How Do Plants “Chill Out”?

The End of Winter?

We experienced a relatively warm January here in western Washington (record-setting, in fact). Some daffodils are already coming up and the witch hazels are blooming.

But most of the trees haven’t started to leaf out because they haven’t yet emerged from winter dormancy.

Most woody perennial plants (mainly trees and shrubs) that must survive winter in the temperate latitudes do so by becoming dormant in the fall.

The deepest state of this dormancy called “endodormancy” – often referred to in horticulture as “rest” – allows them to survive cold temperatures, sometimes well below -30^o F. (This adds new meaning to the phrase “chilling out”.)

Cold Acclimation (a.k.a., Cold Hardening)

Some plants, but not all, can become more cold tolerant or cold hardy simply by being exposed to near freezing temperatures. This is sometimes called cold hardening or cold acclimation. Interestingly, plants that are more cold hardy are generally also more tolerant to cellular desiccation. Indeed, improved cold hardiness may also be induced by mild drought. So, it appears that some of the cellular things the plant does to become cold hardy are the same as it does to become more drought tolerant.

What happens at the cellular level during cold acclimation to make the plants more cold tolerant was described in a previous post. Briefly, the plants may synthesize new proteins that inhibit ice crystal formation or stabilize cellular structures against the cold.

For some plants, it may take only a few days to become cold-hardened. For other plants, especially those entering endodormancy, it may take weeks to become fully cold-hardened.

Of course, the degree of cold hardiness varies greatly among plant species. (USDA Plant Hardiness Zone Map) “So-called chilling-sensitive plants, such as the tropical banana and the semitropical avocado, can be severely injured or even killed by long-term exposure to temperatures (50 degrees Fahrenheit, for example) that are well above freezing. By contrast, chilling-resistant plants, such as garden peas and potatoes, survive brief periods of frost but are killed when freezing conditions continue for more than about four hours. Cold-hardy plants, on the other hand, tolerate extended periods of freezing, and laboratory tests indicate that cold hardness in some of these plants permits them to survive at temperatures as low as minus 75 degrees Fahrenheit.” (from Ref. 1 below)

The Big Chill

Plants that exhibit the greatest cold hardiness are those that become dormant. When these plants make the transition to dormancy, one of the first stages in this process is similar to cold acclimation. This actually may be triggered in many plants by longer nights and reinforced by cooler temperatures.

But these plants go beyond chilling tolerance into a so-called “resting state” (endo-dormancy or mid-winter hardiness) that renders them extremely cold hardy. This resting state is characterized by a temporary suspension of growth and a lower rate of metabolism.

Dormancy is broken after exposure to long periods (weeks to months) of cool temperatures (typically below 40^o F) and shorter nights (among other factors), though cold deacclimation and reacclimation may take place. (see Ref. 3 below)

How global warming may affect the complex process of tree winter dormancy has certainly been on the minds of some plant scientists (e.g., see Ref. 4 below).

The plant hormone ABA is generally thought to be a chemical signal that induces cold acclimation and dormancy in many plants. (Lots of new information about how ABA works has been published in the past few months, so maybe that would be a good subject for next time.)

References

1. John W. Einset “What Determines a Plant’s Cold Hardiness?” Arnold Arboretum, Harvard University (PDF)

2. Mark Longstroth Dormancy and Cold Hardiness in Fruit Crops

3. Kalberer, S.R., M. Wisniewski and R. Arora. (2006) “Deacclimation and reacclimation of cold-hardy plants: Current understanding and emerging concepts.” Plant Science vol. 171, pp.3-16. (PDF)

4. Legave, J.M., I. Farrera, T. Almeras and M. Calleja. (2008) “Selecting models of apple flowering time and understanding how global warming has had an impact on this trait.” Journal of Horticultural Science & Biotechnology vol. 83 pp. 76–84. (PDF)

HowPlantsWork © 2009-2010 All Rights Reserved.

A Step Toward “Fixing” The Most Important Enzyme on Earth

The world’s most abundant and most important enzyme is RuBisCo.

It’s the most abundant because it’s present in relatively large quantities in every photosynthetic organism on the planet – from microscopic cyanobacteria and phytoplankton in the oceans to the leaves of giant-sized trees in the tropics.

It’s also the most important enzyme on Earth because it catalyzes the first step in the photosynthetic conversion of CO₂ into sugars (a.k.a., the Calvin cycle). Indeed, all the organic carbon in the
biosphere is ultimately derived from the CO₂ that RuBisCo captures from the atmosphere.

Because of its primary role in photosynthesis, the enzymatic efficiency of RuBisCo has a major impact on plant productivity. It turns out, however, that RuBisCo is a relatively inefficient enzyme and typically is the chief rate-limiting factor in agricultural productivity.

One reason RuBisCo is so inefficient is that it can react with O₂ instead of CO₂ much of the time. Another reason is that the current levels of atmospheric CO₂ are roughly half the concentration required for RuBisCo to run at top speed. (Scientists hypothesize that the reason for these problems is that RuBisCo first evolved in cyanobacteria 3 billion years ago, when there was little atmospheric O₂ and much higher levels of CO₂.)

This is why scientists have tried to use the genetic engineering of RuBisCo to improve photosynthetic efficiency.

But a major obstacle toward this goal has been scientists’ inability to reconstitute functioning RuBisCo in vitro, that is, in a test tube.

This is mainly because the active form of RuBisCo consists of 16 proteins. (e.g., see image on right)

But a recent report in the scientific journal Nature may represent a major step toward rebuilding RuBisCo.

Reassembling RuBisCo

According to the leader of this research group at the Max Planck Institute of Biochemistry in Martinsried, Germany, Dr. Manajit Hayer-Hartl, the keys to the in vitro assembly of RuBisCo are chaperone proteins.

Chaperone proteins facilitate the correct 3D folding of newly synthesized proteins, which is critical for the optimal enzyme activity. According to Dr. Hayer-Hartl, “With 16 subunits like those of Rubisco, the risk is very high that wrong parts of the protein clump together and form useless aggregates” (1).

The next goal for this research group is to genetically modify the genes coding for the RuBisCo proteins so as to minimize binding to O₂ and maximize the reaction with CO₂.

“Because the modified Rubisco is predicted to absorb carbon dioxide from the atmosphere more effectively,” says Manajit Hayer-Hartl, “it would enhance crop yields and could also be interesting for climate protection.” (1)

Reference

(1) For more information, see the Press Release from the Max Planck Institute of Biochemistry (PDF)

HowPlantsWork © 2009-2010 All Rights Reserved.

Plants That Heat Themselves

“Hot Plants?”

In the previous post, the topic was how plants survive the cold. Although some perennial plants can withstand winter temperatures well below zero (F), plants certainly don’t generate body heat like mammals do in order to warm themselves.

Or do they?

There are a few plants in nature, like the remarkable Voodoo Lily (Sauromatum guttatum), that produce extraordinary heat when they flower. What actually warms up when the plant flowers is part of the inflorescence, called a spadix.

Typically, the plants do this to attract insect pollinators. But some, such as the Eastern skunk cabbage may actually use this mechanism against the cold.

In the case of the Voodoo Lily, flies are lured by chemical attractants, which are volatilized by the heat of the spadix. (The chemicals smell to us like putrid, rotting meat.)

The process of heat production by living organisms is called thermogenesis. And though it’s far from common in the plant kingdom, thermogenic plants occur in several plant families, especially the Araceae. Members of this plant family include the Eastern skunk cabbage and the giant carrion flower.

(from: Giant stinking flower reveals a hot secret)

Much fewer plants, however, are able to thermoregulate, that is, they actually regulate the temperature of thermogenesis within narrow limits. For an excellent slide-show about plant thermoregulation, see here (PDF).

How Do Plants Generate Heat?

Much about what we know about how the Voodoo Lily spadix, for example, generates heat came from the research of Professor Bastiaan J. D. Meeuse.

Among his discoveries about heat production in plants, Dr. Meeuse and co-workers showed that a compound related to aspirin triggers pronounced heat production in the flowers and inflorescences of some thermogenic plants.

Briefly, heat generation in these plants is due to the massive activation of the alternative oxidase metabolic pathway in the mitochondria inside the plant cells.

Simply put, when this happens, instead of generating ATP as result of metabolizing sugars via oxidative phosphorylation, the mitochondria generate heat.

Bottom line: Though some plants can generate heat to promote flower pollination, it’s unlikely that they do so just to survive cold temperatures.

References

1. Meeuse B.J.D. (1966) The Voodoo Lily. Scientific American vol. 218, pp. 80-88.

2. Meeuse, B.J.D. (1975) Thermogenic Respiration in Aroids. Ann. Rev. Plant Physiology vol. 26, pp. 117-126. (Abstract)

HowPlantsWork © 2009-2010 All Rights Reserved.

How Plants Survive The Cold (Or Not)

Plants Can’t Come In From The Cold

Imagine for a moment that you had to stand outside your house or apartment, without moving, all winter long…and that you were naked.

How long do you think you could last?

Not long, especially if the temperature went below freezing. And certainly not if the temperature went below 0^o F (-18^o C).

In temperate zones on Earth that’s what perennial plants must be able to do to survive. And even annual plants may have to withstand an early or late frost in order to complete their life cycles.

But, you may reply, plants are not warm-blooded organisms like mammals. What difference is it to them whether it’s cold or not?

How Cold Kills Plants

What happens if water freezes inside at plant?

At least a couple of things can happen…both bad for the plant.

The first, and likely lethal for the plant, is ice crystal formation inside cells. This has just about the same effect on a plant cell as the little alien chestburster did on the actor John Hurt in the movie Alien. (Sorry, but it’s an effective analogy.) It’s lethal.

If, however, the water freezes outside the cells, in the intercellular spaces, this may lead to the extreme desiccation of the plant. That is, it’s sort of the same as if the plant was drying out.

Other cold-temperature effects on plants include (1) decrease in enzyme activity and (2) changes in the fluidity of cellular membranes, both of which could severely harm plant cells, and, thus, the plant as a whole.

How Do Plants Cope With the Cold?

To answer this question we have to consider plants at the cellular level.

How do the cells of cold-tolerant plants survive sub-freezing temperatures, i.e., withstand dehydration and, more importantly at very low temperatures (below 0^o F or -18^o C) , avoid the formation of ice crystals in the cell?

1. Accumulation of solutes (sucrose, mainly, but also other organic compounds such as proline) by the cells to depress the freezing point of water (think salting ice on the sidewalk) and to stabilize membranes. (But this can only be effective at temperatures from 32^o F to 20^o F.)

2. So-called “antifreeze” proteins help prevent ice crystals from forming in the extracellular spaces (outside cell); plant cells that make these proteins typically secrete them into cell wall region (intercellular spaces).

3. The plant cells may synthesize proteins called “dehydrins”, which are inside the cell (cytoplasm), may bind water molecules and alter the collective structure of water in the cell to stabilize membranes.

4. Plant cells can alter lipid composition of cellular membranes in order to adjust the fluidity (functionality) to colder temperatures.

Can Plants Generate Their Own Heat?

A silly question? I think not.

Some unusual plants, by partially uncoupling their cellular mitochondria, can generate small amounts of heat. (Please see ref #1 below for more information) But this is likely not very significant with regard to cold tolerance, however. (More on this interesting topic here.)

Bottom Line: Plant cells survive sub-freezing temperatures by adjusting their solutes, proteins, and membrane lipids in order to withstand desiccation and to avoid ice crystal formation.

Reference

1. Seymour, Roger S. (1997) “Plants That Warm Themselves.” Scientific American, March 1997, pp. 104-109. (Summary)

HowPlantsWork © 2009-2010 All Rights Reserved.

Plant Mythbusters (#1) – Seeds From Ancient Egyptian Tombs That Germinate

A Truly Ancient Grain?

The wheat variety called Kamut® has a fascinating history.

According to “Kamut®: Ancient Grain, New Cereal”, one of the original growers, and one of the trademark holders, of Kamut®, Robert M. Quinn recounts the story of this unusual wheat variety.

“Following WWII, a US airman claimed to have taken a handful of this grain from a stone box in a tomb near Dashare, Egypt. Thirty-six kernels of the grain were given to a friend who mailed them to his father, a Montana wheat farmer. The farmer planted and harvested a small crop and displayed the grain as a novelty at the local fair. Believing the legend that the giant grain kernels were taken from an Egyptian tomb, the grain was dubbed “King Tut’s Wheat.”

This is certainly not the only story of germinating seeds that are thousands of years old, which were collected from Egyptian tombs. (Please see here and here, for examples.)

The Mummy’s Curse?

On p. 55 of Seeds: The Definitive Guide to Growing, History, and Lore, the author dismisses such claims as being “Right up there with the mummy’s curse that supposedly led to the death of Lord Carnarvon, the archaeologist who uncovered King Tutankhamen’s tomb…”

The oldest claim for longevity (> 10,000 years) cited in this book (published in 2005) is for arctic lupine (Lupinus arcticus) seeds frozen and buried in the Canadian Yukon. The author is skeptical of the claim, and, indeed, a recent scientific report (see ref. 2 below) confirms that the seeds were from modern times.

Seed Longevity: The Facts

Thanks to scores of scientific studies, we now have a pretty good idea of how long most seeds remain viable, that is, able to germinate. Under normal conditions (dry and cool), most seeds will remain viable for only a few years, and anything over 50 to 100 years is quite remarkable. (The reason, of course, is that some, if not most, of the seed is alive and respiring, and, thus, is using up its food supply, albeit very slowly.)

For reference: Table of garden seed longevity and How to test seeds for viability.

To extend the time of seed viability, seed banks may use special storage conditions, such as liquid nitrogen temperatures. (But this will be a subject for another time.)

And coming back around full-circle to the story of Kamut®, Robert M. Quinn admits that“…most scientists believe it probably survived the years as an obscure grain kept alive by the diversity of crops common to small peasant farmers perhaps in Egypt or Asia Minor.”

References

1. SEEDS by Peter Loewer

2. Radiocarbon dates reveal that Lupinus arcticus plants were grown from modern not Pleistocene seeds. (New Phytologist)

HowPlantsWork © 2009-2010 All Rights Reserved.

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

Sniffing 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.)

How 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.

The Ripe Stuff – Part 2: How Plants Make Ethylene

C’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 Signal

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

References:

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)

The Ripe Stuff: Green Tomatoes, Bananas & Ethylene

Fried 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 90^o 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’.

How Plants Make Flowers – Part 5: Photoperiod, Biological Clocks, and Florigen

It’s Time to Flower!

The correct timing of flowering is essential to maximize reproductive success in angiosperms.

And many flowering plants rely on the photoperiod (specifically, the relative night length) as an environmental signal to tell seasonal time. (To see how, please see previous posts about How Plants Tell Time and Why Plants Tell Time.)

As mentioned in the previous post, the so-called “flowering hormone”, historically known as florigen, is likely a small protein called FT.

Briefly, FT is produced in the leaves and is transported via the phloem to the shoot apical meristem (SAM). Here FT acts like a molecular “alarm-clock”, evoking a complex genetic scenario, which culminates in flower formation.

But what sets off this “alarm-clock”, i.e. the production of FT in the leaves?

Turns out the story involves red, far-red, and blue light, the length of the night, and the plant’s biological clock. (Please note: Why night length is more important than day length: animated explanation.)

First some caveats:

1. Most of this information is based on genetic research using the plant Arabidopsis thaliana. (Although specific genes and proteins vary, depending on plant species, it appears that the basic story presented below holds for most photoperiodic flowering plants.)

2. Arabidopsis is a so-called long-day (LD) flowering plant (in reality, a “short-night” plant, but don’t get me started). So, adjustments in the story need to be made for so-called short-day (SD) plants. (Yes, they really are “long-night” plants.)

3. In Arabidopsis florigen is likely the FT protein. In some SD cereals (such as rice), florigen is likely a protein called Hd3a, an ortholog of FT protein.

A Light-Sensitive, Flowering Alarm-Clock

The so-called biological clock in plants is set primarily in the leaves by phytochromes, which are sensitive to red and far-red light. They get help from blue-light-sensitive cryptochrome. These photoreceptors interact with “clock-genes” that cause some proteins in plant cells to cycle with a circadian rhythm.

One of these proteins regulates the gene that codes for florigen (FT in Arabidopsis and Hd3a in rice, for instance).

Thus, florigen cycles in the leaves also with a circadian rhythm.

Briefly, in LD (“short-night”) plants florigen apparently peaks not long after sundown, then slowly degrades during the night. If the nights are too long, the florigen level is below the threshold level to induce flowering at dawn, when the leaves begin to transport material to the SAM via the phloem. (Please note: florigen appears to be synthesized primarily by leaf vein cells adjacent to the phloem.)

Conversely, in SD (“long-night”) plants, the florigen apparently peaks long after sundown. So, if the night is too short, at dawn, the florigen hasn’t exceeded the threshold level to trigger flowering.

For more information, click on image below:

References:

1. Zeevaart, J.A.D. (2007) FT Protein, not mRNA, is the Phloem-Mobile Signal for Flowering. (see here)

2. Bäurle, I. and Dean, C. (2006) The Timing of Developmental Transitions in Plants. Cell, vol. 125, pp. 655-664 (see here)

3. Greenup, A., et al. (2009) The molecular biology of seasonal flowering-responses in Arabidopsis and the cereals. Annals of Botany, vol. 103, pp. 1165-1172. (see here)

How Plants Make Flowers – Part 4: Genetics of Flowering

The Long and Winding Road

So far, this journey through the subject of how plants make flowers has consisted of three parts:

Part 1, an introduction to the flowering hormone florigen,

…Part 2, how environmental cues affect flowering,

..and, Part 3, how the size and age of the plant itself may trigger flowering.

The Players

Because the genetic story of how plants flower turns out to involve many cellular “players”, as well as an intricate plot, perhaps it would be a good idea to first introduce the main “cast of characters”.

Let’s start with florigen.

As previously described, this is the so-called flowering hormone that can trigger the floral transition in plants.

The latest scientific evidence supports the hypothesis that florigen is actually a protein called FT coded for by the gene Flowering Locus T.

Most of the other key genetic “players” turn out to be proteins called transcription factors, which bind to specific DNA sequences and affect gene transcription.

Many of the flowering-related transcription factors (TFs) are members of a “family” called MADS-box TFs.

An especially interesting member of this MADS-box family with regard to flowering is the FLC protein. FLC (the product of a gene called Flowering Locus C) actually represses flowering.

The Genetics of Flowering (A Story in Three “Acts”)

Since flowering takes place in the shoot apical meristem (SAM) , let’s set the stage there. (And please keep in mind (1) that this is a very simplified version of a very complex, and as yet incomplete, story and (2) that most of this story is based on a single plant – Arabidopsis thaliana – though the basic storyline is likely the same for most flowering plants.)

Act 1 – Floral Initiation (From Vegetative To Inflorescence Meristem)

At center stage (currently), is SOC1 (Suppressor of Overexpression of Constans 1), a gene coding for a TF in the MADS-box family. SOC1 protein plays a pivotal roll in the great leap from vegetative meristem to inflorescence meristem (IM). The expression of SOC1 is effected, directly and indirectly, by factors known to induce flowering, such as the plant hormone gibberellin and FT protein (a.k.a., florigen).

FT gets into the act by first binding to a bZip TF called FD protein (gene product of Flowering Locus D). Together FT/FD promote SOC1 gene expression. (Though FT is not a transcription factor, it acts as a “key” to activate FD protein, which is a TF.)

Finally, the antagonist in “Act 1″ is the FLC protein (see above). It inhibits flowering by suppressing the expression of the SOC1 gene. (Further on down the trail, we’ll see how vernalization knocks off FLC and thus promotes flowering.)

Act 2 – “Arranging the Chairs” (From Inflorescence to Floral Meristem – Part 1)

The second act of the story involves the first step in the transition from the inflorescence meristem (IM) to the floral meristem (FM). What’s the difference? Well, think of the transition from vegetative to IM as “making the decision” to flower, without any overt signs of flowering. And the IM –> FM transition is actually starting to build a flower.

The first step in building a flower involves the spatial arrangement of the flower parts, sort of analogous to arranging the chairs in a room for a meeting.

This involves such TF genes as LEAFY (LFY) and APETAL1 (AP1), which are both activated by SOC1 and FT/FD.

Act 3 – “Seating the Guests” (From Inflorescence to Floral Meristem – Part 2)

There are four guests to be seated at the end of our story – sepal, petal, carpel, and stamen – the four basic floral organs.

The genes involved in floral organ identity are called homeotic genes. Together they are responsible for the so-called “ABC model” of floral organ development. (Though I think it’s the ABCD model now, but that’s for a later date.)

Bottom Line: For a visual summary of the above feel free to download and play this PowerPoint file: Flower_Genetics.ppt or see the corresponding YouTube video here.

Next Up: Making a Flower – Part 5: How does photoperiod induce florigen (FT protein) synthesis in leaves?