The joys of jasmonate

What would you say if I were to tell you that there is one molecule out there that can meet all of your fragrance and food-preservation needs? If you were to reply that these are two things not commonly combined, well, you’re right. Perfumes are not normally expected or desired to double as anti-bacterial agents (although, given the alcohol content of most perfumes, you could do worse for an antiseptic). However, thanks to the wonders of methyl jasmonate, you can do both.

Say hello to C₁₃H₂₀O₃, the compound responsible for the smell of jasmine, among other things. Methyl jasmonate actually comes in four flavors - the various stereoisomers. For those you who haven’t taken chemistry lately, stereoisomers are different versions of a molecule - the same atoms are all connected in the same order, but the connections themselves are a little different. Maybe a double bond is in a different position. Maybe the angle between two atoms is different. It seems minor, but two isomeric molecules do totally different things. The thalidomide catastrophe came about because one isomer of thalidomide prevents morning sickness, and another causes birth defects. And even if there had been a way to tell the two apart, thalidomide naturally converts between the two isomers in the body.

Happily, there is no such darkness lurking within the heart of methyl jasmonate. Still, you want to be careful. One of the stereoisomers has a strong odor, one has a weak odor, and two are odorless. The odor in question being jasmine, you may want to go with the strongest-smelling stereoisomer. And that isn’t the only complicated chemical thing about methyl jasmonate. Compared to the process by which is this molecule is synthesized in nature, keeping the various stereoisomers straight is child’s play!

Here’s the short version of jasmonate biosynthesis, or the Jasmonic Acid pathway, as it is sometimes called (for comparison, I spent the better part of a month on this in a college class). Methyl jasmonate ultimately derives from alpha-linoleic acid. Alpha-linoleic acid is a crucial and omnipresent fatty acid. Have you been told to consume more flaxseed or walnut oil? Those health benefits you expect to accrue come from the alpha-linoleic acid contained in said oils. In your body, alpha-linoleic acid reduces inflammation and may protect against heart disease. In a plant, however, alpha-linoleic acid is converted to something called oxophytodienoic acid.

This is not just an intermediate by-product. OPDA, as it is known to its friends, is involved in the regulation of seed germination. Specifically, OPDA inhibits germination, and keeps seeds from sprouting prematurely. One of these days, I’ll do a post (or more likely, a week of posts) on chemical signaling in plants, but for now, let’s just say that a key part of plant chemical ecology is inhibitors. Inhibitors prevent plants from leafing out, dropping leaves, reproducing, producing seeds, releasing seeds, and a host of other life processes. In response to external cues, inhibitor levels decrease, and whatever was being inhibited can proceed. So, for instance, warmer temperatures might signal the start of the growing season, and trigger the decline of growth inhibitors within a plant. OPDA, and other intermediates in the JA pathway are major inhibiting chemicals in plants.

OPDA undergoes several more oxidations to form jasmonic acid (hence the name of the pathway). A further chemical conversion tacks on a methyl group (CH₃), and makes that jasmonic acid into methyl jasmonate. So, that’s all very interesting, but why? What is the purpose of all this jasmonic acid and methyl jasmonate? For that, we return to signaling. Plants don’t synthesize jasmonates at a constant rate - synthesis kicks up in response to herbivory. In English, that means that when something takes a bite out of a plant, the plant begins to synthesize large amounts of jasmonic acid and methyl jasmonate. These compounds accumulate in the damaged tissue. Jasmonic acid triggers the production of toxins, which renders the damaged tissue unpalatable to further herbivory  (theoretically. Build a better plant toxin, and evolution will build a more resistant herbivore). Jasmonic acid is used for all kinds of other signaling in the absence of herbivory, but that is another story. Jasmonic acid synthesis helps to prevent the plant. But what about all the neighboring plants? Often, a plant will be surrounded by members of the same species (quite possibly the offspring of the plant, or part of the same clonal patch). How to warn those neighboring plants that there is a hungry herbivore nearby? Remember how fragrant methyl jasmonate is?

                The lovely jasmine flower cleverly sends its own coded signals to its pals.

There you have it. Plants make their own perfume, but as a warning, rather than an aphrodisiac. Methyl jasmonates waft from the damaged tissue, and signal nearby plants to start upping their own JA synthesis (which in turn makes for more toxic and nasty-tasting tissue, which is more likely to deter an herbivore at the slightest nibble). This, incidentally, is why methyl jasmonate does double duty as a perfume and an antiseptic. It is theorized that the presence of methyl jasmonate prolongs the shelf-life of fresh fruits and vegetables, by virtue of signaling the produce to maintain high levels of natural anti-microbial compounds. Fresh produce, while plucked from the plant, is still living tissue, and retains an active plant chemistry even in storage.

It’s an odd quirk of chemical ecology that a molecule signifying “death to the intruder” would be perceived as a pleasant odor by humans. Further quirks of methyl jasmonate chemistry may even give it anti-cancer properties, another function not commonly met in nature. Evolution is messy that way. A chemical adapted for one particular use often has a host of side-uses and unintended (beneficial or malignant) effects. So, don’t judge a molecule by its “intended” use. You never know where we’ll find the next perfume. Or shelf-life enhancer.