Category Archives: Frozen

PSII is a Fixer-Upper


The final song from our Frozen parody reminds us that just because something is damaged or broken, doesn’t mean it can’t become whole again with a few repairs. This sentiment makes it the perfect theme song for my favorite enzyme, Photosystem II (PSII). Here’s the Disney version…



Is it the slower QB reduction?

Or lack of water oxidation?

No use trying state transitions,

Although we know it transfers well, PSII ends up photodamaged

Such photoinhibition is such an imposition

So it’s a bit of a fixer upper

So it falls behind

Its peculiar mechanism

Is a one-of-a-kind

So it’s a bit of a fixer upper, but we’re certain of this one

You can fix this fixer upper with a newly made D1

Is it the oxygen singlets?

In chlorophyll protein ringlets?

Is it the way the water splits?

Electrons zipping towards quinones

Causing D1’s aches and groans?

Now permanently on the fritz.

PSII’s just a fixer upper

It needs a protein exchange

Its phosphorylation is confirmation

That something is strange

So it’s a bit of a fixer upper

Plant cells know what to do

The way to fix this fixer upper

Is to make D1 anew

Damaged PSII is a bit of a fixer upper

That’s a minor thing

Just disassemble then reassemble

Voila just like recycling!

So PSII’s a fixer upper

It’s function is nixed

Get the damaged protein out of the way

And the whole thing will be fixed

We aren’t saying to remake the whole thing

‘Cause that’s just too much work

We’re only saying that light’s a force that drives PSII berserk

Electrons just excite the wrong things if they go off their normal path

Changing out the D1 protein erases all their wrath

New D1 clears the path!

All PSII’s are fixer uppers

They’re made to fizzle out

DegP, phosphorylation

FtsH, degradation

Get them on the repair route

All PSII’s are fixer uppers

When the electrons start to move

The only fixer upper fixer

That can fix a fixer upper is

To get the damage removed



Photosystem II performs the unique reaction of splitting water to form oxygen and extract electrons used to fuel photosynthesis. Not all of this energy goes in the direction that it should. When energy gets backed up in the system or electrons venture off of the designated path, irreversible damage to the proteins can occur. This damage means that PSII doesn’t work anymore. Because this photodamage is an unavoidable hazard, photosynthetic organisms have an efficient way of dealing with this problem.

For one thing, the D1 protein at the heart of the PSII complex bears the brunt of the irreversible damage. This makes sense because the D1 protein also coordinates many of the cofactors that comprise the electron transfer pathway through the system. On the one hand, damage to this one protein means function gets knocked out as well; on the other hand, it means that the damage is concentrated on just one protein. So, to fix it and restore function to the complex means photosynthesizers mainly focus on replacing one protein, not twenty. That’s what has to happen. The damaged protein must be replaced by a newly synthesized copy.

It sounds simple enough, but anyone who’s done any fixer-upper work knows there’s more to it than that. Repairing the damage starts with recognition; there must be systems in place to differentiate functional PSII from damaged PSII. Phosphorylation of certain residues on PSII subunits labels those complexes as targets for repair. These labels are interpreted by specific proteases, which then remove and chop up the damaged D1 protein. Next, a newly made D1 protein is inserted into the complex to restore function.

The proteases involved in removal of the damaged D1 protein are DegP and FtsH. Researchers still debate over which one is more important, but it is likely to be a combined effort by both. Also, because the D1 protein is located within the middle of the PSII complex, many other subunits and cofactors must partially or transiently disassemble as a result of D1 protein removal. Exactly how this works and what additional proteins are involved in this process are active areas of research in the photosynthesis community.

Photosynthesizers don’t give up on their PSII complexes just because they get a few dings. The constant recycling of PSII complexes through this repair process ensures that the light reactions of photosynthesis will continue to churn away, even in bright light (more energy, higher rates of damage). It may seem like a lot of trouble to run this elaborate repair shop, but it’s still easier than starting from scratch each time PSII is damaged.




References and Links:

PSII damage and repair

Let it Go: Abscission


Up next in the Frozen series: Plants let it go! Here’s the Disney version in case you’ve been living under a rock for the past several months.


The cell walls grow thin in the zone tonight

No chlorophyll to be seen

The leaf is about to fall

Thanks to all the ethylene

In the winter weather those cells would have died

Wouldn’t have mattered how many genes I transcribed!

Turn them red, set them free,

I can’t move I’m just a tree

Breakdown, recycle, not just a show

But, here’s your show!

Let it go, let it go

Not holding on any more

Let it go, let it go

Away they fall, away they soar!

I don’t care

What they’re going to say

Let my limbs lay bare,

The cold never bothered me anyway!

It’s funny how abscission

Makes mincemeat of cell walls

And the genes that once controlled me

Can’t get to my leaves at all!

It’s time to see what I can do

Other organs can shed too

No petals, no flowers for me, I set them free!

Let them go, let them go

Already pollinated, that’s why!

Let them go, let them go

Useless now to me, so let them fly!

Here I stand

And here I’ll stay

I can’t move on!

My fruit flutters through the air onto the ground

My seeds spiraling on the wind all around

The next generation moving forward at last

But I’m never leaving

My roots hold me fast.

Let it go, let it go

It’s really better for me and my spawn

Let it go, let it go

That springtime form is gone!

Here I stand

In the light of day

I can’t move on,

I’m better at biochemistry anyway!



It’s hard to tell if plants have any inner emotional turmoil like the one Elsa had to fuel this song. However, it is safe to say that no matter how stoic they appear, there’s a lot going on inside them. Since they can’t move, plants have to roll with environmental changes using biochemistry and a flexible developmental program. Plants may not run away to the North Mountain, but they know how to ‘let it go’ when necessary. They do this in a process called abscission, a regulated way of shedding parts of themselves for the good of the plant or the next generation.

One of the most spectacular shows of abscission is the autumnal color change and shedding of leaves in deciduous trees. We call it ‘Fall’ because of the dramatic leaf drop before winter. Even though plants can take some measures to protect themselves from the cold, keeping some tissues over the winter requires too much energy of the plant. The trees do what they can to recycle the valuable contents of the leaf cells, which results in their colorful display. Then they coordinate a way to drop their leaves that doesn’t leave open wounds on the plant.

It’s not just letting loose of leaves before winter, abscission is an important plant process for other organs as well. Plants don’t need to waste their energy on maintaining flower petal tissue after they’ve already been pollinated. If seeds are on their way to forming, no need to keep the lush colorful tissues that can’t photosynthesize enough to support themselves. Further down the line, once fruit has formed to encapsulate the seeds, it must also be let go from the mother plant in order for the next generation to find a hospitable place to germinate. These examples represent normal developmental progessions for plant tissues, but sometimes plants have to improvise. When plant tissues become infected with bacteria, viruses, or fungi, they can kick the abscission process into high gear in the hopes that shedding the infected or damaged parts will prevent the death of the whole plant.

The abscission process creates an area of tissue designated the abscission zone, in which the cells take on distinctive characteristics. These cells are smaller and have an extensive network of endoplasmic reticulum and Golgi membranes with connections to the plasma membrane. The specialized cells of the abscission zone acquire the ability to respond to certain triggers to induce cell separation. These triggers can be a combination of environmental (ex. defense proteins induced upon infection) and internal (ex. the plant hormone ethylene) stimuli. When these triggers are perceived, the cells of the abscission zone up-regulate enzymes that breakdown the cell walls making cell separation easier. Ultimately, the abscission zone cells that remain on the main body of the plant differentiate into a protective layer so there is no open wound on the plant. The abscission process requires the coordinated activity of a large number of genes that must straddle the intersections of developmental pathways and environmental sensory integration.

Plant scientists are still working out the details, but the confluence of so many processes during abscission makes it a difficult problem to attack. However, understanding the abscission process remains a high-priority pursuit in the world of plant science. Agriculturally and horticulturally important plants have been heavily selected with respect to their abscission properties over many generations. In some cases, preventing early abscission may increase yields of certain crops (think- use those leaves longer, don’t drop them). Slowing down or halting the abscission process is also important for aesthetic reasons (keep those flowers and leaves around longer). Facilitating the abscission process may be equally useful and aesthetically pleasing. If plants could be engineered to abscise sooner or more completely, harvests would be easier because fruit would require less force to remove from the plant.

Consider the case of the gardenia- a striking example of a plant that needs to learn to let it go. It is perhaps the most perfect garden shrub- beautiful white blooms that coordinate with any background palette and a lovely scent. However, the blooms past their prime are truly one of the most pitiful sights in the botanical world- shriveled and brown and hanging on for dear life many days longer than anyone would care to look upon them. I’m not sure what inner turmoil is raging within this species, but biochemically, the processes of programmed cell death within the petals and their abscission from the plant are not coordinated in a way that is pleasing to the eye. If there were a gardenia variety that timed these processes more closely with one another, then gardeners would not be forced to look at the crumpled brown blooms.




References and Links:

Stomata Open the Door


Next up in the Frozen series… Love may open the door to our hearts, but stomata are the gatekeepers of gas exchange in plants. Here’s the Disney version for your reference.


[Guard Cell1:] Okay, do you feel like we need some CO2?

[Guard Cell2:] I love CO2!

[CO2:] All my life has been just cell walls in my face
And then suddenly I bump into you

[Guard Cell1:]
I was thinking the same thing! ‘Cause like
I’ve been sensing all night, we need some uptake
And maybe it’s the potassium talking or the full vacuole
[Guard Cell2:] [giggles]

[Guard Cell1:] But with you…
[Guard Cell2:] But with you

[Guard Cell1:] I open up…
[Guard Cell2:] I make a space…

And finally those guard cells make a pore!
Stomata, open the door!
Stomata, open the door!
Stomata, open the door!

[Guard Cell1:] With you!
[Guard Cell2:] With you!
[Guard Cell1:] CO2!
[Guard Cell2:] O2 too!
[CO2:] Stomata, open the door…

[Guard Cell1:] I mean it’s crazy…
[Guard Cell2:] What?

[Guard Cell1:] We expose all of the-
[Guard Cell2:] Mesophyll!

[CO2:] That’s what I was gonna say!

[Guard Cell 2:] I’ve never met some cell-

[Guard Cells:]
Who expands so much like me!
Jinx! Jinx again!
Our spatial synchronization
Can have but one explanation

[Guard Cell1:] You-
[Guard Cell2:] And I-
[Guard Cell1:] Were-
[Guard Cell2:] Meant-

[Guard Cells:] Developmentally!

[Guard Cell1:] Say goodbye…
[Guard Cell2:] Say goodbye…

[Guard Cells:]
To the H2O flying past
I think we shouldn’t transpire anymore!

We need to shut this door!
We need to shut this door!
If we want to live much more!

[Guard Cell1:] With you!
[Guard Cell2:] With you!
[Guard Cell1:] Sorry CO2!
[Guard Cell2:] Me too!

[CO2:] Dang it! They shut the door!

[Guard Cell1:] Can I say something crazy?
[Guard Cell2:] [giggles]
[Guard Cell1:] Do this again tomorrow?
[Guard Cell2:] Can I say something even crazier? Yes!


Guard cells, those crazy kids! Am I right? This song only makes them seem fickle. In real life, the motions of the guard cells of the stomata are tightly controlled. They comprise the respiratory system of plants allowing the entry of CO2 and exit of O2 at designated locations on the leaf. Check out this video with excellent illustrations of how these guard cells work together in the plant.

As explained in the video, the opening and closing of stomata must be a tightly controlled process. Plants need to open them up in order to allow for the entry of CO2 and exit of O2. Obviously, this is linked to photosynthetic activity, which increases during the day and ceases at night. Yes, even though those ‘dark’ or light-independent reactions would continue to occur at night, the biggest demand is during the day. Carbon fixation can still occur at night with whatever CO2 reserve remains in the air spaces of the mesophyll layer of the leaf. Stomatal opening is also controlled by CO2 concentration in the atmosphere. When CO2 concentrations are low, more stomata must be opened for longer periods to take in the necessary amount. In the case of increased atmospheric CO2 concentrations, the opposite is true, and plants can leave more of their stomata closed.

All of this gas exchange comes at the expense of water; water loss is the price plants pay for increased access to CO2. During a typical day, the demand for CO2 at night doesn’t justify the water-cost of having the stomata open. When water is at a premium, other signals can override stomatal opening even during the day. For example, the plant hormone ABA is produced at the onset of drought conditions and guard cells respond to this molecule by closing the stomata.

Given that the open/closed state of stomata is dependent on so many environmental factors, guard cells must have systems for integrating many combinations of molecular signals. Guard cells must be able to sense and respond to light, CO2 concentration, plant hormones like ABA, as well as the overall photosynthetic productivity of mesophyll cells. This means that have sophisticated regulatory networks that sort out all of these signals. The exact details of how this works are active areas of research by plant scientists.

Scientists have unraveled many details regarding how exactly guard cells change their shape to create the open or closed states. The path to opening the stomatal door hinges on the activity of an ATPase proton pump at the plasma membrane of the guard cells. This moves H+ ions out of the guard cells. The resulting proton gradient triggers the opening of a gated K+ channel to move K+ ions into the cell in an attempt to keep the appropriate charge balance across the membrane. This movement of positively charged ions also causes the redistribution of negatively charged ions like Cland malate into the guard cells. This change in ion distribution as well as the relative concentrations of sugars within the cell drives the movement of water into the guard cells by osmosis. The increased turgor pressure from the influx of water causes the guard cells to take on the kidney shape which opens the stoma. Signals that trigger the closing of the stoma reverse these ionic distributions, causing the cells to lose water, become flaccid and close the aperture of the stoma.

Finally, stomata are not only interesting to plant scientists. Plant pathogens have long since noticed these openings to interior plant tissue, and have come up with ways to exploit this interest for their own sinister purposes. The fungus Fusicoccum amygdali produces the toxin fusicoccin which activates the proton ATPase pump, in turn causing stomata to irreversibly open. This strategy creates access points for fungal hyphae invasion and ultimately plant death from infection and wilting caused by the constant loss of water through open stomata. Thus, even in the plant world it’s deadly to be betrayed from within by a signal that should have been simpler to interpret.




References and Links:

For the First Time in Forever: Vernalization


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


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, while blocked lines indicate repression.

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.

For more on how plants remember winter, check out this post over at The Quiet Branches.


*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.

References and Links:

Do you want to make a plastid?

FrozenNext up in the Frozen series… Do you want to make a plastid? Here’s the snowman version from Frozen for your reference.

Plant cells…

Do you want to make a plastid?

Come on, differentiate

Time to photosynthesize

Special things to metabolize

C’mon they need a fate

Those used to be proplastids

And now they’re not

We hope genetics tells us why!

Do you want to make a plastid?

It doesn’t have to be a chloroplast

Do you want to make a plastid?

Some grana stacks green and tall?

I think some development is overdue…

Environment gives you cues

From the nucleus transcription calls!

(Induce there GLKs)

It gets a bit confusing

All these proteins whizzing by



Chromoplasts get lots of color

With all these carotenoids

Amyloplasts store starches

For all the tissues underground!

Do you want to make a plastid?

It could even be a tannosome

Yes, etioplasts are in there

In the dark since who knows when

Shine the light to start,

The nucleus is there for them,

No longer inside meristems,

Time for some changes to begin!

They do so many functions,


What can’t plastids do?

Do you want to make a plastid?

Well, if you are a plant cell, the answer to that refrain is always, “Yes!” Plastids are specialized organelles in plants that perform a wide array of specialized biochemistry. The most well-known and recognized of these are chloroplasts. These subcellular compartments are packed full of the thylakoid membranes and enzymes necessary to convert light into sugars. Chloroplasts perform other important biochemical reactions including the synthesis of starches and fatty acids as well as the assimilation of nitrogen into amino acids.

The chloroplast by User:Miguelsierra, adapted by User:Vossman via Wikipedia

There are other types of plastids made in plant cells for other specialized purposes. There are chromoplasts, which are full of carotenoid and other pigments giving them distinctive colors. The cells of tomato flesh, carrots and rose petals contain this type of plastid. Of course, pigments don’t do much good in root tissues. You may not find chloroplasts or chromoplasts there, but they do contain leucoplasts (loosely defined as non-green plastids used for storage of starches and oils). Storage-type plastids aren’t relegated to the roots. Recently other types of plastids have been identified, which specialize in the synthesis and storage of distinctive metabolites. Tannosomes have recently been characterized as specialists in tannin storage. A phenyloplast was also recently described in vanilla fruit as the storage location for vanillin precursor metabolites. In fact, the range of biochemical specialization that plastids perform strains their traditional nomenclature and definitions. As scientists learn more about them, the divisions between traditional types seems to blur. It seems that plants can make them as specialized as they need to be along a gradient of biochemical functions.

Types of plastids by Mariana Ruiz Villarreal LadyofHats via Wikipedia

Plant cells have definitely capitalized on the versatility of the plastid organelle structure to ensure dedicated locations for all manner of biochemical reactions and/or storage of their products. This is no small task. It requires the coordination of genes in two different genomes (that of the plant cell nucleus as well as a small genome in the plastid), trafficking of proteins throughout the cell, sensing of environmental cues, and synchronization with the overall plant developmental program. It’s enough to make any project manager run out of color-coded post-its and lose track of scheduled task times. Here are the highlights:

First of all, plastids do not exist in their mature forms in plant seeds and developing meristem tissues, but as immature and developmentally-flexible proplastids. These proplastids may not be special biochemists in their own right, but they have the potential to become any kind of plastid the plant cell needs. Consequently, proplastids have to know whether they are inside a root cell, petal cell or leaf cell. This means that plastid differentiation (aka development to maturity) must be coordinated with the development of the rest of the plant. Scientists are beginning to learn more about how this works, but this research is difficult since we’re talking about tiny, unremarkable pro-organelles within small portions of tissue. It’s a universal rule of cell biology that studying on small things is much more difficult than studying large things. Genetics has provided some new insights as to which genes have control over this developmental process. Transcription factors like the Golden-like (GLK) family of proteins have been identified as major players in this process, turning on suites of other genes to trigger proplastid development into mature plastids.

Of course, a lot of plant cell and plastid development is tied to environmental cues like light intensity. For example, plants can develop up to a point in darkness, but that doesn’t mean those cells have the same mature chloroplasts present in light-grown plants. Dark-grown plant cells contain plastids termed etioplasts, which are somewhat more differentiated than proplastids but not quite chloroplasts. Upon illumination, etioplasts quickly whip up thylakoid membranes and the photosynthetic machinery and get to the work of photosynthesis.

Plastid development and maintenance requires a large protein migration within plant cells. While plastid genomes make a number of their proteins, they do not make all of their resident proteins. Many essential proteins must come from genes transcribed in the plant cell nucleus and translated in the cytoplasm or endoplasmic reticulum. Thus, plant cells have an elaborate system of trafficking proteins to the proper cellular destination. This is true for all kinds of eukaryotic cells, but plant cells have extra organelles to distinguish among relative to animal cells. For those proteins with final destinations in the chloroplast, they have signals within their sequences that target them there. When they arrive at the chloroplast, they must pass through the surrounding double membranes using the Translocon of Outer Chloroplast Membrane (TOC) and the Translocon of Inner Chloroplast Membrane (TIC). In addition to the large influx of proteins that must be deposited upon initial development, the nucleus continues to provide essential proteins to the chloroplasts throughout their lifetime. It’s a constant flurry of activity maintained by two-way communication between the nucleus and chloroplast such that each organelle knows the biochemical status of the other.

Development into a mature plastid type isn’t the end of the line. There is still some developmental plasticity allowing certain plastids to convert into other plastid types. I’ve mentioned before that chloroplasts convert to chromoplasts in ripening fruit, as can be seen in the characteristic color change of green, unripe fruits into bright yellows, oranges and reds. Chloroplasts also provide the starting point for the development of other plastids specializing in storage of certain biomolecules. Plant cells also have ways of recycling the valuable contents of their plastids when cells and tissues reach the end of their lives (think autumn leaf color-change). As you might expect, this process requires more changes in gene transcription, protein synthesis and membrane structure orchestrated by the cell nucleus in response to more environmental and developmental cues.

Finally, proplastids and plastids of all types have ways of replicating themselves within plant cells. In this way, as plant cells divide each new daughter cell will contain roughly equal numbers of plastids. It wouldn’t be very good if a certain cell line within a tissue ran out of plastids. As much as plastids rely on the nucleus to full development and function, the nucleus cannot spontaneously create plastids from nothing. This wrinkle adds another layer of complexity to plastid biology. It means plastids must have some way of dividing themselves within the cells, and when plant cells divide, they must have some way of equally segregating the multiple plastids between the two new cells.

Basically, plastids are a lot of work for plant cells to make and maintain. However, these high-maintenance organelles are worth it given the biochemical rewards they offer. Scientists are only beginning to understand how plants make, maintain and recycle their plastids. Pieces of the complex system are studied by plant biologists all over the world and will likely keep them busy for many years to come.




References and Links:

Plant Cold Tolerance

FrozenKicking 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-length since these are also tightly connected with seasonal temperature changes.

winteriscomingPlant 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

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.



* 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.

References and Links:


What scientists do… in summer!


Let’s start the Frozen series with some summer fun for everyone. Here’s what Olaf (a snowman) thought about summer…

Have you ever wondered what scientists do in summer?

I’ve always loved the idea of summer… Really, I’m guessing you don’t have much experience with breaks, do you?

Nope, but I like to close my eyes and imagine all the potential productivity when summer does come.

There’s no classes… except that new course you wanted to develop for fall

There’s no students… except the half a dozen HHMI undergrads in the lab

No committees… except that one search that’s planning to beat the competition

PI’s will have time to work in the lab… except they don’t remember how to use the equipment.


A flask in my hand,

A burner flaming under ring-stand,

Squinting, yes, that could be a band,

So many experiments to do in summer!


The joy of preliminary data,

That will be written in grants later,

I hope they meet a generous rater,

But we won’t worry about it now, it’s summer!


Ecologists spend their summer days

Counting Anoles’ dewlap displays

Under the Caribbean rays*

From the cold room, the biochemist says:

I think I picked the wrong discipline for summer!


We can research whatever we please

Because there are no salaries**

Given by universities … in summer!


I hope this transformation gives resistant expressors

Because for reviewers, I’m a persistent addresser

Trying to be less of an #OverlyHonestMethods confessor

If I had my own grant, I be a __________ Happy Postdoc! This summer!***


Research posters, we will assemble

And they just might resemble

The abstracts submitted long ago

To justify a trip to Key Largo

Wait- that conference is really in Fargo… this summer!


Oh! at the meetings, the data will be new

And you’ll all be there too

Because that’s just what scientists do in summer!


// It’s summer, scientists. Enjoy it how you will. Feel free to add your own verses in the comments section below.



* Shout out to my friend Dr. Michele Johnson, WashU alum, now at Trinity University. Go visit her Lizards and Friends webpage for more than you ever wanted to know about lizards and their behavior.

**FYI- Does not apply to postdocs. I still get paid, but many other academic positions are only 9 month appointments.

***Give me a break, it was hard to think of rhymes for assistant professor.