The Fourth of July means red, white and blue to celebrate America’s birthday, but with our mild spring and ample rainfall this year it also heralds fig season in south Louisiana. If your experience with figs is limited to Fig Newtons or once upon a time you had fig preserves on toast, I am pausing for a moment of silence for your taste buds. A fresh fig picked and eaten just off the tree is something else altogether.
Fresh figs do not keep for any significant length of time and you’ll be hard-pressed to ever find them in the grocery store. So, if you’d like to try this summer delicacy, make friends with someone that has a fig tree or grow your own (surprisingly easy for anyone in hardiness zones with winters less than 800 chill hours).The most common varieties grown in the south are the Celeste and the Brown Turkey fig (Texas ever-bearing) which produce small brown figs. The LSU AgCenter has introduced several new varieties in recent years including the LSU Purple and LSU Gold, colored according to their namesakes. I have two LSU Gold trees and as far as taste goes, I cannot sing their praises enough. They have a delicate and very sweet taste. It’s what I imagine heaven must taste like. However, in my n = 2 experience these trees get huge in a hurry. It’s great if you’re impatient for your first fig crop, but beware if your backyard space is limiting. Typically it is not necessary to prune fig trees as with other fruit trees, but you may want to rein in an LSU Gold tree in a small backyard. This is less of a problem with Celeste or Brown Turkey figs.
LSU Gold
If you are new to fig tree culture, you may ask yourself, “I wonder what fig tree blossoms look and smell like? I am sure they must be equally heavenly.” Yes, that’s because the ‘fruit’ you are eating are actually a special type of inflorescence structure (read flower) with the botanical name syconium or synconium. It is basically a modified fleshy stem that encloses numerous ovaries (floral tissue). The inner pulp is the flowers.
You should also beware that fig stems (branches and where the fruit are picked) produce a milky latex material to which some people can be sensitive. It contains the enzyme ficin that will degrade proteins. In fact, this enzyme is used commercially to differentiate blood groups for transfusion purposes. Human blood types go beyond the standard A, B, O or even Rh designations. There are numerous antigens on the surfaces of our blood cells that can affect transfusion success. The Kidd antigen type on your red blood cells and kidneys is difficult to determine in its normal state, but treatment with the enzyme ficin aids in differentiation because the partially degraded product will be more reactive while other variants are resistant to ficin degradation.
Whether or not you care about the finer points of their plant biology or use in biochemical assays, once you have your own fig tree(s), you will inevitably become overwhelmed with the glut of fruit produced in the month of July. You can pawn them off to family, friends, neighbors and acquaintances. Drying them in halves is another great option and intensifies their flavor for use in cooking later. Hardcore enthusiasts will can them as preserves. Now, I was never taught the secret of my grandmother’s fig preserves, but I have read the protocol. Even with a PhD in biochemistry and finely honed protein purification skills at the lab bench, the multi-step process of successfully preparing fig preserves gives me pause. So, who wants figs this Fourth?
January 6 is Epiphany, not a week into the new year and its tradition causes many Louisianians to abandon any resolutions related to gustatory moderation. I’m referring, of course, to the King Cake. In modern tradition, a King Cake is a circular pastry made of Danish-type dough, filled with fruit spread, cream cheese, flavored sugar or some combination thereof topped with an additional layer of icing decorated with purple, yellow and green colored sugar. There is a plastic baby, representing Jesus, inside, and the eater finding the slice with Jesus is charged with purchasing the next King Cake. This continues throughout the Carnival season. It truly is the decadence of Mardi Gras captured in cuisine.
King Cake via Wikimedia
Traditionally, the King Cake has slightly more humble origins. It has always been associated with Epiphany, the church holiday marking the visitation of the Three Kings to see the baby Jesus, but the recipe was not always the refined sugar freight train it is today. Think more bread and dried fruit. Before the advent of plastic trinkets, the baby Jesus was symbolized by the fava bean.
Vicia faba via Wikimedia
The fava bean (Vicia faba) or broad bean is a hardy legume that has been in cultivation for thousands of years. This low maintenance crop has been a source of quality protein for the human diet for just as long. Its class connotations have waxed and waned throughout history, but for some people it can trigger a potentially deadly anemia. The condition is so tightly linked to fava beans, it is known as favism.
The king is dead?
Favism is really just one manifestation of a deficiency in the enzyme Glucose-6-Phosphate Dehydrogenase (G6PD). This is the rate-limiting enzyme within the pentose phosphate pathway, which the cell uses to generate reducing power in the form of NADPH and glutathione as well as 5-carbon sugar groups to use as building blocks of DNA or amino acids. People can display a range of G6PD deficiency levels. This depends on the type of mutation and the relative amounts of the mutant G6PD expressed. This mutation is X-linked, which means you inherit it from your mother. Because males inherit only one X chromosome copy, if they get a defective version, they will always display some level of favism. Female carriers of the G6PD mutation can also show some deficiency as well. Even though female carriers contain two X-chromosomes (of which has a normal G6PD and the other has the mutant version), cells only need to use one copy. Relatively early in development, one copy of the X chromosome in each cell is silenced. Thus, there is a random inactivation of one copy of the G6PD gene in each cell; in some cases the mutant version will be inactivated, in others the normal version. This creates the potential for a range of G6PD deficiency to be observed even when the woman has one copy of a normal G6PD.
So how can fava beans wreak such havoc on basic human metabolism? Fava beans synthesize the alkaloid glycoside, vicine. This substance is a particularly powerful trigger for oxidative damage to the cells. In the red blood cells of G6PD deficient individuals, there’s just not enough reducing power within the cell to protect them from the build-up of hydrogen peroxide and other damaging reactive oxygen species. Consequently, the red blood cells burst open resulting in acute anemia.
Vicine chemical structure via Wikimedia
Long live the king!
How have this metabolic mutation and food crop coexisted for so long? It seems like nature and/or agriculture would select for one or the other. There are other beans out there, ‘Am I right?’ And how could a mutation in such a critical enzyme in central metabolism accumulate in more than 400 million people worldwide? The answer lies within another disease- malaria. The incidence of G6PD deficient versions is higher in individuals of African and Mediterranean descent. There is a working hypothesis that some level of G6PD deficiency offers a fitness advantage over normal individuals when it comes to malaria infections. When the Plasmodium parasite infects red blood cells, some amount of oxidative stress occurs. Because G6PD deficient individuals have a sensitivity to this stress, their red blood cells burst eliminating the parasite’s home. When you consider a population of red blood cells within a G6PD deficient individual infected by the parasite, it’s advantageous to be able to sacrifice some red blood cells in order to give the immune system the chance to clear the parasite. In normal individuals, all red blood cells are easy targets for the parasite, which can enter them and hide more effectively from the host’s immune system. It should be noted though that some malarial treatments given to G6PD deficient patients can be toxic themselves as they also generate a fair amount of oxidative stress.
G6PD deficiency is a relatively benign condition when it is diagnosed and certain oxidative triggers are avoided. So in the same way that it’s good to uncover a plastic Jesus in your King Cake, it’s good to know your G6PD variety. If you’re G6PD deficient, it’s not so good to uncover a fava bean. However, the complicated hidden interrelatedness of each of these things will lead to new epiphanies in malarial infections and their treatment.
If you’re looking for a holiday related diversion, here’s a linkfest of my posts from last year on the Twelve Days of Christmas plants. Understand the plant science behind the traditions. Use these random facts to quickly change the subject when nosy but well meaning friends and family ask you uncomfortable questions.
For many people around the world, tonight is one of the most anticipated nights of the year. In that spirit, here’s some new science, not under the sun, but under the moonlight and starlight. New research from Wegener, Nagarajan and Pakrasi* describe something new about the Photosystem II D1 protein, an unexpected source that photosynthesis researchers had long written off as conquered or fully explained.
Why would we care about photosynthesis at night anyway? It all comes down to the distinctive lifestyle of the cyanobacteriumCyanothece, which belongs to an interesting class called unicellular diazotrophs (word of the day). Like all cyanobacteria, they perform oxygenic photosynthesis but they have the bonus biochemical ability of nitrogen-fixation.
Nitrogen-fixers are capable of pulling nitrogen gas (N2) out of the air and turning it into ammonia which the cells can use as a nitrogen source for important molecules like protein and DNA. Other microbes can perform nitrogen-fixation, and you may remember them as the root nodule symbionts oflegumes. If you’re not a nitrogen-fixer, you have to rely on ammonia or other nitrate compounds present in the soil, sea or your diet (depending on what kind of organism you are) to make the required nitrogenous biomolecules. Since the Earth’s atmosphere is 78% N2, you don’t have to be great at math to figure out that acquiring the ability to tap into the atmospheric nitrogen source advances your species in the game of life a considerable number of squares.
What does this have to do with photosynthesis? Why don’t more plants and cyanobacteria get in on this nitrogen-fixation biochemistry? There’s a critical fatal flaw in the photosynthesis/nitrogen-fixation biochemical tango. Nitrogenase, the enzyme responsible for the nitrogen-fixation reaction is hopelessly and irreversibly killed by oxygen. Oxygen destroys the protein enzyme that’s already been made and tells the genome not to even bother wasting energy trying to make it new. If you’ve been paying attention to the blog, oxygenic photosynthesizers like cyanobacteria and plants make oxygen via their PSII enzyme every time light shines on them. So for nonphotosynthetic soil bacteria and other microbes, it’s not a big deal to avoid oxygen and go anaerobic to fix nitrogen. Cyanobacteria, however, must lead dangerous double lives to combine these two opposing biochemical processes.
Anabeana spherica via Wikimedia Commons The more round cell in the center of the string is the nitrogen-fixing heterocyst.
Some diazotrophic cyanobacteria solve this problem by separating these two processes in space. Species like Anabeana can go through a special type of development where the cells divide themselves, but incompletely to form a connected network like beads on a string. Every tenth cell (heterocyst) gets an extra layer of cell wall, destroys its photosynthetic machinery, and commits itself to a life of nitrogen-fixation. These cells share their fixed nitrogen compounds with their neighbors, which in turn share their fixed-carbon from photosynthesis. This is a fascinating process still hasn’t given up all of its secrets and remains an active area of research.
Cyanothece 51142 by Michelle Liberton, Pakrasi lab
Cyanothece, on the other hand, is a more ruggedly individualistic species that manages to perform both oxygenic photosynthesis and nitrogen-fixation within a single cell. It accomplishes this through a carefully controlled circadian rhythm. During the day, oxygenic photosynthesis occurs. During the night, nitrogen-fixation occurs. It sounds so simple, yet this elegance is far from easy. This is a true circadian process, in that, while some cues are definitely derived from light signals, the cells also have a strong internal clock that keeps the time of day and controls what biochemical machinery is active. Thus, near the hour of dawn and dusk, the cells are actively preparing for the metabolism to come. Also, if you were to train a culture of these cells under a certain day/night cycle for several days then switch them to continuous light, they would still maintain their circadian biochemical cycle for several days after the switch.
One issue that has puzzled researchers for some time is that the photosynthetic machinery, like PSII, is actively shut down at night. It’s not just that it’s dark, so there won’t be any photosynthetic oxygen production. Apparently, that’s not good enough. The cells actively shut it down. When researchers take culture samples of these cells during their dark period and shine light on them to check photosynthetic capability, there is no signal. Sure, there’s probably little chance any significant photosynthesis is occurring at night, but Cyanothece isn’t taking any chances. For these cells, no moonlight, floodlights from passing ships, comets, or even the blessed Eastern Star is going to interfere with their nocturnal nitrogen fixation.
Shutting down photosynthesis is no small feat. Again, if you’ve been paying attention to the blog, you will note that I’ve ranted on numerous occasions about how complex PSII is and how difficult it is to assemble and reassemble from its individual parts. As far as energetics are concerned, it would be a losing battle for Cyanothece to completely disassemble its PSII at dusk only to resynthesize it again the next morning. I don’t care how hard-up it is for a nitrogen source. As it turns out, Cyanothece and other unicellular diazotrophic cyanobacteria solve this problem in a more graceful way, for which Wegener et al have provided new experimental evidence.
Cyanothece, like all other oxygenic photosynthesizers, contains multiple copies of the psbA gene encoding the D1 protein, which is a core subunit of PSII and critical for function. Since the advent of the genomic era, the genomes of numerous photosynthetic organisms have been sequenced revealing these multiple psbA genes, most of which have little or no protein sequence differences. These subtle changes have been linked to cells’ ability to fine-tune photosynthesis under certain conditions. However, Cyanothece and its cousins have a psbA gene copy that is particularly different- psbA4. If one were to take all of the site-directed mutants that photosynthesis researchers made to sort out PSII function over the last few decades since molecular biology techniques were available and threw them altogether into a single mutant gene, you would get psbA4. If PSII contained the D1 protein encoded by psbA4, there would be no C-terminal processing and no active site for water-splitting and oxygen production.
Why would any self-respecting photosynthetic organism retain such an utterly non-functional PSII subunit? The answer is because it does serve a critical function in the daily cycle of Cyanothece, just not during the day. The D1 protein encoded by the psbA4 gene, called a sentinel D1 protein (sD1), is made only for the night, when it does the only thing it still can do- fit right in the center of the PSII complex and prevent PSII function of any kind. There’s no chance of any oxygen production while sentinel D1 is on duty, but the cells can maintain most of the other PSII components in a stable complex (meaning they don’t have to be degraded and made fresh every morning). Then, Cyanothece can turn photosynthesis back on in the morning by replacing a single protein in its PSII complexes. The report by Wegener et al gives the first biochemical characterization of PSII complexes containing a sentinel D1 protein, providing evidence that this strategy works for controlling PSII oxygen production.
Performing oxygenic photosynthesis and nitrogen-fixation within the same cell is biochemically problematic, but the sentinel D1 protein appears to be the secret weapon for this dangerous double life. Through this strategy oxygenic photosynthesis and nitrogen fixation are “Always together, eternally apart.”** Many questions remain regarding the regulation of the transition from functional D1 to sentinel D1 at dusk and the reverse replacement at dawn. There are still outstanding questions regarding the D1 turnover event for any PSII in any photosynthetic organism, so it’s not at all clear what parts of this process Cyanothece uses or whether new factors are involved. Obviously, there must also be some sophisticated regulation to prevent the synthesis of sentinel D1 during the day.
While this work focuses on an organism you’ve never heard of, it has some interesting biotech implications for the future. As I mentioned, being able to both fix CO2 through photosynthesis and N2 through nitrogenase puts you at a significant metabolic advantage. And no, I don’t mean you. Remember, we’ve been through this- people are not photosynthetic. It would be great if one day we could engineer certain crop plants to combine these traits. Legumes already have this trick covered through symbiosis, but many other staple crops require tons of nitrogen fertilizer. If researchers could unlock the secrets of Cyanothece’s double life and translate it to plants, then it may be possible to engineer versions of crop plants that don’t require so much nitrogen fertilizer. Thus, one night in the future, engineered crop plants may be fixing nitrogen thanks to the addition of a variant gene they already had.
Johnna
*I know I’ve posted frequently about Pakrasi lab (my thesis lab) research, but this topic was just developing as I was leaving the lab and it’s too cool to pass up.
**Bonus points to you if you get the movie reference.
Happy Labor Day! I hope you are enjoying your day off of work or for those of you still on duty, I hope you are at least thankful for safe working conditions and reasonable pay. While there may not be an official botanical symbol of Labor Day, today’s post will feature cotton as the ultimate autotrophic symbol of work. So whether your collar is blue or white, even if you don’t have a collar at all, it’s probably still made of some cotton. So, take some time today to consider the labor of cotton in your life.
“All work, even cotton spinning, is noble; work is alone noble … A life of ease is not for any man, nor for any god.” Thomas Carlyle
A cotton field in Texas Credit: Kimberly Vardeman via Wikimedia Commons
Cotton plants have been hard at work for thousands of years supplying us with fiber for clothing and other goods. Also, as far as agricultural products go, cotton has historically set the highest bar in terms of human labor commitment. Consequently, this plant fiber has come to be both the most commonplace fabric as well as the most economically polarizing material in history. It is both a virtuous product as well as a historical symbol of labor exploitation because of the physical demands of its production and processing. ‘High cotton’ is synonymous with prosperity and good times. ‘Picking cotton’ was the epitome of slave labor, tedious and toilsome.
So what exactly is cotton? Plants of the genus Gossypium are perennial shrubs that bloom creamy white flowers. These self-pollinating flowers turn pink later in the day after pollination and begin to form a boll structure at the base of the flower that will contain the mature seeds for the plant. Check out the video below for images of developing cotton flowers and bolls in different stages.*
In generic terms, the boll is the seed pod of the cotton plant. It’s basically like its fruit, but instead of making a juicy delicious flesh around its seeds, cotton plants make soft fluffy fibers. When the seeds begin to mature within the boll, the cells of the outer layer of the seed elongate and kick cellulose production into high gear along their cell walls. It is a precise process that follows a specific pattern for reinforcing the thin cells, but also includes a regular deviation producing kinks and curves. It is these ‘imperfections’ that allow fibers to hold together into long threads as they are spun and thus confer their economic value. Once seed development is complete and the bolls burst open, these elongated cells desiccate, leaving behind shells of thin fluffy fibers hiding the seeds.
Thousands of years of cultivation have yielded a number of agricultural practices that make cotton crops easier to manage. While cotton plants will live as perennials, they are grown as annual crops. In order to have more predictable cotton yields, the fields are typically irrigated; however, cotton has high drought and salinity tolerance. So, for return on water use, it is a good crop choice and thrives in areas with long hot growing seasons. Harvesting is done by mechanical pickers that twist the bolls off of the plant. By weight, the majority of the cotton harvest is the seed. Each boll can contain 24 – 45 seeds entangled in the fibers. Cottonseed is valuable in its own right as a source for oil as well as nutritional meal. The separation of the cotton seeds from the fiber requires an enormous amount of effort. This process is now efficiently handled by mechanized cotton gins. The lint fibers are then baled into 500 lb units, which are the raw materials for textile mills that will then spin the fibers together to form threads and skeins of fabric.
The average acre of cotton in the U.S. will yield about 1 1/3 bales of lint. This is a two-fold increase over cotton production in the 1950s, largely due to improvements in land use, varieties, and irrigation. The vast majority of cotton grown in the U.S. is transgenic. It has been genetically modified to be resistant to certain herbicides or pests or both. Research continues on this economically important crop to improve fiber yield and quality as well as confer disease and pest resistance. Plant scientists are also eager to further push the limits of drought tolerance in this species.
The production and initial processing of cotton is only the beginning when it comes to cotton’s economic impact. According to the National Cotton Council, a bale is enough to make 215 pairs of jeans or 1,217 men’s T-shirts or 313,600 $100 bills. Yes, cotton is literally money. The estimated contribution of the cotton industry to the U.S. is $27 billion.
Olympia Cotton Mills, South Carolina c.1903
So consider cotton this Labor Day, whether you are enjoying a day off or clocking in. It doesn’t matter if your collar is blue or white, it all comes back to green in the plant Gossypium hirsutum. Both the plant and its processing have come a long way.
Johnna
*Video by Janice Person. Also check out the links below from her blog. If you want to know more about cotton, it’s definitely the place to visit. A whole blog about cotton! You can also follow her on twitter @JPLovesCotton (see, she really does love cotton).
Because photosynthetic organisms are the energetic foundation of our biosphere, we always tend to think of them as allies, organisms with a positive connotation. Their trademark color green is universally linked with goodness, growth, and life. However, there are some bad apples in the bunch that just seem to have it out for us heterotrophs. Well, maybe not apples (though I’m sure there are some poisonous apples out there somewhere*), but nature is filled with examples of poisonous plants. Many toxins and pharmaceuticals have botanical origins.
The focus of today’s blog post sinks even lower- algae, pond scum, cyanobacteria. Most of these aquatic photosynthesizers quietly convert sunlight to biochemical energy without any ill effects to anyone. I’ve written previously, that under the right conditions (warm and nutrient-rich waters) these otherwise inconspicuous organisms bloom in great numbers and overwhelm their environments. Like all life on earth, algae are programmed to capitalize on favorable conditions for reproduction. The ultimate crashes of these blooms can result in aquatic dead zones, areas with dissolved oxygen levels too low to support life.**
Algal bloom in Lake Erie 2011 from the NASA Earth Observatory Credit: Jesse Allen and Robert Simmon via Wikimedia
However, in some cases, the effects of these algal ‘blooms’ go beyond sheer numbers. Some algae produce toxins which cause serious health problems for those of us heterotrophs sharing their environment. The individual constituents of these ‘harmful algal blooms’ (HABs) measure in at ~1-2 µm, but they can wreak all kinds of havoc on the scale of large cities. HABs can stop your summer fun by forcing beaches to close or eliminating certain shellfish from your diet, but this summer the problems went beyond recreation to something much more fundamental- potable water.
Clean, safe drinking water is a fundamental service of human civilization. In our modern society, just turn on the tap, cook, clean, bathe, drink. It has been such a staple of American cities that it is taken for granted. That is, until it’s no longer available. That was the exact situation in Toledo earlier this month. A large American city, in the year 2014, was without safe drinking water for a whole weekend. Approximately, 500,000 citizens were affected. All because of toxic algae.
Microcystin-LR chemical structure Credit: cacycle via Wikimedia
In this case, the culprit was a bloom of cyanobacteria which produce the toxin microcystin. This molecule is harmful to the health of humans, pets and wildlife by acting as a liver toxin. It also has neurotoxic effects. The toxicity of microcystins has been extensively characterized and long-known to be associated with certain cyanobacterial species. Because of the potential adverse effects of microcystin-producing cyanobacteria on modern water supplies, treatment facilities routinely check the levels of this toxin. Only one part per billion of this molecule is considered acceptable. When a microcystin-producing algal bloom occurs near the intake of a municipal water supply (as it did for Toledo this month) the facilities can quickly be overwhelmed causing the water supply to exceed acceptable microcystin levels. The situation is compounded by the fact that microcystins are resistant to boiling. While boiling water may destroy other toxins or contaminating bacteria, it only concentrates microcystins. In order to bring the toxin levels down, the problem must be addressed at the water treatment facility (using methods like activated carbon, ozone treatment and membrane filtration). By adjusting the normal procedures to account for increased microcystins, the water supply can be treated to once again safe levels. All of this is accompanied by exhaustive analysis of microcystin levels and vigilant monitoring after the incident.
Scientists and government agencies are always working to monitor our water systems for HABs. Check out some of the links below for descriptions of continuous efforts to monitor our environment for HABs. How do we get to the point of 500,000 people without water for a weekend with everyone watching out for it? I mean, we’re watching it from space! Even with all of these sophisticated tools and models, nature can be surprisingly swift. Check out these images and reports from the NOAA Great Lakes Environmental Research Lab on Aug 1, 2014 and Aug 4, 2014 showing false-colored images tracking the algal growth.
Simultaneously in the news cycle with the Toledo water crisis, two Ebola patients were being treated in premier isolation facilities on American soil. The nation’s attention was rapt with the details of their treatment and speculation was rampant as to the possibility of an outbreak in America (an infinitesimally small probability not worth talking seriously about among scientists and epidemiological experts, but a great ratings-driver). Worldwide, the Ebola death-toll numbers in the thousands, not just from this year, but ever. Based on pure body count, there are many deadlier infectious diseases, which we as the public dismiss more easily. Beyond those numbers, the lack of clean water for drinking, food preparation and sanitation results in the deaths of ~3 million people every year across the globe. A safe and reliable water supply, as a basic right, continues to elude human civilization.
Water, water everywhere, but not a drop to drink… Credit: de:Benutzer:Alex Anlicker
HABs are only a part of the world’s water problem. However, the disruption of Toledo’s water supply should have been an event that caught our attention and held it for a while longer. It may be easy to turn on the tap, but getting the clean water to that point takes a significant amount of effort with infrastructure maintenance, monitoring and treatment. All of these things are largely invisible to us in modern society. Unfortunately, all of these things are affected by other societal choices like economics, aesthetics, environmental regulations, and the practices of our agricultural systems and other industries. As a society, we should start having the longer, difficult conversations necessary to attack this complicated problem rather than the transient chats that occur when we are in crisis mode. Find out about your community’s water situation and the issues related to your supply. Talk to your community leaders today to ensure that safe water is part of your future.
Johnna
*Hey, it’s hard to transition away from the summer’s Disney theme completely in a single post. However, I’m not just talking about the evil queen’s poisoned apple from the fairy tale. Apples have a huge amount of genetic diversity and I’m sure there are some varieties out there that are poisonous or so foul-tasting that you would think they are. After all, apples concentrate toxic substances in their seeds.
**In case you’re wondering, this year’s Gulf of Mexico hypoxic zone measured ~5500 square miles. That’s not breaking any records for size, but still about as large as the state of Connecticut. Read more about it here.
Next up in the Frozen series… we’re talking about flowering for the first time in ‘forever’ (really, just after winter). Here’s the Disney version for your reference.
FRIGIDA’s gone, so’s FLC
Winter is over? Can it be?
We need to transcribe a thousand different genes
For months we’ve waited in dormancy
Halted all pluripotency
Finally, it’s time to make some scenes!
There’ll be actual real live flowers
It’ll be totally great
I’m so ready for this activated state!
‘Cause for the first time in forever
There’ll be flow’ring, there’ll be growth
For the first time in forever
Translating AP1 and LFY both!
It must be the gibberellic acid
There’s active meristematic zones
‘Cause for the first time in forever
FLC is gone
I can’t wait to bloom, everyone!
What if I meet… the one?
This Spring imagine me petals and all,
Fetchingly vining up the wall
My flowers a delicately shaped vase
Ooh! I suddenly see him buzzing by
A striped pollinator that can fly
I’m gonna shove some pollen in his face!
But then we trade pollen and nectar
Which is completely strange
Not like when FLC is in detectable range
For the first time in forever
There’ll be flowers, there’ll be sun
For the first time in forever
I’ll be making AP1
And I know it is totally crazy
Excitement over meristems
But for the first time in forever
There’s activity in them
[FLC:]
Don’t let them out, don’t turn them on
Winter could still go on and on and on
Repress, turn off, it’s not time to grow,
Make one wrong move and get killed by snow
[FLC:] Is it only for today?
[FT:] It seems like Spring today!
[FLC:] It’s agony to wait
[FT:] It’s agony to wait
[FLC:] The VRNs are saying open up the gate
[FT:] The gate
[FT:] For the first time in forever
[FLC:] Don’t turn them on, don’t let them out
[FT:] I’m getting what I’ve waited for
[FLC:] Be the regulator the plant needs about
[FT:] A chance to change my stagnant world
[FLC:] Repress
[FT:] A chance to pollinate!
[FLC:] Repress, turn off, don’t let them out
I know it all ends in autumn,
So it has to start today
‘Cause for the first time in forever
For the first time in forever
Nothing’s in my way!
Flowering is important for plants because it’s how they reproduce. So, they need to have ways of ensuring that this process occurs under conditions that are most favorable for seed production. Plant species solve this problem in a variety of ways. Some annual plants avoid harsh conditions altogether and complete their life cycle within a single warm growing season. Others must find ways of going dormant during the freezing winter months and wait out the season until spring comes back. Plants integrate information on both day-length and duration of cold temperatures so they are not fooled into flowering on a random warm day in winter.
Under any conditions, the transition to flowering requires an elaborate set of gene expression changes so that cells achieve the proper developmental fate. The perennials and winter annual plants that require a cold period of dormancy prior to the flowering transition have an extra layer of regulation to ensure the transition occurs at the right time. Plants accomplish this with a set of gene regulators, some promoting the floral transition and others repressing it. These tiered layers of control allow for seemingly binary (on/off) switches to become a way of fine-tuning the development of flowers in these plants.
It’s not unlike the opposing personalities of Anna and Elsa in the movie Frozen. The gene FLC functions to keep plants from flowering, while genes like AP1, SOC1, FT, and LEAFY turn on genes to promote flower production. In perennials and winter annual plants, FRIGIDA serves to keep plants from flowering through the work of FLC until a certain amount of winter temperatures have passed. The genes VIN3, VRN1 and VRN2 act to let the plants know that enough winter weather has occurred and the hold on flower development (via FLC and FRI) can be let go. The way that the repression system works is also an interesting case. It’s not that these proteins physically block transcription of certain genes; these repressors leave covalent marks on the genome and the histone proteins whose job it is to organize the DNA within the cell nucleus. It takes some effort on the part of the activators to undo these marks to subsequently turn on the necessary genes.
Major players controlling flowering in plants. Pointed arrows mean activation or promotion of the next downstream thing, while blocked lines indicate repression of the next step in the pathway.
It’s interesting to note that all of the genes mentioned in the above paragraph are gene transcription regulators of one variety of another. This highlights a continuing theme in how pathways for development or environmental acclimation are controlled. There are a small set of regulators which control sets of other genes that are also regulators or that actually do the necessary biochemical work. These regulators work together to integrate environmental information (in this case-temperature, light, day-length) and keep developmental programs in check. Scientists tend to identify these factors pretty early in their investigations of these big questions, usually because mutants in these important regulators have obvious defects in the process of interest.
However, I have to admit, this drives me crazy as a biochemist. I want to know what’s going on beyond the nucleus in these processes. Sure, we may know a lot about what conditions turn these regulators and other genes on and off, but we know very little about the physical mechanisms by which plants sense the winter temperatures and time how long they’ve persisted. What is the actual ‘winter sensor’ in plants? How is it different from the cold sensor that plants use for cold acclimation on the timescale of hours or just a few days? How does this winter sensor differ among varieties with different ‘chill requirements’ before they flower and make fruit in the spring?* These components remain a mystery, but one that plant scientists are furtively working to solve.
Vernalization (the plant biology word of the day) is the acquired ability of a plant to flower after a cold season. For our perennials and winter annual plants, the passing of sufficient winter (as measured by the mysterious ‘winter sensor’ and regulated by VIN3, VRN1, VRN2, and FRI) gives these plants the ability to burst forth in flowers in the spring. Even though these regulators have a protective role for the plants in keeping them from trying to flower in the freezing winter, once their control is finally released, the flurry of activity associated with flower development is akin to a grand celebration after what seems like a lifetime of seclusion. Upon flowering, it’s all about reproduction. When it comes to plants, there’s not even a pretense of modesty; they have no problems trading pollen grains with a pollinator they have just met.
A number of economically important agricultural crops, like wheat, cabbage, carrots and most fruit trees, have vernalization requirements for flowering. Understanding how this process works is critical for getting the most out of these plants where they are grown and expanding the arable ranges for these crops. It may be some time before plant biologists make a Honeycrisp apple tree I can grow in Louisiana, but even modest adjustments to vernalization requirements to staple crops like wheat may be needed to accommodate predicted climate changes.
*This is why apple trees (with varieties requiring 400 – 1000 chill hours) don’t flower efficiently and produce fruit in a place as far south as Baton Rouge, LA (~200 – 300 chill hours), but figs (requiring only 100 – 200 chill hours) do.
Kicking off the scientific section of the Frozen series…
Some plants can endure the cold,
Even freezing temps surviving
Gene transcription levels change ten-fold
But the important thing’s the timing.
CBFs start the response pathway,
Activating others to join the fray,
This works when there’s not a sudden freeze one day
It’s bad enough to lose a limb,
But plants must protect their meristems!
For those readers who are not compliant with our rodent overlord and have not seen the movie Frozen, here is a link to the Youtube clip with corresponding song.
Ice in biological systems is just as bad for plants as it was for poor Anna in Frozen. The sharp edges of ice crystals tend to rip biological membranes to shreds in ways they can no longer function or be repaired. In freezing temperatures, crucial biomolecules slowly lose mobility and grind to a halt. Both of these consequences violate central tenets of living systems. Cells need intact membranes to maintain the integrity of the ion gradients responsible for fueling bioenergetics, and all biochemical reactions depend on small motions in all molecules. Thus, all living things want to keep their cytoplasm from turning into snowflakes. So, how do plants deal with freezing temperatures? It’s not like they can just go inside their castles next to a warm fire. And for the record, acts of true love aren’t very helpful either. Today’s post explores how plants adapt to falling temperatures.
Temperature is an important factor governing the molecular details of plants’ lives. The activities of the enzymes that carry out routine metabolism are affected by the ambient temperature. The fluidity of plants’ numerous important membrane systems is also influenced by temperature. Consequently, plants must make significant internal adjustments to adapt to colder temperatures. Even though the leaves of your cold-hardy plants may not look any different in summer compared to winter, there are many molecular-level changes with respect to the types of proteins and membrane lipids that the cells contain. These changes require an energy commitment that makes it wasteful or impractical for plants to always have cold-tolerance turned on, so they have an elaborate system for inducing cold-tolerance.
Very few plant species would be able to survive Elsa’s magical wrath, which turned a normal summer day into deep winter. For the most optimal cold-survival, plants need exposure to lengths of cold-but-not-freezing temperatures to trigger internal pathways to get ready for freezing temperatures. This generally works well for plants on Earth* since the cooling temperatures of autumn precede the first snowfalls of winter. During this time, plants are acclimating at the molecular level for the onslaught of months of freezing temperatures. It shouldn’t be that surprising that cold-acclimation is linked to plants’ circadian clock and timekeeping mechanisms for day-lengthsince these are also tightly connected with seasonal temperature changes.
Plant scientists have been working out the details of just what plant cells are doing during this acclimation time. One of the first things triggered by colder temperatures is the gene expression of the CBFs (C-repeat Binding Factors). These CBF regulatory proteins then activate other genes responsible for the grunt work of protecting cells from freezing temperatures. This layered response gives the plants more ways to regulate the biochemical changes as well as simplifies the initial activation of the pathway. The exact functions of the structural proteins which confer freezing-tolerance are still under investigation, but they have roles like stabilizing membranes under freezing temperatures or producing cryoprotectant molecules like sugars. Plants also change expression of genes controlling development so that growth is controlled during dangerously cold seasons. Teasing out the underlying mechanisms plants use to protect themselves from freezing temperatures is an active area of research in plant science.
Frozen plants by rockmylife via DeviantArt
Researchers are also interested in how cold-acclimation systems differ between plant species in order to gain insights as to why plant species have such differences in cold-tolerance (say, citrus vs. pine). Is it because the less cold-tolerant species don’t have some of the structural proteins necessary to protect cells during freezing temperatures? Or is it because the cold-sensitive species lack or have less responsive regulatory proteins for acclimation? Can the genes responsible for cold-acclimation be transferred to cold-sensitive plants to confer better freezing tolerance? Plant scientists are diligently working to find answers for these questions.
Hey, I’m sure there is some agribusiness that would love to open the market for citrus crops up to farmers in Minnesota,**but I think more modest adjustments in hardiness for certain agriculturally important crops are what they are aiming for. Even so, you may be wondering at this point, “Haven’t scientists been wailing for years about how the climate is getting warmer not colder? Why bother with cold-tolerance now? Can’t we just wait it out?” I’d say, “Sure, when there is beachfront property in Arkansas, go ahead and grow grapefruit there.” However, the story is a little more complicated than that, and it’s also important to mention that freezing-tolerance isn’t all about the thermometer. A big part of dealing with freezing temperatures means coping with less available liquid water. In studying freezing-tolerance, scientists have also uncovered connections with drought tolerance. That’s right, the same systems that kick in to handle frost intersect and merge with those conferring drought-tolerance. Thus, the more we know about freezing tolerance, the more we learn about drought tolerance. I think we can all agree that finding more ways to increase drought tolerance in plants is useful in places other than fairytales.
Johnna
* I can only hypothesize that the flora of fairytale worlds has a much quicker cold-tolerance induction response or that there is other magic to mitigate sudden frost damage.
**Hey, maybe there’s an idea for finally getting rid of that awful citrus greening that’s decimating Florida’s citrus groves. I have a feeling the insect vector that carries the disease will have a difficult time surviving winters in the northern Midwest.
Red fluorescence tells the story, satellites can measure, measure it!
Wait, those aren’t the lyrics to Major Tom Coming Home. Not quite, but more appropriate for the upcoming OCO-2 NASA mission scheduled to launch in less than 24 hours! That stands for Orbiting Carbon Observatory-2, a satellite equipped with instruments to measure carbon dioxide in the Earth’s atmosphere. What does photosynthesis have to do with it? A lot. No matter how the carbon dioxide finds its way into the atmosphere- vehicle emissions, thawing tundra, the panting of my dogs in the Louisiana summer heat- photosynthetic organisms are its ticket out of the atmosphere and back into the solid state. The OCO-2 satellite will be collecting spectral data for direct measurements of atmospheric carbon dioxide as well as sun-induced fluorescence to monitor photosynthesis on a global scale.
Watching in a trance, the crew is certain, Nothing left to chance, all is working…
Now that you know what the OCO stands for, you might be wondering about the 2. Of course there was a ‘1’. Starting with 2 would just drive people like the scientists and engineers at NASA crazy. The OCO-1 launched in 2009 with a similar mission to collect carbon dioxide concentration data, but it failed to launch properly and crashed into the ocean before making it anywhere close to its orbit. Sigh. After I’m sure a lot of this happened, the scientists and engineers got back to work to make the replacement mission even better. You can bet that everything has been quadruple checked this time.*
Starting to collect requested data, What will it effect when all is done?
Remember when I told you how nifty it was that satellites were measuring photosynthesis from space while I was making the same measurements in the lab? Well, it’s not just a scientific novelty being measured because it can be. Chlorophyll fluorescence on a global scale provides critical information for accurate models of primary productivity and global carbon cycles. A recent report in PNAS showed that sun-induced fluorescence data could be used to model gross primary productivity.** The authors found that estimates based on chlorophyll fluorescence data were much higher for major agricultural areas like the U.S. Corn Belt than models using other measures. These findings mean our current models may be underestimating how much modern agriculture and other managed areas contribute to the Earth’s carbon cycle. That report focuses on land photosynthesis, but I hope that the satellites will be collecting the chlorophyll fluorescence signal from both the land and the oceans. Let’s not forget that the photosynthetic bacteria in the ocean account for about half of the Earth’s primary productivity. I’m sure they have it covered since they have long been interested in mapping ocean color.
Check out this video for more on the OCO-2 mission.
There’s a lot of politics behind the amounts of carbon dioxide in the atmosphere, what’s causing them to creep increasingly higher and what that means for global climate patterns. Collecting accurate data on how much carbon dioxide is released into the atmosphere as well as the capacity of photosynthetic organisms to reclaim that carbon dioxide will greatly aid in global climate models that will be used to direct policy.
UPDATE 07/01/14: For those of you that didn’t set your alarms early to watch the launch…
The computer has the evidence, need to abort, the countdown stops…
At T-46 seconds to be precise. There was a problem with the pad’s water system during the launch sequence that caused the mission to be aborted today. The satellite and rocket are all still ready to go, but NASA’s scientists and engineers need to figure out the source of the problem and a new launch date for the OCO-2 mission. Check here for the latest. And follow OCO-2 on Twitter!
UPDATE: 07/02/14
The OCO-2 do-over launch was successful today. Don’t just take my word for it, listen to OCO-2:
*If a launch failure happens again, I’m willing to start entertaining conspiracy theories.
**It should be noted that chlorophyll fluorescence has long been a standard technique in the laboratory for analyzing photosynthetic efficiency. Scientists have even scaled it up for field analysis. The real breakthrough in recent years has been observing this faint signal from plants via satellite using only the incident natural sunlight (not artificially bright light subjected to plants in a very controlled way).
April showers have brought May flowers… to the blog. Today’s post is one of a May Bouquet series focused on flowers one might find in a bouquet. Y’know, leading up to Mother’s Day today! Think of these posts as daily reminders with wonderful suggestions on ways to honor the mothers in your lives.*
Credit: Wikipedia
Today’s post is tip-toeing through the tulips. They rank at the top of lists for most popular cut flowers and bulb plants in gardens. The flowers provide intense spring color in such uniformity that they are easy to incorporate into any arrangement- vase or plot.
Tulip Credit: John O’Neill via Wikipedia
These flowers originated in central Asia, but their introduction to Europe in the late 1500s created such a stir in the Netherlands it has come to be known as ‘tulip mania.’ The Dutch economy was good at the turn of the 17th century, so people had time to invest in aesthetics. The recently introduced tulip was the perfect medium with its dazzling capacity for intense color on a consistent form. New color varieties were introduced with names like Viceroy and Semper Augustus and demand caused their prices to skyrocket.
Semper Augustus print via Wikipedia
However, basic tenets of tulip biology made the economic speculation craze dangerous and untenable. While tulips are perennials that can be grown from bulbs year after year, it takes as along as 4-6 years to go from seed to a bulb large enough to flower. This makes introducing new varieties slow, even when vegetatively propagating them from bulb offsets. Plus, as they are flowers, their beauty is by definition fleeting. They bloom for a short time during the spring then exist as bulbs for the remainder of the year.
Furthermore, the most desired tulips were the ‘broken’ varieties with blooms containing streaks of two colors. During this period, the streaks were not due to some inheritable genetic mutation, but infection with Tulip Breaking Virus. It caused pleasing visual appeal, but also weakened its host. Eventually, the bulbs weakened to the point of not being able to flower or produce additional bulb offsets. Thus, the most expensive tulips in history have gone extinct. Many of the streaked varieties available on today’s market are the result of stable genetic mutations that affect flower coloration, but not the vigor of the plant. There are only a few truly ‘broken’ varieties left (like Absalon), which are infected with TBV, but for some reason the infection has not manifested itself beyond the effects on flower color pattern.
The Viceroy Credit: Wikipedia
So just how much money are we talking about? More than anyone in modern times has spent at a garden center for a single bulb. For example, records indicate that a bulb for ‘The Viceroy’ sold for approximately ten times the annual earnings of a skilled craftsman. The peak of tulip bulb speculation was the winter of 1636-1637. Of course, at this time tulips are only bulbs with no flowers at all, hardly things that look worthy of fortunes. Tulip trading was a futures market, and contracts were written based on what traders thought the bulbs would be worth to consumers at spring planting time. At some point that winter, people came to their senses. The first few that cashed in their contracts set off a selling frenzy that caused the bottom to drop out of the market.
In the end, fortunes were lost and some were left with lots of worthless bulbs. I’m sure their beauty that spring was just salt on the wound. It was even difficult to eat their losses. Tulip bulbs taste awful and when not prepared correctly, they are poisonous. They are really only a food source of last resort in extreme situations, like the Nazi occupation of the Netherlands during World War II.
Today’s tulip markets are more rational, but still huge business in floriculture. New colors, shapes and patterns are being developed, but the source of the broken tulips, Tulip Breaking Virus, is no longer coveted, but eliminated. The ultimate damage this pathogen does to vigor of the tulip bulbs outweighs the production of any desirable color patterns. The spread of this infection is controlled by using pesticides and other measures to reduce aphids on the tulips that spread the virus as they eat on one plant then another. TBV is detected by experts trained to spot the symptoms in the tulip plants in the field. Infected plants are removed and destroyed. A new report out this year describes an instrument capable of scanning plants in the field for TBV to improve this laborious process.
Flaming Parrot Tulip Cultivar Credit: PierreSelim via Wikipedia
So, if tulips find their way into your bouquet today, enjoy them- just don’t go crazy.
Credit: McBeth via Flickr
Johnna
*Maybe you’ve learned something about plants along the way. Maybe these posts have helped you remember to pick up flowers for the mothers in your life. But let me just add, if one of those mothers still has small children, say that you sired or otherwise claim, make sure your bouquet also includes species like folded laundry, extra sleep, cooked meal, clean kitchen and bathroom. These varieties, while difficult to cultivate without the help of a mother, will surely reap you returns greater than those seen during tulip mania.
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