Tuesday, November 24, 2015

Corn Color Concepts

Biology concepts – maize, transposon, antigenic variation, cereal grain, food grain, caryopsis

The Corn Palace in Mitchell, South Dakota, uses corncobs
to make murals on the sides of the building - yes, the mural
on the right is made of corncobs. Each year’s murals have a
different theme, and they use 13 different shades of corn in
their artwork, but after the drought of 2012 they only had 8
shades to work with for 2013. This is a picture of the palace
as it appeared in 1907. Notice the questionable decoration
on the center minaret – of course this was 25 years before
the rise of the Nazi party.
Thanksgiving decorations typically include some colorful earns of dried corn, commonly referred to as “Indian corn.” However, this corn has a history much more involved than mere decoration. People might be less inclined to hang it around their house if they knew how much it has in common with the organisms that cause gonorrhea, Lyme disease, and Pneumocystis pneumonia.

One of the first misconceptions we have to get out of the way is that corn is actually corn. The word corn doesn’t literally refer to the stuff on the cob we eat in the summer and the stuff we pop on a cold afternoon. What we call corn is much more accurately called maize.

The word "corn" comes from an old german/french word. In most uses before the 1600’s, corn meant the major crop for one particular area or region. In England, corn meant wheat; in Scotland or Ireland, it most likely means oats. There is even mention of corn in the King James Bible. This was translated several times and hundreds of years before maize arrived in Europe. The “corn” of the Bible most likely means the wheat and barley that were grown in the Middle East at the time.

When Columbus took maize (Zea mays) across the Atlantic to Europe, he might have referred to it as the chief crop of the Indians; therefore, it was Indian corn. After a while, domesticated maize became so ubiquitous that the word “Indian” was dropped, and all maize became corn – like all facial tissue becoming Kleenex.

The history of maize is, well, a-maizing. The corn we know today is the most domesticated of all crops. It can’t survive on its own; it has to be managed by man. Rice and wheat have naturally wild versions of themselves that still grow in nature, but there is no wild corn, it is purely man-made.

Today’s “corn” is actually a selective breeding result from a
grass called teosinte and a grass called gamagrass. Genetic
experiments have confirmed that each of these grasses was
involved in the evolution of maize. There was also some back
crossing of early maize with the grasses again. You can see
how the kernels and plants have changed over time.
The earliest corn-like plant was called teosinte. It's a grain plant with very small, vertical kernels. This plant was bred with something else, maybe gamagrass, and over time became early maize. Early maize was then bred back to teosinte, and the cob emerged. A recent article from Florida State shows that corn was being bred and harvested as early as 5300 BCE.

The early plants were quite variable, growing from 2 to 20 feet tall. The ears, when they developed, were small and had only eight rows of kernels. More breeding took place, especially when the plants were brought north. At that time, ears grew near the top of the plant, and the growing season in the north was too short to allow full development.

Maize is a grass, so it has the nodes and internodal growth as we discussed a few months ago. Corn grows about 1 node unit for each full moon; the Indians needed a corn that would mature in just three moon cycles. So they planted kernels from stalks that had the lowest ears, thereby selecting for plants they could harvest before it got too cold. Their selection was for size and production, but colors came along for the ride.

There are many color genes possible in maize. A new version, called glass gem corn, shows just how many colors are possible (see picture). Indian corn, as we define it now, can be found in most of these colors; sometimes ears are all one color, sometimes they are combinations of colors. It all depends on who is growing nearby, but we need to know a little more about corn in general to explain this.

This Carl’s glass gem corn. The photographer swears there
was no manipulation of this image. The corn is just this
pretty! I’d hate to eat it. This strain was the result of many
years of selective breeding, and the seeds were passed
down through a couple growers before they got this result.

Maize is a food grain, meaning that has small fruits with hard seeds, with or without the hulls or fruit layers attached. More specifically, maize is a cereal grain, because it comes from a grass. Wheat is a grass, so is barley, rice, and oats. Basically, these are the grains your morning cereal is made from, so which came first, the breakfast “cereal” or the “cereal” grain? The answer is out there.

And by the way - yes, grains are types of fruits. The fruit is more precisely called a caryopsis (karyon means seed); a small fruit and seed from a single ovary, which doesn’t split open when mature (indehiscent). One of the characteristics of most grains is that the pericarp (the fruit) is fused to the seed coat, so it is difficult to talk of the fruit without including the seed.

The point of this cartoon is to show you that there are
many layers to the kernel. The whole thing is not the
embryonic plant, just the germ. Some people say wheat
germ is healthy to eat. It would take a lot of kernels to get
much germ. You can see the hull is made up of several
layers as well, this is here the color is expressed. The
endosperm is what tastes food. It is many cells, all
storing the sugars.
The hull is a little more vague. Corn has a husk (the leaves that surround the ear), which is often considered the same thing as a hull. But each kernel on the ear also has a hull, the epidermis that is more brittle when dried. In other plants, husk and hull mean the same thing.

It's the hull that shows the color of a kernel of maize. You can pop blue, red, or purple corn, but the popcorn will still be whitish yellow. The color genes are present in all the cells of a kernel, but they are only expressed in the epidermis or hull; this will be important in a minute or two.

So how can Indian corn have kernels of different colors? The same way that you and your siblings look different. Each kernel is a different seed, so each is a different potential plant. The male flowers of the corn tassel send out grains of pollen to pollinate the female flowers. Each pollen grain has a sperm cell, and each has undergone the same process of mitosis and meiosis as human sperm – there is genetic variation there.

The female flowers are the silks on the ear of corn. Each silk is connected to a different ovary (potential kernel). Again, each egg is a different version of the maternal plant’s genome. Different silks could be pollinated by different male plant pollens floating around in the air – nothing says that all the kernels must have the same dad.

What we call Indian corn is just corn that has not been bred
so much as to have only color gene, and can be pollinated by
different dads. You can see that Indian corn can have several
colors or one major color. The interesting parts are those
spots and streaks. Read on for more about them.

So, it isn’t to difficult to see that different kernels could be different colors, either from random assortment and mendelian genetics, or from different pollens meeting different eggs. The reason we eat yellow corn or white corn or yellow/white corn is because the color genes have been selected for by breeding, and the pollination process is highly controlled. This is not the case with Indian corn.

So that’s the story for corn color – or is there more? Look closely at Indian corn above; some kernels have streaks or spots of color. How does that happen?! This is completely different from having kernels of different color, and relates to one of the great exceptions in DNA biology.

Barbara McClintock found that by observing the chromosomes of maize very carefully, specifically chromosome nine, and by looking at the resulting kernels from selective breedings, she could match changes in the chromosome to changes in color streaks and spotting.

She noticed changes in the length of the arm in some cells, and related this to the movement of genes along the chromosome. To this point, all scientists believed that genes stayed in the same place on a chromosome forever. McClintock saw genes jumping from one place to another. She called them transposons.

The mechanism of transposon control in corn is a bit
complicated. The C gene codes for pigment, but can be
disrupted by the Ds transposon. (top). If Ds never moves
out, then the kernel will be white in this example. If the Ds
gene never moves in, the kernel will be completely purple.
If it jumps out and in or in and out, then you get spots. The
bottom image shows that the early the change, the larger the
spot, because more daughter cells will have the functional
or dysfunctional gene.
But this jumping is not haphazard. It was under the control of another gene. When one gene (Ds) was activated to jump by another gene (Ac), its new position disrupted a third gene’s (C) sequence (Ds = disrupter, Ac = activator, and C = color).

When Ds was located inside C, no color was produced, but when it was not, the daughter cells could produce color. A kernel has many cells that divide and divide, so some progeny could switch back and forth and produce cells on the hull that may or may not be able to produce the color protein (see picture). If the move to disrupt C occurred early, more daughters would be produced and more of the surface would lack color. If it was late, the spot would be smaller (see bottom image to left).

This idea of jumping genes was revolutionary …. and not well accepted at first. Even though Barbara’s science was impeccable, others just weren’t as good at spying the small changes in the chromosome. It took a while for the laboratory techniques to catch up to Barb’s eyes – then they gave her the Nobel Prize.

From our new knowledge of transposons have come many discoveries – some not so savory. Some infectious agents, both bacterial and eukaryotic, use jumping genes to escape our immune system. Neisseria gonorrhea was one of the first shown to do this. Our immune system, given time, will find bacteria that have taken up residence inside us; in gonorrhea's case, through sexual transmission.

N. gonorrhea has found that if it can change its costume, our immune system must start over looking for it. The proteins it has on its surface are what our immune cells recognize, we call them antigens. Gonorrhea organisms can go through antigen variation; they have many surface antigen genes, and can switch them out if they are detected.

Variable surface glycoproteins are like selecting for antibiotic resistant
bacteria. One organism may switch its VSG for antigenic variation,
just like one bacterium might pick up a resistance gene.
When the immune system finds and mounts a response to the
organisms with the “blue” VSG, they are killed, but now the “green”
VSG organisms can proliferate. This is like when the antibiotics kill
off the susceptible bacteria, the resistant ones (green) then
have more room and food to overgrow.
They do this by moving different surface antigen genes in and out of an expression site. Only the surface antigen gene in the expression site is transcribed and translated to protein, but they can jump in and jump out when needed. Antigenic variation also occurs with Borrelia burgdorferi, the causative agent of Lyme disease, the Plasmodium falciparum of malaria, and Pneymocystis jirovecii, a eukaryote that causes the pneumonia most AIDS patients contract.

In the case of Pneumocystis, a 2009 study showed that there are over 73 major surface glycoprotein (MSG) genes that can be switched in and out. They differ by an average of 19%, so the protein sequence of each is markedly different. Even though we don’t know the function of the MSG, it would appear that it is designed to increase the variation of the organism, probably to avoid an immune response.

Still have that warm and fuzzy feeling about Indian corn as a representative of Thanksgiving?

Next week, we start to look at the last of the four biomolecules - lipids. Can you believe some people can't carry any fat on their body, no matter how much they eat?

It just so happens that Barbara McClintock and her corn made up a portion of a recent exhibition at the Grolier Club in NYC, entitled, "Extraordinary Women of Science and Medicine: Four Centuries of Achievement." The exhibit included one of Barbara's ears of corn and some of her breeding materials. The catalogue is available from Oak Knoll Books. Thanks to Karen Reeds, independent curator and museum consultant for the heads up.

Pohl ME, Piperno DR, Pope KO, Jones JG. (2007). Microfossil evidence for pre-Columbian maize dispersals in the neotropics from San Andres, Tabasco, Mexico. Proc Natl Acad Sci U S A. , 104 (16), 6870-6875 DOI: 10.1073/pnas.0701425104

Keely SP, & Stringer JR (2009). Complexity of the MSG gene family of Pneumocystis carinii. BMC genomics, 10 PMID: 19664205

For more information or classroom activities, see:

History of maize –

Transposons –

Antigenic variation -

Wednesday, November 18, 2015

Give Thanks For The Cranberry

Biology concepts – epigynous berries, seed dispersion, scarification, drupe, endocarp

Ocean Spray alone sells 86.4 million cans of jellied cranberry
sauce each year. No matter which sauce you prefer, I bet it
has a lot of added sugar. Cranberries alone are tart enough
to shrink your head.
Cranberry sauce is a Thanksgiving staple, but it’s a lot like fruitcake at Christmas – you either love it or hate it. Let me give you some reasons to love it.

Cranberry (Vaccinium macrocarpon) is one of very few commercially grown fruits native to North America. The vine needs cool temperatures and acidic, sandy soil conditions, so New England, Southern Canada and the Pacific Northwest are prime growing locations. Similar latitudes in Europe also support growth of cranberries (Vaccinium oxycoccus) in their bogs. We have previously talked about bogs where the acid conditions preserve human remains and produce bog mummies.

But there is an exception in the Southern Hemisphere – Chile in South America. In the northern part of Southern Chile, volcanic ash soils mimic the sandy soils of peat bogs, both in consistency and acidity. Runoff from the Andes Mountains allows for water, and the temperatures are similar to those in Washington and Oregon - perfect for cranberry growing.

The Ocean Spray Company harvests berries in North America in autumn, but it needs berries in the summer too. In January of 2013, Ocean Spray bought the cranberry processing interests in Chile. The harvesting period in Chile is March to May, just in time to supplement Ocean Spray’s dwindling supplies.

Cranberries are tart compared to other fruits; they have five times as much acid as their close cousins, the blueberries. Why? It may be the acidic soils they grow in. In terms of evolution, growing in peat bogs was a good choice. Not many things can grow in a bog, so competition is low. Competition for what is the question – there is very little nitrogen in the soil of a bog, and the water is acidic too.

Plants need fresh water and nitrogen to survive, so the cranberry evolved better nitrogen tapping mechanisms, as well as leaves and stems that can retain their fresh water very well. Not many other organisms have adapted to these conditions, but the cranberry thrives, transferring the acids to its leaves, stems and fruits.

This is the bog copper butterfly (Lycaena epixanthe) that
lives its entire life on a cranberry vine. It not only survives
the acidic condition of the plant – it eats it up. It lays its eggs
on the under side of the leaf, and the pupa and the larva can
survive a flood that covers the plant for months.

This acidity is also a help when it comes to pests. Several acidic compounds have been isolated from V. macrocarpon that stop insects from eating the leaves and stems. I’m guessing insects don’t like Sour Patch Kids. The exception is the butterfly Lycaena epixanthe; it spends its entire life feeding on the cranberry plant.

The second reason for the high acid content of the cranberry is that it doesn’t need to be sweet. The blueberry is much sweeter, but it  has to be. Blueberry bushes spread their seeds by having birds, rodents, or humans eat them one place and excrete them in their feces somewhere else; sweetness promotes consumption.

Seed dispersal is the most basic reason for any plant producing a fruit. If a seed falls directly beneath the parent plant, no one wins. Both patent and child will require the same nutrients, and they will end up competing for everything. Things would also get very crowded.

Several mechanisms of seed dispersal have evolved. Wind is a popular way to disperse seeds. You’ve seen those helicopter seeds from Maple trees – they catch the air and twirl down vertically, but also move horizontally. Sycamore trees have tufts on their seeds to catch the wind as well.

Fruiting is also a way to disperse seeds. Animals need carbohydrates, and fruits are an important source for many animals. When they eat the fruit, they also eat the seeds. Later on, the animal grabs a copy of Sports Illustrated, locks the door, and deposit the seeds somewhere else.

These are some of the types of fruits. The peach is a drupe. It
has an edible mesocarp. The coconut is also a drupe, but its
mesocarp is more fibrous (flake coconut). The tomato is a true
berry. It’s pericarp and locules or all edible. The raspberry is an
aggregate fruit, many ovules and mesocarps held together. The
raspberry is also a drupe, which you know when you get those
seeds stuck in your teeth. Each little fruit is a druplet.
In fact, some seeds must pass through the digestive tract of an animal in order to germinate. Some seeds, like those of drupes (drupa = overripe olive), have a hard endocarp (seed coat), derived from the ovary wall. In fact, that’s what makes a drupe a drupe. Fruits like peaches, almonds, coconuts, olives, are considered drupes and each little part of a blackberry or raspberry is a druplet.

The germinating embryonic plant isn’t strong enough to break through the drupe endocarp on its own. Something must be done to weaken the endocarp. The weakening (scarification) may come from scratching the surface, freeze/thaw, fire (for the Ponderosa Pine), or perhaps from the digestive enzymes of an animal. Many berries, like blackberries, currants, and raspberries require digestive scarification in order to germinate. But the cranberry isn’t one of these berries.

Why don’t cranberries need to be eaten for seed dispersal? Because they float! When the bog (or similar sandy wetland) floods, the berries are carried away from the parent plant, away to some far off place that may or may not be suitable for cranberry vine growth. That’s the problem with floating; you gotta go with the flow.

Cranberries float because they have air pockets trapped within them. Floating fruit isn’t that exceptional, apples float too. It’s a good thing; think how may lives this has saved during bobbing for apples season!

On top we see the coconut – it’s a drupe with a tough exocarp.
You can see the germinating plant coming through one of the
eyes. Seed dispersal for the coconut is shown on top right. We
don’t know where palms come from originally, because they
could spread around the world in just one generation. The
cranberry also floats, because of the air pockets shown on the
bottom right. The frog is just a bonus – cute, huh?

Given their bouyancy, it amazes me that it wasn’t until the 1960’s that someone thought of flooding the bogs in order to harvest the cranberries. They have machines that shake the vines and release the ripe berries.

Cranberry plants grow very low to the ground, they have long runners (rhizomes), that can extend six or more feet from the parent vines, and these can sink roots to become new plants. Because of their short stature, it only takes about 18 inches of water to flood a cranberry bog for the wet harvest. So those commercials with the two goobers standing waist high in water in their waders are a bit of a stretch.

The cranberry was probably at the first Thanksgiving; they are hearty and ready to be harvested just about the time we are sitting down to our turkey and stuffing.  But, the pilgrims misled us – the cranberry isn’t a real berry! And don’t say it was because the pilgrims were from across the ocean. The cranberry is closely related to the European lingonberry, so the mistake had already been made.

The cranberry is a false berry, also called an epigynous berry (epi = in addition to, and gynous = ovary). A berry is a fleshy fruit derived from a single ovary. False berries develop from an inferior ovule and contain tissues from parts of the flower other than the ovary, while true berries develop from superior ovary tissue only (see picture). Other examples of epigynous berry-producing plants are bananas, coffee and cucumbers.

Here is one difference between real and false berries. All true
berries are hypogynous, where the ovary (in red) is above
where the petals and pistil come out. False berries have an
inferior ovary. Another difference is that the true berry is
made from only the ovary, while the false berry incorporates
other parts of the flower. Below on the left is the red currant,
and on the right is the cranberry. As a berry, the currant is true
and the cranberry is false. But really, can you tell the difference?
The V. macrocarpon false berry fruit is indispensible as a Thanksgiving sauce, but medicine has found other uses for cranberry compounds. In the first 10 months of 2013 alone there were 86 papers published on the merits of cranberry compounds.

Most people who know about medicinal cranberries have had a urinary tract infection (UTI). For a hundred years or so, old wives (and young wives) have espoused the virtues of cranberry juice in preventing or treating UTIs.

Recent years have seen many studies try to validate the home remedy. As for if cranberries work, there is evidence on both sides. Hundreds of published reports say it’s the best thing since sliced bread, and hundreds say it doesn’t do a darn thing. Such is science – and that’s a good thing. Argue away so we know we get it right in the end.

One 2013 study found that sweetened dried cranberries added to the diet made a real difference in women who were susceptible to UTIs. Half the women in the study didn’t have even one UTI while on the study, and they all had reduced numbers of incidents.

As for why caranberries may work, scientists first thought it was the acid that killed the UTI-causing bacteria. Then it was believed that cranberry compounds prevented the attachment of the bacteria to the wall of the urogenitial epithelium via the bacterial fimbriae (appendages for attachment). This may actually be true, but other actions are also possible.

Another 2013 study showed that for the UTI causative agent Proteus mirabilis, eating powdered cranberry was very effective for preventing UTI. In this experiment, the researchers found that the organisms did not swim well or swarm when exposed to cranberry compounds. In fact, the gene that expresses proteins for their flagella (for motility) were inhibited by cranberry powder.

In addition, their urease virulence factor was also suppressed. A virulence factor is any molecule that helps an infectious organism to colonize and/or obtain nutrition from a host, or helps it to evade or suppress the host immune system.

This is a dividing bacterium showing the fimbriae that help it
attach to surfaces. You can see the difference between these
and the flagella that help in the motility of the organism. It
may be that cranberry compounds mess with both to
prevent UTIs.

Not to be a downer, but a different group carried out a meta-analysis (an organized compilation of many studies involving a lot of statistical math) of many cranberry/UTI studies in 2013 and determined that cranberry compounds have no effect on the prevention or treatment of UTIs. So, all that talk about just how cranberry molecules suppress UTIs (fimbriae, acid, down regulation of host molecules) can be ignored if you don't believe they work.

The news is better on other fronts. In obese men, cranberry juice was able to inhibit the stiffening of blood vessels, an important factor in development of cardiovascular disease (CVD). The effect was greatest in men with metabolic syndrome – a combination of high blood pressure, blood glucose, and cholesterol, as well as obesity.

A second study confirmed this by showing that 1 cup of cranberry juice each day reduces blood glucose levels and CVD risk in men with type II diabetes. And this is just the beginning; 2013 studies also show how cranberry compounds may help you age well – this makes sense, some vines have been producing cranberries since before the American Civil War. Other studies show that cranberry is a potent anti-viral agent as well as preventing bacterial UTIs. Respect the berry – uh, false berry!

Next week, let’s talk about another symbol of Thanksgiving, the indian corn that you think is just decorative is actually a fascinating story of discovery.

Burleigh AE, Benck SM, McAchran SE, Reed JD, Krueger CG, & Hopkins WJ (2013). Consumption of sweetened, dried cranberries may reduce urinary tract infection incidence in susceptible women -- a modified observational study. Nutrition journal, 12 (1) PMID: 24139545

McCall J, Hidalgo G, Asadishad B, & Tufenkji N (2013). Cranberry impairs selected behaviors essential for virulence in Proteus mirabilis HI4320. Canadian journal of microbiology, 59 (6), 430-6 PMID: 23750959

Lorenzo AJ, & Braga LH (2013). Use of cranberry products does not appear to be associated with a significant reduction in incidence of recurrent urinary tract infections. Evidence-based medicine, 18 (5), 181-2 PMID: 23416416

Ruel G, Lapointe A, Pomerleau S, Couture P, Lemieux S, Lamarche B, & Couillard C (2013). Evidence that cranberry juice may improve augmentation index in overweight men. Nutrition research (New York, N.Y.), 33 (1), 41-9 PMID: 23351409

Shidfar F, Heydari I, Hajimiresmaiel SJ, Hosseini S, Shidfar S, & Amiri F (2012). The effects of cranberry juice on serum glucose, apoB, apoA-I, Lp(a), and Paraoxonase-1 activity in type 2 diabetic male patients. Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences, 17 (4), 355-60 PMID: 23267397

For more information or classroom activities, see:

Seed dispersal mechanisms –

Scarification –

Different types of fruits –

Fimbriae and flagellae –

Wednesday, November 11, 2015

Fish Guts and Cancer – Giant Bacteria, part 2

The gut of a fish is a strange place to go looking for bacteria. It’s an even stranger place to find the second largest bacterium on Earth.

Epulopiscium fishelsoni (E. fishelsoni) hangs out in the intestinal tract of the brown surgeonfish, commonly called the lavender tang. While it seems logical that E. fishelsoni would be named for the site where it was found – inside a fish – it was actually named for its discoverer, Lev Fishelson of Tel Aviv University.  

Epulopiscium fishelsoni is shown in the left image. The white line is approximately 100 µm. On the right is the Lavender Tang.  E. fishelsoni lives in this fish’s gut, and only in this fish’s gut.

Before T. namibiensis (last week’s post) was discovered, E. fishelsoni was the biggest kid on the block, having been first seen in 1985. It can be seen with the naked eye, reaching a maximum length of 0.7 mm, but it also has large size variations. In fact, this is one of the keys to its success.

E. fishelsoni’s changing size is a daily routine. In the early morning, E. fishelsoni is only about 10 µm long, only 2-5 times bigger than typical bacteria. As the surgeonfish starts to feed, more food is available to the bacteria in its gut. With this signal, E. fishelsoni starts to grow. By late afternoon into evening, the maximum size has been reached and they can be seen with the unaided eye (if you happened to be in the fish’s gut to see it – I wouldn’t recommend it as a holiday destination).

However, after the night passes, you would find just the small cells again in the morning. You would also see that the number of bacteria has increased.  The large cells have divided into daughter cells, splitting their cellular contents between their two or three new partners. Then, as a new day passes and food becomes available in the gut, these cells grow large and divide overnight. 

Could you imagine having your baby grow 75x bigger in one day?
Think of it this way: you bring home your 22-inch long newborn baby in the morning and place it in its crib.  That night, you find that you have a baby that is 140 ft. tall. You start to build the world’s largest crib, but by morning, the giant is gone and you find two 22-inch babies in the crib. It would continue like this everyday. Parenting is difficult.

E. fishelsoni’s shape is also different than that of T. namibiensis. E. fishelsoni is shaped like a long grain of rice, as opposed to the spherical T. namibinesis. This can help meet diffusion needs (see this post), since the distance to travel is much shorter for molecules brought in on its long sides. The elongated shape is enough to make the new daughter cells viable. But as the cells grow during the day, merely being longer than they are wide isn’t enough to overcome diffusion rate, mixing rate, and traffic time limits. E. fishelsoni must know another trick in order to survive at is maximum size.

In the majority of molecular interactions, it is a cellular protein that partners with a molecule that has diffused into the cell. What might E. fishelsoni do to increase the chance that an enzyme will find its substrate (the molecule an enzyme acts on and changes in some way) quickly?

Remember in the “It’s all in the Numbers” post, we saw that one way to reduce traffic time was to increase the number of one or the other interacting molecule. It is impossible for the bacterium to raise the concentration of nutrients, but it can raise the number of proteins made by the bacterium.

The central dogma of molecular
We need a bit of background to help explain E. fishelsoni’s trick to producing more copies of its proteins. There is a central dogma (core belief) to cell molecular biology: DNA goes to RNA goes to protein. This means that DNA is transcribed to a message (mRNA), which is then translated into a protein. However, if you want to make more protein, you can’t just transcribe more RNA from the DNA in the cell. This process is highly regulated and can only be manipulated to a certain degree. The other problem with this solution is that the proteins would be produced near the site of the DNA, so these extra proteins would have to travel a long distance to mix through the entire cell – this wouldn’t solve the mixing time (diffusion) problem.

What if the cell made more copies of its DNA and spread them out through the cell? Then the cell could produce much more RNA and hence much more protein. Having the DNA spread throughout the entire bacterium would solve the mixing time problem.

Fold number of chromosomes is a cell’s ploidy. 
N= haploid number of chromosomes, N in humans = 23, 
but we are diploid, so the total number of 
chromosomes is 2 x 23 = 46.
How would a bacterium make more copies of its entire DNA (its genome)? Isn’t the number of copies of DNA determined and unchangeable? In general, bacteria are haploid, meaning that they have one copy of each (usually just one) chromosome. Human cells (except for sex cells) are diploid, meaning they have two copies of each chromosome (one from Ma and one from Pa). Some plants exhibit triploidy, especially the seedless varieties of fruit, like bananas and watermelons. Finally, while polyploid cells (poly = many and ploid = fold) can occur naturally in lower animals and some plants, in humans it is often associated with cancer cells. The more copies of the genome there are in a cancer cell, the worse the prognosis (predictable outcome) for the patient.

E. fishelsoni has found a way to make being polyploid work for it. The early morning version of the bacterium (the small cell) is haploid, but as the cell volume increases hour by hour, the amount of bacterial DNA also increases through the circadian cycle (the daily sequence of physiological events).

Green color in inset shows the huge amount of DNA dispersed throughout  
E. fishelsoni. Courtesy of: Ward, R.J., Clements, K.D., Choat, J,.H. 
and Angert, E.R..  2009.  Cytology of terminally differentiated  
Epulopiscium mother cells.  DNA and Cell Biology 28:  57-64.
By evening, the mega-E. fishelsoni has 85,000 copies of its genome! Scientists don’t have a -ploidy name for a number that big; just plain polyploid. This is a huge amount of DNA for a prokaryotic cell, and is 25% more DNA than contained in a human cell.  The new DNA copies are spread throughout the cytoplasm to provide thousands of local protein factories. Wherever there is a diffused nutrient, the proper protein it needs to interact with won’t be too far away. Therefore, E. fishelsoni can disregard the usual size limitations placed on it by diffusion.

This bacterium still has much to teach us; for instance, I wondered about all that extra DNA. If there are 85,000 copies in the parent cell, but the two or three daughters that result from it are haploid (1 copy/daughter cell), what happened to the other 84,997 or 84,998 copies of the genome? I asked Dr. Fishelson about this, and he said, “there are several questions concerning this enigmatic bacterium, one of which is what you are asking about - what is the fate of the ‘surplus DNA’ as the daughter cells are produced?” If we figure out how E. fishelsoni gets rid of its extra DNA, we could take advantage of the process. Wouldn’t it be something if we learned how to beat cancer by studying a bacterium in the gut of a fish?

Bresler V, Montgomery WL, Fishelson L, Pollak PE. (1998). Gigantism in a bacterium, Epulopiscium fishelsoni, correlates with complex patterns in arrangement, quantity, and segregation of DNA J Bacteriol., 180 (21), 5061-5611 : 9791108

  For more information and activities on ploidy, central dogma, see below:

Ploidy –

Central dogma –