Archive for the ‘Plant Hormones’ Category

joker-card-01.jpgHow To Screw Organic Farmers

In a recent issue of our local paper, there was a tragic story about how several organic farmers in the region had unknowingly purchased manure which turned out to be contaminated with a powerful herbicide. Consequently, they lost most of their crops. And they certainly lost their organic seal of approval.

How did this happen? And how common is it for organic growers to be screwed in this way?

This story led me to investigate instances of herbicide contamination in so-called “organic” manure.

It turns out that instances of this problem have been reported for several years. Cases were well documented in England in 2008 and 2009. ( Map of contaminated manure UK 2008/2009 ) Indeed, the herbicide in question was banned in the UK, at least, for time. (UK ban petition) It was reinstated in April, 2010.

Here’s the story.

As described in a previous posting, many herbicides work by interfering with the plant hormone auxin. These so-called auxinic herbicides have been around for long time. So long that some plant species targeted by these herbicides have developed resistance to them.

Chemical companies such as Dow Chemical have overcome this resistance by making chemical modifications to these herbicides in order to create new versions. An example of this is the herbicide aminopyralid.

This herbicide was introduced several years ago and is proven to be a problem because of its resistance to biological breakdown. It persists in hay, manure, compost, and grass clippings (also, see refs below).

From the makers of this product: DOW Agrosciences UK and DOW Agrosciences USA

Does your manure contain herbicides?

Bioassay for herbicides in manure – Mother Earth News

And, finally, a personal story – Persephone Farms.


1. Aminopyralid Residues in Compost and other Organic Amendments – Whatcom County Extension

2. Persistent Pesticide As Organics Recycling Foe

3. Davis, J., S.E. Johnson, and K. Jennings (2010) “Herbicide Carryover in Hay, Manure, Compost, and Grass Clippings: Caution to Hay Producers, Livestock Owners, Farmers, and Home Gardeners”, North Carolina Cooperative Extension. (PDF)

4. Aminopyralid Family of Herbicides, Dow AgroSciences (2010) (PDF)

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Can Chemically Inducing Dormancy Help Plants Cope With Stress?

sleepyhead.jpgThis was a very bad year for wheat in Russia because of an extraordinarily hot and dry summer. And many climatologists believe this may be only a glimpse of the not-too-distant future in many parts of the world. If so, then it is of critical importance to find ways to make crop plants more drought and heat tolerant.

One way to do this, of course, is to develop new varieties of crops that can better withstand hot, dry summers. Unfortunately, using conventional plant breeding, this typically takes a very long time, sometimes decades.

But what if it was possible to spray plants with a chemical that induces them to become more tolerant of heat and drought?

Some scientists believe that research reported in the last couple of years have brought us steps closer to such a scenario.

Abscisic Acid = The Plant’s “Sleeping Pill”?

green_pills.jpgAs mentioned in a previous post, the plant hormone Abscisic Acid (ABA) triggers the closing of stomata in plant leaves in response to water stress. It also is well known in promoting dormancy in seeds of many plant species. (ABA may also play a role in maintaining a state of dormancy in other parts of plants, but scientific evidence for this is equivocal.)

In a way, plant dormancy is somewhat analogous to sleep in that it may induce a sort of near inactive metabolic state in plants.

In such a state, plant cells and tissues are usually better able to withstand extremes of cold, heat, and drought. Briefly, this is due to the expression of protective proteins, such as dehydrins, and to changes in the cellular structures, such as the composition of cell membranes.

What ABA does is trigger the cellular processes involved in such changes. The question that has confounded scientists for many years is exactly how ABA does this.

Targets and messengers.

It turns out that 2009 and 2010 have been very good years for research on the mode of action of the plant hormone ABA.

In 2009, several laboratories, including Sean Cutler’s lab at UC Riverside, identified ABA receptors, that is, cellular proteins that specifically bind to ABA.

And this year, much more was learned about the docking site for ABA on these proteins and about what these proteins do. (See here and here for more about this.)

Briefly, these proteins function as phosphatases, which often function to regulate the activity of other enzymes. In this way, they act as an army of messengers, greatly amplifying and elaborating the ABA signal.

Artificially Inducing Dormancy?

Information about the ABA docking site may allow scientists to develop chemicals, such as pyrabactin, that can mimic the action of ABA, but that are way more stable and cheaper than the natural plant hormone ABA itself.
Some scientists envision the use of such chemicals as a way to artificially induce a transient dormancy-like state in growing crop plants, such as wheat for example, in order for them to survive episodes of extreme heat and drought.

For example, Dr. Mike Sussman, from a recent article regarding his work on ABA puts it this way: “”Since they cannot walk or run, plants have developed an interesting and complicated system for sensing and responding very quickly to dehydration and other stresses,” says Sussman, noting that, on average, a plant is composed of 95 percent water. “Most plants have what’s called a permanent wilting point, where if water content goes below 90 percent or so, they don’t just dehydrate and go dormant, they dehydrate and die.”

Figuring out how to trigger a dormant state, such as exists naturally in seeds, which are 10 percent water and can in some cases remain viable for hundreds of years, could be key to creating plants that survive drought in the field, Sussman explains.

It’s possible that someday farmers will spray their wheat fields with such chemicals, which will induce the plants to “sleep through” an unusually hot, dry period.

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apical_dom.jpgPlant Cut-Backs

Pruning is one of the most important cultural practices for maintaining woody plants, including ornamental trees and shrubs, fruits and nuts. It involves both art and science: art in making the pruning cuts properly, and science in knowing how and when to prune for maximum benefits.” (from ref. 1 below)

Briefly, the main effect of pruning a plant is to stimulate the growth of axillary buds (a.k.a., lateral buds).

But why is the growth of axillary buds stimulated by cutting off the terminal (or apical) bud?

The most common explanation to this question, dear readers, is the long-known, and somewhat confounding, phenomenon called “apical dominance”.

The Curious Case of Apical Dominance

Apical dominance is defined as the control exerted by the shoot tip on the outgrowth of axillary buds, whereas correlative inhibition includes the suppression of growth by other growing buds or shoots. The level, signaling, and/or flow of the plant hormone auxin in stems and buds is thought to be involved in these processes.” (from ref. 2 below)

But hold on a second, I thought auxin stimulated plant growth.

Apical_Dominance.jpgThis contradiction was noted way back in 1933 by the eminent plant physiologists Kenneth Thimann and Folke Skoog – “…it seems paradoxical that a substance promoting cell extension can also act as an inhibitor….” (from ref. 3 below)

New Evidence

In a previous post back in the fall of 2008, I reported on the discovery of proposed new class of plant hormones called strigolactones.

These compounds, derived from carotenoids, were shown to inhibit shoot branching.

Since then, research on strigolactones, especially as they relate to apical dominance, has yielded evidence that auxin may indirectly stimulate the production of strigolactones (see ref 4 below).

So, does reducing auxin in the plant by removing the apex via pruning also reduce the levels of strigolactones, which, in turn, may increase the growth of axillary buds?

It’s likely not that simple an answer. Other factors such as the plant hormone cytokinin are also involved.

Bottom Line: Pruning works by disrupting a natural process we call apical dominance, which is likely the result of complex interactions among two classic plant hormones (auxin and cytokinin) and one new one (strigolactones).


1. Wade, G.L. and R.R. Westerfield “Basic Principles of Pruning Woody Plants” The University of Georgia Cooperative Extension.

2. Ferguson, B. J. and C. A. Beveridge (2009) “Roles for Auxin, Cytokinin, and Strigolactone in Regulating Shoot Branching” Plant Physiology vol. 149, pp. 1929-1944.

3. Thimann, K. V. and F. Skoog (1933) “Studies on the Growth Hormone of Plants III. The Inhibiting Action of the Growth Substance on Bud Development” Proc Natl Acad Sci (USA) vol.19 pp.714–716.

4. Hayward, A., P. Stirnberg, C. Beveridge, and O. Leyser (2009) “Interactions between Auxin and Strigolactone in Shoot Branching Control” Plant Physiology vol. 151, pp. 400-412.

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379759639_4afaae1d71_m.jpgSniffing Out Ethylene

In the previous post I summarized the latest information on how the plant hormone ethylene is made (at least in the model plant Arabidopsis).

Though most people are familiar with the plant hormone ethylene mainly because of its effects on fruit ripening, the list of plant responses to ethylene is long.

How do plants manage to detect (“sniff out”) minute quantities of this gaseous plant hormone?

And how do minute quantities of ethylene, once detected by the plant, elicit such a wide array plant responses, from stimulating seed germination in some plants to promoting aging in others, for example?

Detecting the Ethylene Signal

In order to listen to FM radio, you have to have a FM receiver.

That is, in order to detect FM radio signals (at frequencies invisible to our eyes), you have to have a way to detect such weak signals. (The rest of the radio is for amplifying the signal so you can hear it.)

gymnist.jpgHow do plants detect the weak ethylene signal?

They have ethylene receivers, or in biological terms, ethylene “receptors” that can very specifically discern ethylene from other small molecules. (Hormone receptors are typically proteins because they have the ability to form very complex and precise 3D structures. This allows for their high specificity in recognizing distinct molecular structures.)

It turns out that each ethylene molecule interacts with two receptors, which are paired together to form a pair or “dimer”.

In the photo on the right, the two rings are like the two individual ethylene receptors, and the gymnast is like ethylene.

Interestingly, these ethylene receptors are transmembrane proteins located inside plant cells in the endoplasmic reticulum (ER). (Since ethylene is a relatively small gas molecule, it can easily pass through the plant cell membrane from outside to inside the cells.)

In Arabidopsis there apparently is a 5-member family of these individual ethylene receptors. Each member of the family can pair with another copy of itself to form a “homodimer” functional ethylene receptor or with other members of the family to form a “heterodimer”. (The term “homodimer” is used when the two molecules are identical, e.g. A-A, and “heterodimer” when they are not, e.g. A-B.)

Thus, the ethylene serves as a “key” in the receptors’ “lock”, setting in motion a cascade of events…….

Amplifying the Ethylene Signal
You text a secret to two friends. Then each of your friends texts the secret to two more people. Then each of these people text the secret to two of their friends. And on, and on, and pretty soon it’s no longer a secret.

This “cascade” of events effectively “amplifies” the original text message. The ethylene signal is similarly amplified via a cascade of cellular events. For example, when ethylene binds to its receptors, this causes conformational changes in these receptor proteins, which then “activates” them…somewhat analogous to you using your car key (ethylene) to start your car (receptor proteins).

The “activated” receptor proteins, in turn, initiate an intracellular signal cascade ultimately leading to the expression of an array of genes, which collectively result in the “display” we observe, whether it be inhibition of shoot growth or fruit ripening.

Which genes ethylene “turns on” depends on the biological “context”, that is, what part of the plant?, what stage of the plant’s development?, what plant species?, etc.

Qiagen offers an illustration of “The Big Picture” of the ethylene signaling pathway in Arabidopsis, though it’s somewhat technical.

Bottom line: Decades of scientific research has revealed not only the receptors for ethylene in several plant species but also a complex cascade of cellular events leading to the plants’ responses to ethylene that we can observe in nature.

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ethylene_T.jpgC’est un gaz. Es un gas. Es ist ein gas. It’s a Gas!

If you are familiar with the gaseous plant hormone ethylene, it’s most likely because of its ability to promote fruit ripening in apples, bananas, tomatoes, etc..

Ethylene also affects many other aspects of a plant’s life cycle, including seed germination, growth and development, responses to physical and biological stress, leaf abscission, and senescence.

It may even be responsible for how some herbicides kill plants.

But how does ethylene work?

That is, how can this simple gas (CH2-CH2) mediate so many different processes in plants? Where and how is this chemical signal produced in plants? And how is this signal received by plant cells and then amplified into the responses we observe?

Making the Signalethylene_T2.jpg

Virtually all the cells in a plant have the potential to make ethylene. Plant cells make ethylene starting from the amino acid methionine (see below).

And it turns out that during the course of a plant’s life – from seed germination to senescence – ethylene may be made not only as part of the developmental program of the plant, but also in response to random events, such as wounding and pathogen attack.

The primary way plants (at least Arabidopsis) regulate the amount of ethylene is through the expression of a family of genes that encode enzymes (the ACS protein family) that catalyze the synthesis of the key metabolic precursor to ethylene, namely, ACC*.

Methionine –> SAM* –ACS proteins –> ACC* + O2 –> Ethylene
* SAM = S-Adenosyl-L-Methionine, ACC = 1-AmminoCyclopropane-Carboxylate

(Please see here for diagram of ethylene biosynthetic pathway in plants.)

Quoting part of a recent report (ref. 1 below) on the genetics of ethylene biosynthesis:

“We view the ACS protein family as a “Symphony Orchestra” (45-member when all nine genes are expressed in a cell) that regulates ethylene-mediated processes by generating appropriate amounts of ACC in the proper spatial and temporal manner through their harmonious interplay. At any given moment, the orchestra is tuned by various inducers to produce ACC sufficient to mediate myriad ethylene responses…”


So, this may explain why the biosynthesis of ethylene in plants can be affected by so many different factors.

Next-time: The Ripe Stuff – Part 3: How Plants Respond to Ethylene


1. Tsuchisaka, A., et al. (November 2009) “A Combinatorial Interplay Among the 1-Aminocyclopropane-1-Carboxylate Isoforms Regulates Ethylene Biosynthesis in Arabidopsis thaliana.” Genetics vol. 183, pp. 979-1003. (PDF)

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green_tomatoes.jpgFried Green Tomatoes

About this time of year in the North Temperate Zone people may be getting very tired of fried green tomatoes and green tomato pie.

As a plant physiologist, I was often asked how to ripen green tomatoes. (Rather than go into this here, I’ll refer you to this recent blogpost.)

You probably already know that tomato ripening is promoted by the gaseous plant hormone ethylene.

Regarding ethylene, one of the best online resources I’ve found provides comprehensive information about this gas, including a table listing the relative production of, and sensitivity to, ethylene in a large number of fruits and vegetables.

And if you want to inhibit fruit ripening, there’s even a commercial website for reducing ethylene.

Going Green to Red (or Yellow)

But what’s happening to the tomato when it ripens from green to red? And to the banana when it goes green to yellow (and then brown)?

The change in color is primarily the result in the active conversion of chloroplasts to chromoplasts. The chlorophyll is actively (enzymatically) broken down, and the red and yellow colors are due mainly to carotenoid pigments in the chromoplasts.

Since the fruits are there primarily to promote seed dispersal by animals, red colors apparently tend to attract birds, for example. Interestingly, as reported here, at tropical temperatures (about 90o F), the Cavendish banana skin tends to stay green, though the fruit ripens.

“Over-ripe” fruits (the brown banana, for example) tend to be primarily the result of senescence.

Fruit Softening

The “softening” of the fruit is the result of the breakdown of plant cell walls by cell wall-digesting enzymes such as cellulases, pectinases, and expansins.

Indeed, scientists were able to extend the shelf-life of the Flavr Savr tomato by effectively turning off the gene coding for a pectinase.

Getting Sweeter

Another characteristic of fruits that tends to attract some animals for seed dispersal is the presence of sugars. Increased sugars in the process of fruit ripening is due mainly to the production of enzymes that break down starch.

Interestingly, the process of fruit ripening involves many enzymes that digest polymers of sugar molecules (i.e., cell walls and starch).

How does ethylene promote ripening?

The expression of many of the above enzymes is promoted by ethylene in plant species that have so-called climacteric fruits, such as tomatoes and bananas. (Please see here for a list of climacteric and non-climacteric fruits.)

Climacteric fruits are characterized by a burst of cellular respiration that is often immediately preceded by, or happens simultaneously with, a sharp increase in ethylene. (Ethylene also may promote its own biosynthesis.)

Ethylene is an essential component of climacteric fruit ripening. Blocking ethylene biosynthesis or action prevents ripening.

Ethylene apparently regulates the expression of many ripening-associated genes, including those coding for enzymes involved in color change, fruit softening, and starch breakdown. (How ethylene activates such genes is a topic for another day.)

How “One Bad Apple Spoils the Bunch” (and ripens your green tomatoes).

As mentioned above, ethylene may promote its own biosynthesis in climacteric fruits.

So an over-ripe apple producing a lot of ethylene gas – which diffuses throughout the bunch – triggers the biosynthesis of ethylene in the rest of the apples (and also in your green tomatoes), thus promoting the ripening process.

Bottom line: For climacteric fruits, the gaseous hormone ethylene is indeed “the ripe stuff’.

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dandy1.jpgWhat Do Suburban Lawns and the Vietnam War Have in Common?

Answer: The herbicide 2,4-D.

You may be familiar with this herbicide as an active ingredient in “Weed ‘n Feed®”, “Weed B Gon MAX®”, Turf Builder® With Weed Control”, etc..

During the Vietnam War, it was an active ingredient in Agent Orange.

On lawns it’s used to kill the dandelions, but NOT the grass. (Find out how it does this below).

In the Vietnam War the U.S. military used it to defoliate the trees (so that they could more easily spot the Viet Cong).

You’re likely familiar with the term “Agent Orange” because of the controversy regarding the tragic health problems it caused to U. S. soldiers. (For current info re. this issue see here).

The serious health issues to both Americans and Vietnamese caused by Agent Orange are due to contaminants called dioxins produced during its chemical synthesis. (For more info on this see 2,4-D and dioxins and also here.)

But since this post is about how such herbicides work on the plants, let’s leave dioxin issues aside (for now).

Herbicides Such as 2,4-D are Auxinsdandy3.jpg

Auxin in perhaps the most well-known plant hormone. (I’ve previously discussed auxin in this blog here.)

The herbicide 2,4-D is a synthetic auxin first produced in the 1940’s. It is one of many so-called phenoxy herbicides. These herbicides all are both structural and functional analogs of the natural auxin indole-3-acetic acid (IAA). That is, these synthetic auxins not only are structurally similar to IAA, but they are also biologically active as auxins in plants.

Although they both look and act like auxins, plants can not metabolize these phenoxy herbicides as they can with IAA, the natural auxin.

This turns out to be the key to why phenoxy herbicides such as 2,4 D are able to kill some plants.

How Does 2,4-D Kill Dandelions…?

Auxin-based herbicides are referred to as “selective” herbicides because they kill so-called “broadleaf” plants (a.k.a., dicots) but not grasses, for example. (Hence, that’s why they’re such popular herbicides with both growers of lawns as well as of wheatfields.)

But how exactly does spraying 2,4-D on susceptible plants kill them?

This turns out to be very poorly understood, and it’s also the subject of much misinformation. For example, I’ve heard people say that such herbicides “grow the plant to death” and read that 2,4-D “…simply confuses the plant to death”. Huh?

dandy2.jpgAt the present time nobody really knows precisely how the auxin-like herbicides kill susceptible plants. As with most effects of plant hormones, it probably has a lot to do with the plant species in question.

However, recent findings have provided important clues. And these clues support the idea that plant death may occur as a result of a combination of factors.

Here’s a summary of the story:

First off, one of the well-know effects of excess amounts of auxin on dicots is to cause them to overproduce the plant hormone ethylene. For example, in 1969, Mary Hallaway and Daphne J. Osborne first showed that ethylene is a factor in defoliation caused by 2,4-D.

Because plants can’t break down 2,4-D, it’s action persists. This action includes the excess production of ethylene, which may result in a number of plant responses, including epinasty and senescence.

Another effect of excess ethylene production in response to 2,4-D is to stimulate the production of yet another plant hormone, abscisic acid (ABA). The effects of ABA on the plant may contribute to eventual plant death. (For an illustration of the complex effects of auxin-based herbicides on plants, see Figure 1 in the reference listed below.)

…and why doesn’t 2,4, D Kill the Grass? (and You?)

Perhaps the simplest explanation for both questions has to do with sensitivity to the plant hormone auxin.

In general, grasses are much less sensitive to synthetic auxin herbicides than are dicots. That is, a much higher threshold level of auxin-based herbicide is required to elicit physiological responses in grasses versus the so-called “broadleaf” plants. So, at the doses used to kill dandelions, for example, grasses are largely unaffected. (Higher doses of 2,4-D may kill the grass, too, however.) Grasses may be more resistant to such herbicides because of differences in leaf morphology, translocation of the herbicide inside the plant, and the ability to metabolize (breakdown) synthetic auxins.

Aside from the toxic contaminant dioxin, 2,4-D has no physiological effects on animals at hormonal levels, that is, at the concentrations that affect plants. (Indeed, there is no reputable evidence that any of the five main plant hormones affects animals.)

Grossmann, K. (2007) “Auxin Herbicide Action: Lifting the Veil Step by Step”, Plant Signaling & Behavior 2:421-423. (PDF)

Bottom Line: The herbicide 2,4-D mimics the plant hormone auxin and sets off a complex series of events – involving two other plant hormones – that eventually lead to the death of susceptible plants. At hormonal levels, auxins affect plants but not people.

Next-Time: More on Herbicides (Is Roundup® Losing Its Punch?)

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