A Survey of Phytohormones

Good afternoon, everyone! (It certainly doesn’t feel like afternoon. I woke up two hours ago, and I’ve been novel-writing, as promised, since, so my perception of time is a bit wonky.) I’ve returned from the depths of my own despair to bring you another post on phytohormones, courtesy of my plant biology notes! Buckle up, though—this one’s gonna be a bit of a doozy.

(If this gets a bit incoherent at times, I apologize. I’m listening to The Bus is Late in the background, and I might get strangled. Sapphire hates it. Well, you know what, Sapphire? COME IN HERE AND FITE ME LIKE A—)

Ahem. Anyway. In my last post, I gave you a brief introduction to phytohormones, complete with some passing remarks about their synthesis, transport, and perception. Now, it’s time to get down and dirty and talk about things in more detail—that’s right, we’re getting specific up in here.

You remember that list of hormones that I gave you before? Well, just watch—I’m about to blow through it in less than an hour. (That’s writing time. Hopefully, it’ll take you like… ten minutes. Less, if you’re a freak like Finn.)

Here we go!


Like most stories in biology, the story of auxin begins with Darwin.

In the 1890s, Darwin studied phototropism in plants. “Phototropism” refers to a plant’s ability to “see” light, and it’s something you’ve already seen in action—when plants grow, they grow towards sunlight.

Darwin had the bright idea to cut off the tip of a plant’s coleoptile—a protective sheath in germinating cereal plants—to see what happened. (He also covered only the tips of the coleoptiles, so that they weren’t exposed to light.) He found that, unlike control plants, they exhibited no phototropism—they made no attempt to bend toward a light source. The conclusion, from this data, was that the signal that gave plants the ability to perceive sunlight must travel from the tip of the plant downward.

Forty years later, auxin (indole-3-acetic acid, or IAA) was purified and shown to promote growth. (It’s actually really cool how they did the experiment—they got auxin to soak into agar blocks, and then placed them on decapitated plants. The ones with auxin blocks behaved like they hadn’t had their heads chopped off.) It was also shown that auxin could only move in one direction through the plant—from tip to root. (Remember, we called this “polar transport.”) Using the agar blocks, it was also shown that auxin plays a role in apical dominance; in simple terms, when auxin can travel from the tip of the shoot, branching is suppressed.

In the 21st century, we now have a whole host of molecular tools with which to study auxin. With all these fancy bells and whistles, we’ve managed to pretty much figure this sucker out, from beginning (biosynthesis) to end (signal transduction).


Auxin, or indole-3-acetic acid, is made from indole. (Shocking, I know.) However, most of its biosynthetic pathway use a modified form of indole called tryptophan (an amino acid!). The biosynthetic pathway is very tightly regulated, and is influenced by other hormones and environmental factors (such as temperature or red light/far-red light ratio).

As we said before, hormones can be conjugated to alter their activity. Auxin is no exception. Conjugation to alanine or leucine (nonpolar amino acids) marks it for storage, while conjugation to aspartate or glutamate (basic amino acids) marks it for degradation. (The genes that control Asp- and Glu- conjugation are called GH3 genes, and their overexpression leads to dwarf phenotypes.)


As we established, auxin transport is polar. Specifically, auxin moves from shoot tip to root tip through the phloem (which conducts nutrients from the shoot to the root—remember what we said about the phloem being the plant’s “nervous system?”). This is called “basipetal transport” in the shoot, where it moves from tip to base, but in the root, it becomes “acropetal” (movement from base to tip). At the very tip of the root, auxin turns around and travels up a little again (this time, through transport channels called PINs).


There are two types of receptors for auxin—ABP1 and TIR1. We don’t really understand how ABP1 works yet, but we do get how the TIR1 pathway works. Let’s look, shall we?

TIR1 is an F-box protein, an exchangeable piece of a larger complex called the SCF ubiquitin ligase complex. (“SCF” refers to “SKP1, CUL1 and F-box,” the three components that make up the complex. Ubiquitination is a way that cells mark proteins for degradation. A ligase is an enzyme that attaches something to something else.) When TIR1 is attached, this complex is called the SCFTIR1 complex. Auxin works by being a kind of “molecular glue” that attaches TIR1 to target proteins. Once the target proteins are bound, the ubiquitin ligase complex attaches ubiquitin to the protein, and it is broken down by an apparatus called the 26S proteosome.

Now, you may be asking, how the heck does breaking something down accomplish growth? Well, typical targets of the SCFTIR1 complex are Aux/IAA proteins, which are transcriptional repressors. They live short, crazy lives in the nucleus (their half-life is roughly 6.5 minutes). When they’re broken down, they no longer act as repressors, and the genes they were repressing become activated.


Now that we know how auxin works, we can ask ourselves, what does auxin signaling accomplish? Well, we already said that Darwin found that it plays a role in phototropism. As it turns out, it also plays a role in gravitropism (response to gravity). The “bending” that changes the direction of a root’s growth (so that it’s always going down) results from changes in auxin concentration—more auxin on one side means more cell elongation on one side in relation to the other, which makes the root bend.

More generally, auxin promotes lateral organ initiation and inhibits branching in the shoot, while maintaining stem cells and promoting branching in the root. It also plays a role in embryo patterning and organ development—messing with auxin in embryos results in plants without roots. How’s that for the holy grail of growth hormones?

Auxin also has lots of friends that influence how it does its job. Auxin and cytokinin don’t get along at all (my professors calls them “arch-nemeses”). For example, if you plate plant cells with auxin, you’ll grow only roots, and if you plate them with cytokinin, you’ll grow only shoots. However, if you plate them with both, you get a mess of undifferentiated cells, because cytokinin and auxin are too busy fighting with each other to get anything done. (You can, however, grow shoots with cytokinin and then roots with auxin. Just not at the same time.) Auxin and ethylene are BFFs—the presence of one promotes production of the other. Auxin can also scream loud enough to drown out salicylic acid, prioritizing growth over immune response.

Alright! That’s plenty complicated, isn’t it? Well, we’re just getting started. Let’s keep going—!


Gibberellins get their name from a species of Japanese rice fungus known as Gibberella fujikuroi. Infection with this fungus resulted in a disease called “bakanae disease.” (馬鹿苗, or “bakanae,” is Japanese for “foolish seedling.”) The fungus excretes gibberellic acid, which causes rice plants to rapidly elongate until they cannot support themselves.

Sometime later, it was discovered that gibberellins aren’t just some weird poison made by fungi. Plants make them for themselves! (In fact, Mendel’s “dwarf peas” had a mutation that prevented them from making gibberellins.) Turns out, they’re plant hormones that promote cell elongation by inhibiting inhibitors. Sound confusing? Don’t worry, it only gets worse from here!


The synthesis pathway for GAs is, in my professor’s words, “outrageous.” It starts in plastids, and is made from a precursor called GGPP. Synthesis then moves into endomembrane systems, finally to be exported into the cytoplasm. I could go into detail, but, well, I won’t. Just take my word for it?

You remember when we talked about conjugation, right? Well, GA deactivation can take place through a couple of different processes—oxidation, methylation, or epoxidation. Again, that’s about as much detail as we need. Okay?


Gibberellin transport is a lot less complicated than auxin’s, because gibberellins aren’t picky. They move both ways, although not for long distances. (GAs also move from the embryo to the aleurone, or stored protein, in seeds to stimulate amylase production during germination. Amylase breaks down starch into sugar for the baby plant.)


Gibberellin signaling also uses the SCF ubiquitination complex. Gibberellins bind DELLA proteins (a class of repressor proteins) to GID1. The DELLA protein is then targeted by the SCFSLY1/GID2 complex for ubiquitination and, therefore, degradation.


As you’ve already noticed, Gibberellins have a big effect on the plant as a whole. They promote cell elongation, which allows plants to grow very quickly to avoid, for example, being submerged in flooding. They also promote nutrient mobilization in seeds, which is useful not only if you’re a germinating embryo, but if you’re interested in making beer. (To get malt, they trick those poor embryos into breaking down their starch stores using GAs—rude.) They are also, interestingly, necessary for flower.

Phew. I need to stand up for a minute.


Cytokinins, auxin’s arch-nemeses, were discovered when desperate researchers took desperate measures. In the 1950s, people wanted to find compounds that would increase cell growth in plant cell cultures, so they started putting whatever they could think of in with the cells—including coconut milk. Turns out, there was something present in coconut milk that increased cell growth. What was it? Kinetin, a cytokinin!

Cytokinins, as hormones, do a lot of stuff, but perhaps their most famous function is in delaying senescence (read: delaying death). That got a lot of people thinking, “Hey, we’ll overexpress cytokinins, and our plants will never die!” Turns out, that’s not as great an idea as it sounds.


Cytokinins are adenine-related compounds substituted at the N6 position. The two most notable among them are trans-zeatine (tZ) and isopentanyl-adenine (iP). Starting with ADP or ATP, they’re made in basically all plant tissues (although the location of synthesis in the cell isn’t yet known).

As you’d expect, cytokinins can undergo conjugation to modulate their activity. Reversible conjugation to a carbohydrate marks them for storage, while oxidation marks them for degradation.


Cytokinins are transported through both the xylem and the phloem. However, fascinatingly enough, all cytokinins aren’t present in equal amounts in both tissues. Xylem contains mostly tZ and tZ riboside, while phloem contains iP and tZ. It’s not yet understood exactly why this is, but it’s expected to be, as always, caught up in nuances of signaling.


Unlike the receptors for auxin and gibberellins, the receptors for cytokinins are the membrane-bound components of a two-component system. Without getting into too much detail (that’s what the Wiki link is for), signaling in the cytokinin pathway requires two pieces—a histidine kinase (HK) and a response regulator (RR). Perception at what is called the “input domain” activates the histidine kinase, and a phosphate group is transferred to one of its histidines. This is then transferred to an aspartate on the response regulator’s “receiver domain,” where it causes a conformational change that effects a kind of response.

(If this sounds complicated, it is—my professor, upon learning that few people in the class had taken a microbiology course, facetiously gushed, “Oh, yay, I have the honor of being the first to teach this to you!”)

If you’re asking about the names of the particular components, you’re asking for even more problems. There are three receptor proteins—AHK2, AHK3, and AHK4–as well as five “histidine-containing phosphotransfer factors (HPts),” called AHPs, and twenty-three RRs (ARRs). That’s… a huge freaking mess, so we’re just going to talk about them in general.

The AHKs form transmembrane homodimers, which is a fancy way of saying they’re stuck in the plasma membrane, and they pair up with themselves. When they perceive cytokinins, they transfer a phosphogroup to one of the five AHPs, which then shuttles into the nucleus to pass it to an ARR. That’s it. That’s the basic gist.

If you’re asking, “Plant, why so many of everything?” the answer is essentially, “So I can’t screw it up.” Redundancy is a big thing in biological systems, and it’s really useful—for example, you have to mutate three of the five AHPs before you get a “no-signaling” phenotype. Having multiple copies of everything also lets you toy around with what they do—the many ARRs, for example, can have diverse effects on signaling. (Evolution does this like… a lot. Hemoglobin is a fantastic example.)


As I said before, cytokinins do lots of things. Famously, they play a role in senescence and shoot growth. They also have something to do with nutrient uptake and pathogen responses. As with all hormones, CKs aren’t one-trick ponies… which makes them a pain to study.

As said above, leaf senescence is regulated by cytokinins. In plants expressing cytokinin during times when they’re supposed to be dropping leaves, leaves stay alive longer. However, longevity has its costs—for example, keeping a plant alive for a long time doesn’t do good things to the seed it produces.

Cytokinins also play a role in drought and freezing resistance—overexpression of or pretreatment with CKs improves a plant’s ability to survive drought or freezing. One of the ARRs, ARR2, also interacts with parts of the salicylic acid pathway to improve immune response to pathogens such as P. syringae. You gotta give it props, don’t you?

Okay. We’re basically halfway there. (Woah-oh, dog elected mayor….)

Abscisic Acid

Let’s face it: life is stressful, no matter what kingdom of life you belong to. Hey, it’s cool. Abscisic acid understands. Abscisic acid will protect you. Well, not you, not so much. But plants? Yeah, it’s got plants’ backs.

(Is Tangled too old to reference now? Okay. Well, you get it.)


Abscisic acid (ABA) is synthesized in the plastid and the cytoplasm from zeaxanthin, a forty-carbon carotenoid. The resulting compound can be marked for degradation through conversion to phaseic acid, which is something that happens when you rehydrate a plant that’s got its drought-response engaged. Glycosylation reversibly marks it for storage in the vacuole, which doesn’t surprise anyone at this point. (This is also how it’s transported in general.)


ABA moves in the exact opposite way that auxin does—through polar transport from root to tip, through the xylem. This makes a lot of sense, if you think about it: if ABA is to get the plant to conserve water, it needs to move from the root (“There’s no water down here!”) to the shoot (“Hey, leaves, close those stomata!”). It can also travel short distances through the apoplast.


ABA has sort of unique receptors called PYR/RCAR receptors. Essentially, ABA binds in a complex to PYR/RCAR receptors and AB1 (or other PP2C phosphatases). When PYR/RCAR and ABA bind PP2C, PP2C is inactivated, and it can no longer inactivate another protein called SnRK2. SnRK2 phosphorylates other proteins, such as ion channels and transcription factors, to bring about downstream effects. (Does this “inhibiting and inhibitor” paradigm sound familiar at all?)


ABA plays a role in a lot of different physiological processes, including guard cell response, root growth, dehydration response, and seed development. For example, ABA allows SnRK2s to open ion channels that move ions out of guard cells, which gets water to move out of the cells. The ultimate result is that the stomata close, which decreases water loss.

Similarly, ABA pushes plants to make roots instead of shoots when the plant is experiencing drought. It also suppress root branching (get down there to the water—don’t worry about branches!).

Finally, ABA works with gibberellins (GAs) to control seed germination. While ABA is present in the seed, germination is suppressed, and the seed remains dormant. As ABA tapers off, GA levels rise, and the seed starts to grow.


Ethylene is freaky weird for one reason: it’s a gas. Yup, you read that right. It’s a hormone. That’s also a gas.

Like all good discoveries, it was accidental—it was found that plants grew toward gas lamps. Afterwards, it was purified from ripening apples, which proved that it’s something plants actually make. Which is, you know, cool if you think you’ve stumbled across a new hormone.

This tiny molecule is famous for its role in ripening, but it also plays a role in senescence and cell expansion. Can you think of any ways in which it messing with these things while being a gas might be inconvenient? Because, whether you can or not, you’ve probably experienced it already. Because it is. Darn inconvenient, that is.


Ethylene synthesis is complicated, so we won’t talk too much about it. Essentially, you start with methionine, a sulfur-containing amino acid, and, through a series of steps, make ACC. (You can, therefore, consider both methionine and ACC precursors.) ACC is then converted into ethylene by ACC oxidase. We’re pretty sure this takes place in the cytoplasm. Pretty sure.

This pathway is really tightly regulated, and mostly is dependent upon the stability of the enzymes that carry it out (ACS and ACO). Usually, both are really unstable, but wounding or other hormones make them more stable.

There are actually nine genes for ACS, which each have both unique and common functions. The more of them you knock out, the sicker the plant gets—if you knock out all nine, it’s nonviable. (In other words, plants cannot live without ethylene.)

As you might expect, there exist certain mutants in plants that overproduce ethylene. In these mutants, a protein called ETO1 is mutated. ETO1 is an F-box protein, and, when it’s part of the SCF complex, it targets ACS for degradation. Without it, ACS isn’t degraded, and more ethylene is produced than is necessary.


Interestingly enough, ETR1, ethylene’s receptor, was the first phytohormone receptor ever identified. ETR1 is a membrane-bound receptor that initiates a pathway very similar manner to the cytokinin two-component system.


Like everything else, ethylene meddles with an awful lot of plant processes. It’s well-known for promoting ripening and senescence, but it also plays a role in shoot/root elongation, flooding responses, and pathogen responses.

For example, ethylene puts a damper on elongation while promoting swelling while in the dark. This is useful because it’s a way for a germinating seed to deal with obstructions in the soil—the resulting “triple response” causes the shoot to thicken and form a hook that can help it respond to impediments. It’s also important in the immune system—with lowered amounts of it, plants get sick.

The most famous function of ethylene, of course, is in ripening and senescence. Ethylene dictates when the petals fall off your flowers, as well as when you apples, bananas and tomatoes ripen. This is inconvenient, because it means that ripening in one fruit can set off ripening in another. (You can use it for good, though—next time you buy some green bananas, store them with an apple. They’ll ripen right up.)

Alright, I’m exhausted, but we’re almost there. Onward, to my favorite hormone!

Salicylic Acid

Humans get lots and lots of useful things from plants, and salicylic acid is a perfect example. It turns out that, by complete coincidence, what functions as an immune hormone in plants functions as a painkiller in animal. Salicylic acid is named for Salix alba, or white willow—willow bark is used by animals and humans alike as a natural remedy for pain and fever. (When you acetylate it, you make acetylsalicylic acid, which is also known as Aspirin—and also named for a plant. You can’t escape plants. Don’t even try.)


Salicylic acid is made using two completely separate pathways, one in the chloroplast, and one in the cytoplasm. (The chloroplast supposedly accounts for 95% of SA production, although my professor contests those numbers.) In the chloroplast, it’s made from chorismate (a key enzyme is ICS), whereas in the cytoplasm, it’s made from phenylalanine (key enzyme: PAL).

SA undergoes lots of conjugation, too, because why wouldn’t it be complicated? [salts] Methyl-salicylate is its transport form (which we’ll revisit), while glucosyl esters are its inactive storage forms.

Salicylic acid synthesis is instigated by, as you might expect, stress and pathogens. Salicylic acid primarily deals with biotrophic pathogens (pathogens that feed upon living tissue, such as bacteria). They respond, therefore, to receptors that detect flagellin, a component of bacterial flagella.


NPR1, which my professor said is named for the radio station, is a strong candidate for the salicylic acid receptor. (The other candidates are NPR3 and NPR4. While my professor has an opinion, she claimed she wouldn’t drag “thirty-five innocent students” into her battles.) It usually oligomerizes by formation of bisulfite bridges between monomers, linking up many small pieces into something big and bulky. However, in the presence of SA, the environment becomes reducing, and those bonds break. The monomers are free to move into the nucleus, where they can affect transcription in some way.

The targets of salicylic acid are a group of genes called “PR (pathogenesis related)” genes. Increased salicylic acid ramps up expression of these genes, which results in an immune response. Nifty, eh?


Salicylic acid plays a huge role in plant immunity, including systemic acquired resistance and hypersensitive response. It also functions in response to abiotic stress, and plays around with seed germination, flowering and senescence. Because of course it does.

The hypersensitive response describes a mechanism by which a plant manages to “quarantine” infected cells. Basically, this involves killing infected cells and the cells around them so that pathogens can’t travel. Systemic acquired resistance, on the other hand, is the mechanism by which an infected tissue alerts other tissues of the presence of a pathogen, essentially urging them to prepare themselves. In both cases, salicylic acid appears to have an important role.

Okay, I’m seeing double by this point. After writing this post, I think I’m going to need a salicylic acid derivative…

Jasmonic Acid

You know how nice jasmine smells, don’t you? Because you’re cultured, unlike me? Well, turns out that lovely smell is a plant hormone called jasmonic acid. That’s right. Sniff those plant hormones. Because that’s not weird.


Jasmonates are made from alpha-linolenic acid, an unsaturated fatty acid commonly found in plant cell membranes. Synthesis starts in the plastid, then moves to the peroxisome, and finally to the cytoplasm. Because plants, as we’ve learned by now, like to make a mess of things.

Jasmonates have two notable conjugate forms—Ile-JA and me-JA. Conjugation to isoleucine (a nonpolar amino acid) through the enzyme JAR1 results in the active form of the hormone. Methylation produces a stable form that can be more easily transported (and stored, according to my professor, who apparently worked in a jasmonate lab. “It smells great.”)


Ile-JA is recognized by COI1-JAZ, which are coreceptors. COI1 is an F-box protein, which means, you guessed it, it’s messing around with SCF. JAZ is a repressor that typically prevents MYC2, a transcriptional activator, from, um, activating transcription. When jasmonic acid binds to COI1, however, the SCF complex targets  JAZ for breakdown, and transcription is activated.


Jasmonates act primarily in response to necrotrophic pathogens (pathogens that feed on dead tissue, such as fungi) and insects. They also, of course, play roles in development, but are we surprised at this point?

A primary way that jasmonates protect the plant against herbivory is through the production of proteinase inhibitors. When insects eat plants, they, unsurprisingly, produce proteinases in their gut to break down any protein they eat. The plant can secrete proteinase inhibitors, which prevent proteinases from working properly. This can weaken or even kill insects feeding on the plant.

They also communicate with salicylic acid, although salicylic acid is a bit of a bully when it comes to playing with other hormones. If both jasmonates and salicylates are present, salicylate signaling wins—in other words, if a plant is infected with both a fungus and a bacterium, it will fight off the bacterium before it fights off the fungus. (Which I don’t understand, because, quite frankly, fungi are terrifying.)

Wow, okay! I’m exhausted. This took a lot longer than I thought it would, but it’s also like… 75% of my test material. I guess, in the long run, the time investment paid off. I’m gonna skedaddle, though—I’m seeing crosseyed.

Have fun, friends!


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