (2013) demonstrates that sucrose plays the primary role in promoting axillary bud outgrowth, with auxin playing a secondary role later in the process. The study in question showed that the exogenous application of sucrose broke axillary bud dormancy, thereby triggering lateral growth and reducing apical dominance.[14] Additionally, earlier research has shown that bud break in Rose sp. is related to the stimulation of sugar metabolism (sucrose transporter).[15] However, this is relatively new information and there is still much to be understood about the mechanisms by which sucrose releases the axillary buds. Further, both sucrose/sugars and phytohormones play a complex role in breaking bud dormancy and further research is needed to understand this process fully.[16]



Cytokinin Additives



6-Benzylaminopurine, benzyladenine or BAP is a first-generation synthetic cytokinin that elicits plant growth and development responses, setting blossoms and stimulating fruit richness by stimulating cell division.


Research by Paul T. Wismer et al (1995) showed that when Benzyladenine (BA) was used on apples in comparative trials against NAA, carbaryl, and daminozide, BA produced the best results of all the chemicals with increases in fruit size and weight.  It was shown that BA increased the rate of cell layer formation in the fruit cortex, indicating that BA stimulated cortical cell division. The number of cells in an apple may be increased in three ways: 1) by more rapid cell division during the cell-division phase of fruit growth, 2) by extending cell division for a longer period than normal, or 3) by some combination of these two phenomena.[17]


Research by Kevin E. Crosby et al (1981) on soybean notes:




Of the five cytokinins tested at 0.1 mm concentration in 1977, BA was found to be most effective in promoting fruit-set.”


[End Quote]


In the same research it was shown that BA increased soybean yields, hypothesizing that:




 “BA may act by increasing the ability of the treated fruits to competitively mobilize nutrients. Shortages of assimilates, particularly during the period of fruit-set, may intensify nutrient competition between developing fruits and vegetative organs. This might cause abscission of young fruits deficient in substrate or hormones. Cytokinins are known to attract nutrients to sites of application.”[18]


[End Quote]


Exogenous Application of Cytokinin Potentially Speeds Up Flowering Times


Some recent evidence suggests that the exogenous application of cytokinin can speed up flowering times in certain crops. For example, research by Nisha Nambiar et al. (2012) with Dendrobium orchid showed that the exogenous application of BAP increased the percentage of inflorescence production, induced earlier flowering, and contributed to the differences in inflorescence length and the number of leaves and flowers produced. This study showed that BAP is a potential plant growth regulator that can speed up the flowering process of Dendrobium orchid.


Similarly, in research by Zhang Rui and Terukatsu Ito (2000) it was shown that BAP could accelerate blossom in P. maosonian. [19]


Conclusion and Discussion


The correct useage of auxins and cytokinins used at varying ratios and times during the grow and flowering cycles can greatly stimulate desirable effects in plants. Auxins used in early grow, promote adventurous rooting, help relieve plant stress, and promote plant health/vigour.


Cytokinins, used during early bloom, can greatly aid in setting up a better plant structure (short squat plants with close internodes), and used thereafter can stimulate cell division (growth rates), resulting in increased yields and potentially and earlier harvest times due to cytokinins having the potential to speed up flowering times. .






In the early part of the twentieth century, Japanese farmers noticed that some rice plants would randomly shoot up to such great heights that they would collapse, becoming impossible to harvest. They named this disease “bakanae”, meaning foolish seedlings. Sawada (1912) suggested that the disease was due to a ‘substance’ secreted by a parasitic fungus, Gibberella fujikuroi.


This theory was supported by Ewiti Kurosawa (1926) who found that sterile filtrates of the fungus could initiate symptoms of bakanae disease in healthy rice seedlings.


Later, in 1939, Yabuta and Hayashi isolated the growth promoting substance ‘gibberellin A’ which has now been shown as a mixture of many growth promoters, collectively known as gibberellins.


Today, there are 126 known gibberellins, divided into two classes, and more may be discovered in the future. Plants produce these hormones naturally through biosynthesis as they grow, ensuring that they have the hormones they need to develop normally, and these hormones can also be applied to plants to achieve specific desired outcomes.


One of the primary functions of gibberellin in plants is to regulate the growth of the stems. Many members of the cabbage family, for example, release gibberellin when they “bolt” to produce long flowering stalks.


Gibberellins also influence sex expression. That is, research has shown that while auxin and cytokinin promote female sex expression in plants, gibberellins promote male sex expression.


The Role of Gibberellins (GA) and Auxin in Stem Elongation (Stretch)


Auxin and gibberellin control separate processes that, when combined, contribute to stem elongation and fruit set (including ovary growth), suggesting an additive effect, in which the auxin stimulates growth by cell expansion/elongation and cell division while gibberellin acts in the expansion/elongation of cells (Yang et al., 1996). Further, it has been shown that auxin stimulates GA biosynthesis[20] which leads to higher levels of endogenous GA which, in turn, encourages stretch. Put simply, GA, in conjunction with auxin, plays a key role in cell elongation (i.e. stretching an existing cell) and this results in stem elongation.


Auxins and gibberellins, besides inducing cell elongation, are known to promote ‘cell division’ (i.e. through cytokinesis the parent cell splits forming two daughter cells with identical DNA) under certain conditions, but this behaviour is an exception rather than a rule. Cytokinin, on the other hand, promotes cell division as an absolute rule.


Cross Talk Between Gibberellins, Auxin and Cytokinin


Research has shown there is a ‘cross talk’ between GA (gibberellins) and cytokinin (CK).

Several recent studies have shown development-dependent reciprocal interactions between the two hormones, where cytokinin inhibits the production of GA and promotes its deactivation, while GA inhibits cytokinin responses. Thus, GA and CK exhibit antagonistic effects towards each other and thus illicit different growth responses in plants. The ratio between the two hormones, rather than their absolute levels, determines the final response.[21]


One of these antagonistic effects on plants is that GA promotes stretch in plants (The role of gibberellins in promoting stem elongation is due to an enhancement of cell division or cell elongation[22]), while exogenously applied cytokinins alter the GA CK ratio (leaning towards a higher CK to GA ratio) and can offset this situation. As Lata et al. (2008) put it: Cytokinins commonly stimulate shoot proliferation and inhibit their elongation.”[23]This is useful for the development of short, bushy plants.


However, it is important to note that phytohormone and plant interactions are yin and yang. That is, the application of any one hormone may elicit desirable traits in a plant, while also promoting undesirable traits/outcomes. So, for instance, GA encourages stretch while CK encourages a more compact plant through reducing stretch. This said, GA e.g. encourages intermodal growth while CK is shown to reduce internodal growth. On the other hand, auxin, while causing apical dominance and elongating plant cells, is important in the regulation of physiological growth responses, such as greening, flowering time, and senescence. Other than this, auxins regulate other important physiological processes in plants. By shifting the ratio/amount of any one hormone we are then altering the levels of other important hormones which impact on how the plant grows and forms. Therefore, while creating a short bushy plant through the use of exogenously applied cytokinin sounds straight forward things aren’t nearly as simple as this and factors such as; 1) the type of cytokinin used (i.e. there are two types of cytokinins: adenine-type cytokinins represented by kinetin, zeatin, and 6 benzylaminopurine, and phenylurea-type cytokinins such as diphenylurea and thidiazuron); 2) the level of use (i.e. ppm of application); 3) the time of application (e.g. grow or bloom); 4) what other hormones (if any) are applied in conjunction with cytokinin; 5) the plant species and; 6) the genetics (phenotype) of that species will influence outcomes.


While the research is variable it is often shown that combinations of exogenously applied hormones at varying ratios elicit the best response in growth and yields. For example, in research by Stella C Cato et al (2013), where gibberellins (GA3), auxins (indolbutyric acid) and cytokinin (kinetin) were tested, both independently and together, on Micro-Tom tomato it was shown that the plants treated with kinetin (cytokinin) alone presented reduced internodes and excessive stimulus to the development of lateral buds. On the other hand, where plants were treated with GA3 (gibberellin) alone longer internodes and delayed flowering were observed. Where plants were treated with indolbutyric acid (auxin) alone they produced no axillary buds (apical dominance). However, When applied in pairs, GA3 + IBA; GA3 + kinetin (KIN); and IBA + KIN or the three altogether (GA3 + IBA + KIN), it appears that there was a combination of the effects of each of plant growth regulators to promote a more balanced shoot development.


The following treatments were sprayed three times on tomato plants, with one spray during the growing season and twice during flowering: GA3 (5 mg L-1); IBA (5 mg L-1); KIN (9 mg L-1); GA3 + IBA (5 mg L-1 + 5 mg L-1), GA3 + KIN (5 mg L-1 + 9 mg L-1); IBA + KIN (5 mg L-1 + 9 mg L-1), GA3 + IBA + KIN (5 mg L-1 + 5 mg L-1 + 9 mg L-1) and Stimulate® (100 mL L-1). The control plants were sprayed with water.


Stimulate® is a commercial liquid formulation comprised of a molecule of cytokinin group at 90 mg L-1; a molecule of gibberelin group at 50 mg L-1, and an auxin at 50 mg L-1.


Thus, basically, when scrutinizing these treatments, in all instances, a higher cytokinin to auxin and gibberellin ratio was applied.


The research concluded: that the combined application of GA3, IBA and KIN or Stimulate® promote significant increases in the dry matter accumulation in roots and fresh and dry matter of fruits of tomato ‘Micro-Tom’ in relation to control.”[24]


This research is inline to other research that shows a somewhat higher cytokinin to auxin and gibberllin ratio can improve growth and yields.


Chemical GA Biosynthesis Inhibitors Reduce Plant Stretch


Chemical plant growth regulators (subclass growth retardants) such as paclobutrazol (PBZ) and chlomequat chloride (CCC) are used by some indoor growers to reduce stretch. These products/actives act as GA antagonists (GA biosynthesis inhibitors) which interfere with the GA pathway. This leads to severely depleted levels of bioactive GA within the plant, which results in producing short squat plants with close internodes and heavy floral clusters through inhibiting stem elongation and thereby producing stunted plants.

Chlormequat chloride (CCC) is shown not only to antagonise GA, leading to severely depleted levels of bioactive GA, but also to increase endogenous levels of cytokinins. For example, Skene (1968) reported a 10-20 fold increase in the cytokinin content of xylem sap from grapevines treated with CCC.[25] This demonstrates that where there are higher levels of endogenous CK to GA, along with other factors, the result is a shorter, denser plant (i.e. reduced stem elongation, closer internodes and heavier flowering).

Other than GA biosynthesis inhibitors (growth retardants) such as PBZ and CCC, chemicals such as morphactin are shown to produce morphological changes that suppress stretch in plants (producing short squat plants with close internodes and heavy floral clusters). Zieglar et al have claimed that methyl-morphactin is a competitive inhibitor of the action of gibberellin, while Masayuki Katsumi (1973) has claimed that Fluoren-9-carboxylic acid (a morphactin) acts as an auxin and gibberellin-antagonist and thereby produces short squat plants.[26] Morphactins are shown to produce similar results in plant growth, formation and yields when compared to chemical GA biosynthesis inhibitors such as PBZ and CCC.[27], [28]


Additionally, similar to chemical GA biosynthesis inhibitors such as CCC, morphactin has been shown to increase the endogenous levels of cytokinins.[29] However, the effect of morphactin, though diverse, is more like an anti-auxin and effects vegetative and reproductive organs including polarity disturbance*.[30]


Morphactin also plays a powerful role in the sex expression of plants. For example, the Mohan Ram group (1970) concluded that morphactin (2-chloroethanephosphonic acid) affects the sexual flower differentiation in Cannabis sativa L, in the sense of feminization of flowers. This study demonstrated that male plants could be turned into female plants through the use of morphactin at treatments of 250 – 500ppm. The research concluding that morphactin induced an “extreme degree of feminization” in Cannabis sativa L.[31]


* Re “polarity disturbance”: Cell polarity refers to the differences in the shape, structure, and function of plant cells. Almost all cell types exhibit some sort of polarity, which enables them to carry out specialized functions. Therefore, where a chemical changes/disturbs the natural process of cell polarity this is “polarity disturbance”.


The Yin and Yang of Chemical GA Biosynthesis Inhibitors (Growth Retardants)


I have previously spoken about the use of chemical PGRs (chemical GA biosynthesis inhibitors) when discussing natural, non-chemical methods for reducing stretch (see page….). However, to reassert a very important point….


I tend to be a great believer in the philosophy that any chemical that profoundly alters the natural growth processes of a plant must then have a payoff. A case of yin and yang…. all things in nature have a balance. Interfere with or alter this balance and unforeseen/undesirable outcomes may result. This is certainly the case with chemical GA biosynthesis inhibitors such as PBZ and CCC.


That is, many chemical GA biosynthesis inhibitors have known toxicity issues (i.e. their residues are potentially harmful to human health) and they are known to seriously impact on the quality of produce. i.e. plant enzymes, similar to the ones involved in GA biosynthesis, are also important in the formation of abscisic acid, ethylene, sterols, flavonoids, terpenes and other important plant constituents. Thus, by antagonizing GA we are also blocking/limiting/effecting the pathway/mechanism responsible for essential oil and flavonoid production. [32] Therefore, while chemical GA biosynthesis inhibitors can increase yields through antagonizing GA biosyntesis their use will also result in lower quality and potentially harmful to human health produce. For example, chlormequat chloride is a known human immune toxin, while PBZ is toxic to the liver. Other chemical GA biosynthesis inhibitors (e.g. daminozide/Alar) that are used in just some hydroponic industry flowering additives (e.g. Superbud/Phosphoload, Flower Dragon and Top Load) are considered to be “potent” human carcinogens.


Many chemical GA biosynthesis inhibitors have extremely long withholding periods (months in some cases) which makes them completely unsuitable for use on short-term indoor deciduous crops. For example, I have been informed by the California based Werc Shop (medical marijuana testing laboratory) that 15% of medical marijuana they test fails the ‘pesticide screen’, of which roughly 50% fails on the basis of testing positive for paclobutrazol. See lab results following (with thanks to the good folk of ‘The Werc Shop’)


In many countries these actives (PBZ, CCC etc) are not permitted for use on consumable crops and daminozide/Alar is banned for use on any consumable crop, worldwide. Therefore, products containing these actives are, typically, sold through the agricultural sector with license for use on ornamental crops only. Unfortunately, a few unethical hydroponic manufacturers have used these actives in bloom additives, which they have then marketed as containing safe and organic components.


GA biosynthesis inhibitor containing products are relatively easy to spot. Basically, their use has a very immediate and pronounced effect on upward growth, significantly inhibiting or stopping it completely. Thereafter, lateral branching begins and nodes form closer than would be expected. Other than this, the floral clusters are tight, dense and heavier than would be case without the use of GA biosynthesis inhibitors.


While some hormone based products may elicit similar responses in plants (forming shorter, bushier plants) their effects aren’t nearly as pronounced as when using chemical GA biosynthesis inhibitors and typically the upward growth of the plant will continue as would be the norm.


Therefore, if you are looking to grow non-toxic, high quality produce, any product that significantly inhibits or stops upward growth and induces early flowerset is a product that is best avoided. This applies to both registered and non-registered products. For instance, through sleight of hand registrations several PGR (GA biosynthesis inhibitor) products are legally able to be sold through the hydroponics retail sector. These include, but are not limited to, Mr No, formerly Dr Nodes (0.4% paclobutrazol, sold in North America through General Hydroponics), Yield Masta/Sudden Impact (paclobutrazol and chlormequat chloride, sold in Australia and New Zealand), U-Turn (paclobutrazol, sold in Australia), Cyco Flower (paclobutrazol and chlormequat chloride, sold in Australia), and Bonza Bud (paclobutrazol, sold in Australia).


While the aforementioned products are registered, don’t be deceived – they are registered only for use on ornamental crops. For instance, U-Turn’s (APVMA reg 58890/100ml/0506) label states,




“For growth control of container grown ornamentals only as per directions for use.”


[End Quote]


As for Cyco Flower (Australia), another paclobutrazol containing product marketed with “APVMA approved PGR”, its APVMA registration, 64027/1L/0110, 64027/0110, reads,




“ Active Constituent/s: 4g/L paclobutrazol….For growth control of container grown ornamentals.”


[End Quote] 


And in the case of Dr Nodes (North America, 0.4% paclobutrazol, EPA registration number 80697-3), recently renamed Mr No, one hydroponic store notes,




“This product was designed specifically to shorten internodes, stop vertical growth, increases lateral growth and produce larger, more rigid flowers. This product is EPA registered for use on ornamental plants (i.e. bedding plants, flowering/foliage plants, woody plants or bulb crops).”


[End Quote] 


Perhaps you’re getting the picture. i.e. The last time I checked GA biosynthesis inhibitor products sold through the hydroponics retail sector weren’t being sold to Geranium, Chrysanthemum, Poinsetta, Rhododendron, Camelia and/or Daffodil growers. Quite simply, paclobutrazol and other chemical GA biosynthesis inhibitors are, in many instances, not intended for use on ANY consumable crop (eaten or ingested via any other means).


It’s not up to me to tell growers what they should and shouldn’t use in the production of consumable crops. However, as an author for hydroponic consumers I do have a responsibility to, at least, inform growers about these products, so they (you) can make informed purchasing decisions. Consider yourself now informed (knowledge is power)! Now it’s up to you…


This said, let’s leave gibberellins, stretch and the interactions/’cross-talk’ between auxin, cytokinin and gibberellins there and move on to the recently discovered phytohormone, brassenosteroids which, much like gibberellins, also play an important role in promoting stretch in certain plants.





Brassinosteroids (BRs), are a group of plant-specific polyhydroxylated steroidal hormones that were first discovered over 40 years ago by Mitchell et al (1970) after it was observed that organic extracts of Brassica napus pollen promoted stem elongation and cell division in plants.


BRs regulate a wide range of growth and developmental processes, including cell elongation, seed germination, stomata formation, vascular differentiation, plant architecture, flowering, male fertility and senescence.


Accumulating evidence supports the fact that there is a crosstalk between BR and GA signaling pathways.[33] While the science surrounding this crosstalk is complex (among other things, involving the concentration and ratio/balance of each phytohormone), BRs and GAs act synergistically to promote cell elongation. As a result, this crosstalk promotes stem elongation (stretch) in plants.


Plants with blocked BR biosynthesis result in a dwarf phenotype. Conversely, the application of BRs, at extremely low levels, causes pronounced elongation of hypocotyls, epicotyls, and peduncles of dicot specie plants (e.g. tomato, chili and bell pepper). Young vegetative tissue is particularly responsive to BRs. This means that the application of brassinosteroids can prove beneficial when used in the vegetative stage of the crop cycle. For example, one product/plant growth stimulant that is available through the agricultural sector and that is used with seedlings and vegetative plants is Vitazyme™, which contains brassinosteroids, triacontanol and other growth stimulants that are ideal for vegetative growth.


Conversely, brassinosteroids, when used alone (i.e. without other hormones to offset the BR to other phytohormone ratio), could/would prove counterproductive, due to promoting stem elongation (stretch), when used in bloom.


Brassinosteroids (BRs) and BR Biosynthesis Inhibitors


Brassinosteroid induced plant stretch can be overcome through the use of chemical or synthetic BR biosynthesis inhibitors. One such BR biosynthesis inhibitor that has been studied extensively is brassinazole. The molecular structure of brassinazole is similar to paclobutrazol which acts as a gibberellin biosynthesis inhibitor. In studies with cress (Lepidium sativum), brassinazole-treated plants did not show recovery after the addition of gibberellin but showed good recovery after the addition of the brassinosteroid, brassinolide. This study and others have demonstrated that brassinazole is a specific BR biosynthesis inhibitor.[34]


This said, brassinozole (a triazole derivative) is prohibitively expensive. For example, 100 milligrams (0.1g) of brassinozole could cost anywhere between $1000 – 2000 USD.   This excludes its use in hydroponic additive formulations and really only of use for research purposes.  


However, Burkhard Schulz has shown that the relatively cheap to purchase propiconazole acts in a very similar manner to brassinozole by inhibiting the brassinosteroid function in corn plants. In this study, and following studies, it was demonstrated that the application of propiconazole resulted in short, squat plants that only have female characteristics, and that develop more kernels where pollen would normally grow.[35]


Propiconazole (Pcz) is classed as a ‘triazole’ which are a group of agricultural chemicals that were initially developed as fungicides, but were also found to retard plant growth. The most typical plant growth responses to triazoles is a reduction in stem length, but they also have been found to increase leaf thickness, thicken stems, and increase root development. There are several triazole compounds (e.g. voriconazole, uniconazole, tebuconazole and propiconazole) that are shown to act as plant growth retardants.


Pcz acts in a similar way to paclobutrazol (PBZ) and other chemical plant growth retardants (i.e. it promotes shorter plants, with close internodes which, in turn, encourages dense, well formed flower clusters); however, the effect is not as pronounced. For example, a study by Zandstra J. W et al (2004) showed Pcz treated plants demonstrated a growth response similar to paclobutrazol; however, the effect was not as great. “By the end of the 42 day greenhouse production period, propiconazole treated transplants had greater top fresh weights, root fresh weights, and stem diameters than untreated, but generally not as great as paclobutrazol treated transplants.”


The research concluding:




“Total yields did not differ statistically amoung treatments, but tended to be greater when transplants were treated with paclobutrazol. However, all treatments (propiconazole and paclobutrazol) increased the percent red fruit and decreased the percent green fruit when compared to untreated, with paclobutrazol generally giving a greater effect.” [36]


(End Quote)


Pcz is of particular interest to agricultural researchers because it is less active than paclobutrazol and other chemical plant growth retardants (e.g. chlormequat chloride and daminozide/Alar) and needs to be used at higher rates, which provides a greater margin of safety.


Pcz is registered for use on a variety of food crops, most notably banana, nuts, barley, corn, stone fruits, wheat, cereal grains, citrus, oats, rice, rye, sugarcane, and wheat.[37]


Burkhard Schulz has said that Pcz is a safe chemical to use and poses no risk to humans. However, this view is perhaps (arguably) overly optimistic. For instance, chronic toxicity tests on rats and mice found benign and malignant liver tumors to occur in males at doses as low as 3.6 mg/kg daily.[38] As a result, the EPA has categorized Pcz as a possible human carcinogen.


This said, by the oral route of exposure, triazoles are considered as having low to moderate toxicity. The main concern, with at least some triazole fungicides, is the potential to cause birth defects, although data suggests that, in humans, such effects would occur only at moderate to high doses of exposure.


The EU estimate for acceptable daily intake of Pcz for humans is 0–0.07mg/kg ‘bw’ (body weight).


The body absorbs 86% of a Pcz dose in 48 hours. Excretion occurs at 95% in 48 hours.


When compared to chemicals such as PBZ, CCC and daminozide/Alar, triazole BR biosynthesis inhibitors, therefore, given current knowledge, may offer a safer, less toxic alternative to chemical GA biosynthesis inhibitor containing additives (e.g. Yield Masta, Phosphoload, Emerald Triangle Gravity, General Hydroponics Dr No etc) for controlling stem elongation (stretch) in indoor crops.


However, much like GA biosynthesis inhibitors triazoles such as Pcz are shown to have long withholding periods and, therefore, remain residual in the harvested product.


For example, a study by Garland S.M. et al (1999) showed that Pcz and tebuconazole (Tbz) residues were present in peppermint (Mentha piperita L.) plant tissue 64 to 89 days after application. The authors of this study noting:




“propiconazole was detected at levels of 0.06 mg/kg and 0.09 mg/kg of dry weight, and tebuconazole was detected at 0.26 and 0.80 mg/kg dry weight, in identical trials…. .”[39]


(End Quote)


When scrutinizing these figures, the Pcz residues fall below various country-by-country maximum residue limits (MRLs). For example, the EPA MRL for Pcz is, in or on bean at 0.70 ppm; vegetable, foliage of legume at 30 ppm; tomato at 3.0 ppm; citrus fruit at 8.0 ppm; stone fruit, except plum, at 4.0 ppm; and plum at 0.60 ppm.


Keep in mind that 1ppm (part per million) of a solid is the same as 1mg/kg. Therefore, when looking at the research on Pcz residues in peppermint by Garland et al (1999), 0.06 mg/kg is 0.06ppm and 0.09 mg/kg is 0.09ppm. Given that the EU estimate for acceptable daily intake of Pcz for humans is 0–0.07mg/kg bw a lot of peppermint would need to be ingested in a day (many kilos) to meet, or exceed, the EU limit.


Conversely, while research on Pcz and other triazole residues in indoor crops is extremely limited, a study by Serge Schneider et al (2014) found triazole residues in samples of seized cannabis.


A total of 50 samples were tested for 160 different pesticides. Seven different pesticides were detected in 19 samples and five samples contained two pesticides. Four of the pesticides detected were fungicides (propamocarb, tebuconazole, propiconazole and tolylfluanid).[40]


One sample that was tested showed a whopping (massive!) 800mg/kg (800ppm) of the triazole tebuconazole, with another sample showing 80mg/kg (80ppm – well above MRL). Tebuconazole is listed as a possible human carcinogen by the US Environmental Protection Agency (EPA) and is linked to birth defects.


Concerning toxicity to the end user and how much triazole exposure cannabis smokers would be exposed to; in research conducted by the California based Werc Shop (Independent medical marijauana testing laboratory) risk of pesticide exposure to medical cannabis patients was explored. A laboratory setup was constructed in which the mouthpiece of the smoking device was fixed to tubing leading to a cold trap containing an organic solvent at low temperature. Inhalations were simulated using a vacuum pump and timed valve. The settings were made such as to represent the smoking behaviour of a typical adult cannabis smoker. The material used for this study was a single batch of medical cannabis which was prepared for use by applying ~750μg of various pesticides, diluted in acetonitrile (all pesticides adjusted for purity) one at a time to 5 separate sample lots containing ~2.3g of cannabis in round bottomed flasks. The pesticides tested were imidacloprid, permethrin, bifenthrin, pyridaben, cypermethrin, indoxacarb, t-fluvalinate, deltamethrin, carbaryl, propiconazole, acetamiprid, dicofol, diazinon, malathion, thiamethoxam, tetramethrin, bifenazate, and tebuconazol.


The results found a relatively large difference in recovery of residues between the different pesticides. The authors concluded that this was due primarily to the stability of each compound and to what extent degradation/pyrolysis occurs under combustion.


The relative recovery of pesticide residues in the smoke stream ranged from 11.4% – 95.0% recovery from a non-filtered glass pipe, 10.6% – 71.9% from the waterpipe without filters, and 0.3% – 20.4% from a triple-filtered waterpipe with filters.


The authors noting:




“The recovery levels from the unfiltered devices were alarmingly high, demonstrating the resilience of pesticides to heat degradation.”


[End Quote]


It is important to note that when compared to most other pesticides and fungicides that were tested in this study, a high degree of triazole residues remained present in the cannabis smoke stream. For example 95% and 53.1% of tebuconazole and propiconazole respectively were present in the smoke stream where an unfiltered glass pipe was used. What this really means is that where using actives such as Pcz as growth retardants, residues will be present in the harvested product, and a high percentage of these residues can be ingested (through combustion and inhalation) directly into the lungs (re medical cannabis crops).


Basically, as with chemical GA biosynthesis inhibitors such as paclobutrazol, the use of chemical BR biosynthesis inhibitors may present with health implications for the end user. This is particularly true for immune suppressed individuals who are exposed to pesticide and/or fungicide residues.


There are undoubtedly flowering additives available through the hydroponics industry that contain triazole BR biosynthesis inhibitors. These products, much like chemical GA biosynthesis inhibitor containing additives can be identified (regardless of listed actives or their marketing) through their ability to dramatically reduce stretch.


Note that some hormone based additives elicit similar responses in plants (i.e. reduced stem elongation and closer internodes); however, their effect isn’t as pronounced. For instance, recently it was shown that there is a cross-talk between cytokinin (CK) and BRs.[41] Therefore, not only does CK offset stem elongation through altering the endogenous GA to CK ratio, but also it is possible that a similar response may occur due to the cross-talk between CK and BRs.


To put things very simply, given the phytohormones we have covered to date, when discussing stretch (cell/stem elongation), GA and BRs promote stretch, auxins promote GA biosynthesis[42] (Ross et al., 2000, 2003) and, thus, promote stretch (Cleland, 2010), while cytokinins promote short bushy plants. The ratio between the hormones will determine the final response.


Anyway, auxins, cytokinins, gibberellins and brassinosteroids aside, let’s now have a look at a phytohormone that acts to antagonize GA biosynthesis and elicit other desirable traits in plants (e.g. increased trichome production).


Jasmonic Acid (JA)


Growth and defense tradeoffs are thought to occur in plants due to ‘biotic’ (i.e. living disturbances such as fungi and pests) and ‘abiotic’ (i.e. factors that occur in nature such as high temperatures, drought, extreme sunlight and high UV) stresses, which demand prioritization towards either growth or defense, depending on external and internal factors. These tradeoffs have significant implications to growth because both processes are vital for plant survival, reproduction, and, ultimately, plant health.


While many of the molecular mechanisms underlying growth and defense tradeoffs remain to be fully understood, phytohormone cross-talk has emerged as a major player in regulating the balance between growth and plant defense.


For example, increased levels of the phytohormone jasmonic acid (JA) are found in plants challenged with biotic and abiotic stresses.[43] The increased JA levels are usually associated to enhanced defense, reduced growth and decreased stem elongation in many species.[44] These growth, stress responses are attributed to several things.


Firstly, JA is shown to antagonize gibberellin (GA) biosynthesis. For example, a study by Maria Heinrich et al (2013) with Nicotiana attenuata, a species of wild tobacco, demonstrated that high levels of JA inhibit stem elongation through antagonizing the biosynthesis of gibberellins.[45] Keep in mind that gibberellins are plant hormones that are primarily responsible for stem elongation. Most synthetic plant growth regulators/retardants (PGRs) antagonize GA biosynthesis in plants. Therefore, because JA antagonizes GA biosynthesis, this acts to reduce stem elongation.


Secondly, JA increases ethylene production.[46] This acts to, among other things, reduce stem elongation/stretch. For instance, when discussing the chemical PGRs that reduce stretch, n example of one such PGR is ethephon. Unlike other PGRs, ethephon does not inhibit gibberellin or brassinosteroid biosynthesis. Instead, plants take up ethephon where it is converted to ethylene in plant cells. The increased ethylene causes cells to limit elongation and increase in width. Besides this, the release of ethylene reduces apical dominance, which can increase axillary branching. Additionally, JA has been shown to stimulate fruit ripening, most likely through its action on ethylene biosynthesis.[47] This means that JA can speed up the flowering process.


Thirdly, JA is shown to cross-talk with IAA (auxin) which plays a role in reducing stem elongation. For example, a study by Ueda et al (1994) showed exogenously applied JA substantially inhibited IAA-induced elongation of oat coleoptile (tissue surrounding the shoot axis or tissue in young leaves) segments.[48] Several other authors report similar findings.


So, all of this information sounds great!! Jasmonic acid, much like chemical GA biosynthesis inhibitors, antagonizes GA and much like ethephon stimulates ethylene production which, in turn, reduces stem elongation/stretch. Therefore, given the material we have covered to date surrounding stretch and chemical PGRs the application of jasmonic acid, theoretically, should elicit desirable outcomes re growth and yields in several types of indoor crops… Yes?


Well, not quite!


Unfortunately, increasing yields through growth retardation/regulation is extremely complex biochemistry involving e.g. up regulation, down regulation, the GA pathway, GA1, hydroxyl groups, carboxyl groups, DELLA proteins, enzymes, GA production sites, cross-talk, brassinosteroids, brassinosteroid biosynthesis inhibitors and so many phytohormone specific pathways criss-crossing and intersecting one tends to become easily lost. However, let’s not get caught up too much in this lest we become bogged down in a quagmire of indecipherable plant physiology jargon.


To put things simply, while JA inhibits GA biosynthesis this doesn’t mean it operates at the same level as the various chemical GA biosynthesis inhibitors (which, in themselves, operate at several different levels). Further, while JA stimulates ethylene production, this doesn’t mean it equates to the same thing as the PGR ethephon.


Even subtle/minute differences between hormone ratios and levels can result in quite different morphological responses in plants and different for each genus/species. Therefore, while JA antagonizes GA biosynthesis and increases endogenous ethylene levels its application results in quite different responses than would occur when synthetic PGRs are applied. In fact, while PGRs can increase yields through reducing stretch and increasing lateral branching, bud sites and bud growth, the application of JA is shown in many species to have the opposite outcome. That is, the application of JA is shown, in many cases, to reduce yields (put simply).


Keep in mind that growth and defense tradeoffs are thought to occur in plants due to ‘biotic’ and ‘abiotic’ stresses, which demand prioritization towards either growth or defense, depending on external and internal factors. These tradeoffs have significant implications to growth, hence yields, because both processes are vital for plant survival, reproduction, and, ultimately, plant health. Therefore, when a plant directs its energy towards defense it has less energy to direct towards growth and yields suffer as a result.


The problem here is that JA acts as a signal that directs plants towards defense and as a result the trade off is growth. For example, various studies have shown reduced yields in several species where JA has been exogenously applied or induced through stress.[49], [50], [51]


However, conversely, in many cases, these studies also demonstrate increased terpenoid and phenolic production[52] and this is where JA can become a beneficial element/additive for indoor hydroponic growers (and others). Further, it has been my experience that JA has limited use as an effective, non-toxic growth/stretch retardant (i.e. a safe, non-toxic alternative to synthetic PGRs) when used via foliar spray as a one off or, at most, when applied twice, a week apart, during the stretch cycle (i.e. the first 2 – 4 weeks – strain dependent – of the 12/12 light cycle) with particularly leggy genetics/strains.


Jasmonic Acid – An Essential Oil Elicitor (+Trichomes, + Terpenes, + Phenolics ++)


Virtually all plant species possess some kind of hair-like epidermal structures. When these structures are present on the aerial parts of a plant, they are commonly referred to as trichomes. Trichomes are, in most cases, not connected to the vascular system of the plant, but instead are extensions of the epidermis from which they originate.


There are two types of trichomes found in plants, non-glandular and glandular. Non- glandular trichomes are unicellular, while glandular trichomes are usually multicellular, consisting of a differentiated basal, stalk and apical cells and can be found on approximately 30% of all vascular plants.[53] Glandular trichomes, also referred to as secretory or peltate trichomes, have in common the capacity to produce, store and secrete large amounts of different classes of secondary metabolites such as terpenes (compounds that are responsible for the taste and smell of many plants), phenolics, lignans and alkaloids.


Trichomes play important protective roles as structural defenses upon biotic attacks such as pest and fungal infections, and against abiotic stress factors such as drought, heat, and excess light. .


Trichomes can be induced by wounding and insect attack[54] and the phytohormones involved in signalling these stress responses are jasmonic acid (JA) and salicylic acid. That is, there is a ‘negative’ cross-talk between these two phyothormones and the positive effect of jasmonic acid on trichome production is antagonized by salicylic acid.[55] For example, in research by Traw et al with Arabidopsis (2003) it was shown that the exogenous application of JA caused significant increases in both trichome density and number. Conversely, where salicylic acid was applied it caused significant decreases in both trichome density and number. Additionally, it was shown that gibberellin and jasmonic acid have a synergistic effect on the induction of trichomes, suggesting important interactions between these two compounds.[56]

In another study, Richard Karban et al clipped leaves of sagebrush plants to mimic insects eating their leaves. The cut sagebrush released jasmonic acid’s volatile ester, methyl jasmonate (MeJA), which the wind carried to nearby downwind tobacco plants. The plants sensed the MeJA, and this induced a defense response which resulted in increased trichome production. Additionally, jasmonate treatment significantly increased nicotine concentrations in the leaves of treated plants 22-54% above their water-treated counterparts (control).[57]

In yet another study, it was shown that 7 and 14 days after treatment with MeJA, the mean density of glandular trichomes on new leaves of MeJA-treated tomato plants was nine fold higher than on leaves of non-treated plants.[58]


JA, Secondary Metabolites (e.g. terpenes/terpenoids, phenolics, lignans, alkaloids)


Having covered that a large degree of secondary metabolites form/occur in/on the trichomes of plants, and having highlighted JAs capacity to increase trichome density and number, let’s now look at JA and its role in stimulating/manipulating secondary metabolites.


I’ll try to keep this as simple as possible because an entire book could be written on the subject (several, in fact) and there are numerous secondary metabolites and mechanisms that are involved in their production. For now, in brief…


Plants produce a large and diverse array of secondary metabolites. These secondary metabolites appear to have no direct function in growth and development; i.e. they have no role in the process of photosynthesis, respiration, nutrient assimilation etc.[59]


Although the situation is not fully understood it is believed that most of the 100,000 known secondary metabolites are involved in plant defense systems, which were formed over the millennia during which plants have co-existed with biotic and abiotic stressors.[60] Thus, secondary metabolites, including terpenes, phenolics and nitrogen (N) and sulphur (S) containing compounds, defend plants against a variety of herbivores and pathogenic microorganisms as well as various kinds of abiotic stresses (e.g. extreme heat, drought, UV light).


The main classes of secondary metabolites that have been found to be produced in trichomes include terpenes/terpenoids, phenolics, methyl ketones, acylsugars and defensive proteins.


Although higher concentrations of secondary metabolites might result in a more resistant plant, the production of secondary metabolites is thought to consume a lot of energy and, as a result, reduces plant growth and reproduction.[61] Therefore, the production of secondary metabolites falls within the growth, defense tradeoff’ paradigm. Keep in mind that these tradeoffs have significant implications to growth because both processes are vital for plant survival, reproduction, and, ultimately, plant health – hence yields. Put simply, if a plant directs energy towards defense this leaves it with less energy to direct towards growth and vice versa. Therefore, inducing plant defense to increase quality (i.e. increase trichome size and density and stimulate secondary metabolites) needs to be handled with care.


Terpenes constitute the largest class of secondary metabolites.[62] Terpenes are the primary constituents of the essential oils of many types of plants and flowers. They are extremely important secondary metabolites because, among other things, they are ‘quality’ secondary metabolites and are associated to the colours, taste and flavour of the plant. For example, terpenes contribute to the scent of eucalyptus, the flavors of cinnamon, cloves, and ginger, and the color of some flowers. Well-known terpenes include citral, menthol and cannabinoids. Therefore, through stimulating/increasing the terpene production of a plant we can enhance and/or modify its qualities.


Other than terpenes, for purposes of interest here, phenolics are another extremely important secondary metabolite that influences flavour and colour. Phenolics include flavonoids, isoflavonoids and tannins. There are about 8000 known phenolic compounds found in plants. They are often found conjugated to sugars and organic acids. Phenolics are categorized into two groups, flavonoids and non-flavonoids. Flavonoids make up the largest number with about 4500 known flavonoids in plants. Among the important flavonoids are the flavAnols, cachtechin (found in green tea, cocoa powder and red wine), epicactechin, anthocycanins (influence fruit colour), flavones, flavanones (found in high concentrations in citrus fruit) flavOnols and more. Preharvest, applications of JA/MeJA have been shown to increase total phenolics in fruit and flowers. For example, studies have shown that the application of MeJA and benzothiadiazole (an analog of salicylic acid, and methyl jasmonate) increases phenolic compounds in grapes. One study that spanned two years concluded both compounds increased grape flavonoids, including anthocyanins, proanthocyanidins, and flavonols in both years of the study. Further, wine from the treated grapes showed a higher total phenolic content when compared with wine that was made from untreated grapes.[63]


Elicitors are compounds, which activate chemical defences in plants. Various biosynthetic pathways are activated in treated plants depending on the compound that is used. The most studied and understood elicitor is jasmonic acid and/or its derivative, methyl jasmonate (MeJA), which modify the production of secondary metabolites such as terpenes and flavonoids. For example, JA/MeJA treatment can give rise to increased trichome densities on newly formed leaves. Additionally, terpene emission can be induced in tomato glandular trichomes by spraying plants with JA/MeJA. Apart from terpenes and defensive proteins, also acylsugars and alkaloids can be induced in glandular trichomes by spraying plants with MeJA.[64] Additionally, MeJA, due to being a chiral compound (there are two chiral carbon atoms in the methyl jasmonate molecule), is described by John Leffingwell (2003) as a valuable fragrance material (whose stereoisomers have remarkably different odor intensities).”[65] For example, MeJA makes up some 2-3% of jasmine oil while methyl epijasmonate, which exhibits a powerful lemon and jasmine-like odor, was identified for the first time in lemon peel by Nishida and Acree (1984). Basically, methyl jasmonate and a diasteroisomer of methyl jasmonate, methyl epijasmonate, can play an extremely important role in the odor that a plant and its produce emits.


Volatile compounds are responsible for odor. Odorous plants synthesize and constitutively store relatively large amounts of volatiles, and these may play a role in defense against herbivores. At least one study has shown that where odorous plants are exposed to herbivore wounding or applied with MeJA, increased existing volatile emissions predominated; however some new volatiles were detected only in response to herbivory damage and MeJA treatment suggesting de novo synthesis (i.e. new/novel odors were produced or, more technically, complex molecules from simple molecules resulted).[66]



Radhika Venkatesan, a PhD student at the International Max Planck Research School in Jena, studied Brassica napus, a widespread and agriculturally important plant species. She found that when its flower tissues produced jasmonates during an early developmental stage, nectar production was immediately activated, regardless of whether the plant had been attacked by herbivores or not. Additionally, the study showed that the floral tissues of plants produce jasmonic acid (JA) endogenously, and JA concentrations peak shortly before nectar secretion is at its highest. The exogenous application of JA to flowers induced nectar secretion, which is suppressed by treatment with phenidone, an inhibitor of JA biosynthesis.[67]


In a study by Wang et al (2005) MeJA was applied to black and red raspberry being grown under field conditions. Raspberries treated with MeJA had higher soluble solids content, total sugars, fructose, glucose, sucrose and lower titratable acids, malic acid and citric acid than untreated fruit. MeJA application also significantly enhanced the content of flavonoids and the antioxidant capacities in the fruit.[68]


You’re perhaps getting the idea by now, so let’s leave the phytohormone jasmonic acid there.


To wrap it up, JA/MeJA can be used during the stretch cycle (with care) to reduce stem elongation/stretch. Further, the key benefit to applying JA/MeJA is that it increases terpenes, phenolics and volatile compounds which results in higher quality yields (improved resin production, flavour, odour and potency).


We will add more to the article shortly




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