The Nature of Science

Showing posts with label evolution. Show all posts

As A Bird - It's No Turkey

Mr. Carlson and Herb Tarlek had to deal with the

aftermath of bombing Cincinnati with live turkeys.

The line about turkeys being able to fly is one of the

most famous in TV history. But he should have at least

questioned whether they could fly, there are more than

50 species of flightless bird alive as we speak.

In a famous 1978 episode of the TV sitcom, WKRP In Cincinnati, station manager Arthur Carlson releases turkeys from a helicopter to a waiting crowd below as part of a holiday publicity stunt. The birds crashed to the ground (off camera), as intrepid reporter Less Nessman described the carnage. You can find the entire episode here; it’s as funny now as it ever was.

This comedy had a 1940’s parallel in real life, when the town of Yellville, Arkansas dropped Thanksgiving turkeys off the courthouse roof for several years in succession, and then from low flying planes. They didn’t seem to have any qualms about the flight problems of the domesticated turkey.

In contrast, the North and South American wild turkeys would have survived the stunts. In the genus Meleagris, there are several species of wild turkey, and they can and do fly short distances. In fact, they spend their nights perched in the low branches of trees from Maine to Peru.

The Aztecs introduced the Spanish to Southern Mexican turkeys (Meleagris gallopavo gallopavo), who took them back to Europe in the 1520’s. The Spanish trade capital at the time was Turkey, and from there turkeys spread all across the continent by the 1550’s. Therefore, the English called them turkeys, because they thought the birds originated in Turkey.

The Meleagris g. gallopavabirds brought back to Europe were domesticated and became the eating turkeys of today. They were bred for large breast muscles, and being raised in domestication caused them to lose much of their flying musculature; the domesticated turkey is flightless and mimics a bowling ball when released from a helicopter.

Here’s proof for you city folks that turkeys can fly.

Their perch is bird-like, drawing up one leg. This might

be to conserve heat, or to change their outline and

make them look like a plant in order to avoid predation.

Truly, that is one hypothesis… I mean it….really I do.

In animals, only birds have a vertical extension (keel) on their breastbone to allow for attachment of the large breast muscles required for flight. Birds are also the only animals to have fused collarbones, called a furcula. This bone attaches to the muscles important in the down stroke of wings, and also helps to pump air into the lungs - we know this structure as the wishbone. The furcula is more massive in the middle, and can flex and act like a spring during flight.

We use the furcula as a sign of good luck, but for domesticated turkeys it is just an unfortunate reminder that they used to have a fighting chance at avoiding a gravy bath. It's ironic that breeding to increase the size of their flight muscles is exactly why the domesticated turkey can’t fly.

Over many generations, the domesticated turkey’s muscles have become too big to allow it to fly and its legs have becomes shorter, so it has a hard time running. In fact, they are so large and cumbersome that they can’t even mate; they are inseminated artificially in order to breed them further. Many have been bred for white plumage, so that the small pin feathers left after plucking are harder to see.

But the noble turkey (Benjamin Franklin suggested the turkey as our national bird) can trace its line back to about 1100 CE, with the Spanish entering the picture about 400 years later. But new evidence suggests turkeys were raised in captivity much earlier than either of these estimates.

A recent study based on excavations of Mayan ruins shows that as early as 300 BCE there were male, female, and juvenile M. gallopava within the settlements, and some reduced flight morphology suggests that they had begun to be domesticated by that time. What is more, the native turkeys in southern Mexico were M. ocellata, not M. gallopava (from northern Mexico and America), suggesting that trade in the animals with the north had already commenced by this time period.

All this traveling suggests that by the time the pilgrims landed in Massachusetts they were already familiar with the turkey, and its inclusion in the first Thanksgiving feast was probably not a surprise to them. There is no evidence that turkey was the served at the first Thanksgiving, but it makes sense; both cultures were familiar with the bird. American Indians even had tribes named for turkeys and believed that their feathers had mystical powers; Central American Indians had turkey gods.

I find it a little odd that the turkey was revered as a god, considering its looks – that is truly a face only a mother could love. It has appendages and little growths everywhere. If a turkey spins its head around when startled, it could slap itself silly! But as nature proves again and again, everything has a purpose – or did.

You can see the differences between wild turkeys and those bred

for lots of meat. True, the domesticated version is puffed up in

a display, but he is much bigger weighing twice as much as

the wild version on average (16-50 lb.s/7.25-22.5 kg for domestic).

The fleshy appendage around the head a throat of many bird species is called the wattle. In turkeys, the wattle hangs from under the beak and down the throat, but in pheasants it is located around the eye and cheek. Another name for this structure is the dewlap, and many animals have these. Even your grandmother might have a dewlap under her chin or upper arms!

The wattle is a mark of sexual dimorphism in many birds (di = two, and morph = shape). The males and females look different in species that are sexually dimorphic. It is hypothesized that birds’ wattles are a form of ornament for mate selection. A male with a larger wattle may be seen as more fit and a may have more reproductive success. The hypothesis states that a large ornament is energetically costly, so only the strongest, most disease resistant males will be able to survive the cost of a large ornament and still live to reproduce.

In terms of the female turkey, picking a male with a bigger wattle would be the same as picking a male with stronger genes. Indeed, a 2010 study in pheasants showed that there were different immune genotypes (MHC, major histocompatibility complex) associated with wattle size. The functional difference between the different MHC genotypes is not known, but they did show a significant difference in the genotypes of males with larger wattles, and those are the more highly preferred mates, so it may also represent stronger MHC types.

But domesticated turkeys don’t worry about selecting mates or appearing healthy, all decisions are made by the breeder, so why do they still have wattles? It may be because their breeding is anything but true natural selection, but it may also be that the wattle has another function. Being highly vascularized (having many blood vessels), the wattle can release body heat by placing a large amount of blood close to the surface, thereby acting as a physiologic control.

Use this picture to memorize the parts of the turkey’s

head. Cousin Eddie asked Clark to save him the neck

in National Lampoon’s Christmas Vacation, but I doubt

that anyone ever specifically for the snood! There are

no snood recipes - believe me, I looked.

On top of a turkey’s head and down its wattle are smooth surfaced growths called caruncles. At the base of the wattle are larger growths called the major caruncles (not very imaginative). The exact function of the caruncles is not known, but they are significantly larger on males than on females, so sexual ornamentation might be one of their functions. Together, the wattle and caruncles are also a mood detector. When threatened or ready to mate, the wattle on a tom turkey will turn bright red.

Thestrangest part of a turkey’s head is the snood. The English word “snood” was around long before the English were aware of turkeys. It referred to a decorative hair net or bag worn by women on the back of the head to confine their hair. The resulting mass of hair does look something like the snood that hangs over a turkey’s beak, and this might be where the name came from (see below).

While many animals have wattles, and several different kinds of fowl have caruncles, the turkey is the exception in that it is the only animal with a snood. Its functions may be similar to those of the wattle and caruncles, as they are much larger in males than in females. The snood length in males is linked to testosterone levels, and males are more likely to dominate or steal food from shorter snooded (just made up that word) males than long snooded (there it is again) ones.

I haven’t found any documentation that the turkey

snood is named after the hair snood, but it makes sense.

The snood as a garment makes a comeback every 100

years or so, now they are all the rage in McDonalds and

abattoirs (slaughterhouse) –turkeys with snoods are

processed by workers wearing snoods!

But turkeys are rarely served with the head intact, and eating them is what we are most interested in at Thanksgiving. Like chickens, turkeys have both dark and white meat. The difference in color is due to the makeup of the muscles and how they store and use energy.

The red meat of mammals and the dark meat of birds are similar in that they contain high amounts of myoglobin. The muscles that have myoglobin are for prolonged use; muscles used most of the time require lots of oxygen to make lots of ATP. Myoglobin is to muscles cells what hemoglobin is to red blood cells; it is a molecule that binds and holds oxygen. In the muscle cell, the myoglobin will release the oxygen as needed to allow the muscle to make more ATP and then use that ATP for contraction.

Myoglobinis highly pigmented, so the muscles look darker (redder). When denatured by temperature, the myoglobin turns a tan to dark brown color, giving the cooked meat its look.

Myoglobin is structurally similar to hemoglobin, in that it

looks like one of hemoglobin’s subunits. Each subunit in

hemoglobin can carry one oxygen molecule, but act in

cooperative behavior; the first one is hard to bind, the

second is easier and so on. Myoglobin stores oxygen within

the muscle cell. The more you exercise that muscle, the

more myoglobin it will produce.

White meat, on the other hand, has much less myoglobin. Why? The muscles with white meat (like flight muscles) need energy in short bursts, perhaps to evade predation. To do this, they need less oxygen most of the time, but need lots of glucose some of the time. Therefore, they have less myoglobin but more glycogen (a storage form of glucose) so they can react quickly, rather than waiting for the blood to bring more glucose. The glycogen makes the cooked meat look white and glossy.

So, we have a big bird (did you know that Big Bird’s costume is made of turkey feathers painted yellow?) providing us with a big meal on a big holiday. Next week, we look at a final implication of immune responses and when infections might be helpful - sick bacteria are good for us.

Baratti, M., Ammannati, M., Magnelli, C., Massolo, A., & Dessì-Fulgheri, F. (2010). Are large wattles related to particular MHC genotypes in the male pheasant? Genetica, 138 (6), 657-665 DOI: 10.1007/s10709-010-9440-5

Thornton, E., Emery, K., Steadman, D., Speller, C., Matheny, R., & Yang, D. (2012). Earliest Mexican Turkeys (Meleagris gallopavo) in the Maya Region: Implications for Pre-Hispanic Animal Trade and the Timing of Turkey Domestication PLoS ONE, 7 (8) DOI: 10.1371/journal.pone.0042630

For more information or classroom activities, see:

Sexual dimorphism –

www.bio.indiana.edu/community/faculty/ICE.../Selection-All.pdf

http://www.enotes.com/sexual-dimorphism-reference/sexual-dimorphism

http://www2.nau.edu/~bio372-c/class/behavior/lesson1-1-1.htm

http://scienceblogs.com/tetrapodzoology/2008/07/17/bird-bills-sexual-dimorphism/

http://www.bbc.co.uk/nature/adaptations/Sexual_dimorphism

http://animals.about.com/od/zoology12/f/sexualdimorphis.htm

http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=8&ved=0CEwQFjAH&url=http%3A%2F%2Ffall2009bsc307.wikispaces.com%2Ffile%2Fview%2F11th%2BGrade%2BLesson%2BPlan-Martinelli.doc&ei=mfqXUMi2Bc-30AHR24GoCA&usg=AFQjCNE0O1piSijdgE-k9_YJaQR7_SzFTg

http://www.ck12.org/book/Biology-I---Honors-%2528CA-DTI3%2529/r2/section/25.1/Reproductive-System-and-Human-Development-%253A%253Arev%253A%253A-1-%253A%253Aof%253A%253A-Biology-I---Honors-%2528CA-DTI3%2529/

http://www.bioedonline.org/slides/slide01.cfm?tk=60&dpg=5

http://www.agfc.com/education/justForEducators/Pages/lessonPlanDetails.aspx?show=114

Myoglobin –

http://www.personal.kent.edu/~cearley/PChem/jmol/heme/myoglobin.htm

http://www.exploratorium.edu/cooking/meat/INT-what-meat-color.html

http://meat.tamu.edu/color.html

http://www.loc.gov/rr/scitech/mysteries/turkeymeat.html

http://higheredbcs.wiley.com/legacy/college/boyer/0471661791/structure/HbMb/hbmb.htm

http://bittelmethis.com/bittel-me-this-whats-the-difference-between-red-meat-white-meat-dark-meat/

http://www.getbodysmart.com/ap/respiratorysystem/physiology/gases/myoglobin/animation.html

Tricky Little Buggers

Biology concepts – immune defense, antibiotic resistance

Naim Süleymanoğlu is better known as Pocket

Hercules (4' 10"). He was born in Bulgaria, but is

of Turkish descent. He competed and retired

several times, and won gold medals from 1983

to 1998. He is one of the first competitors to

lift more than 2.5x his own body weight.

Therewas a small Turkish weightlifter a few years back whose nickname was “Pocket Hercules.” He won gold medals in three separate Olympics and was the one the best examples of big things in little packages. Last week we talked about the immune systems of vertebrates, invertebrates and plants, now let’s talk about the defenses of the smallest organisms – bacteria are the Pocket Hercules of biology.

Do bacteria have defense mechanisms? You bet – they get attacked all the time. For bacteria that stray into or purposefully target animal or plant hosts, the perils are many and varied. Antimicrobial peptides try to burst them, antibodies try to bind them up and point them out to killer cells. Macrophages and other phagocytic cells try to eat them or wall them off from the other host cells. Organisms will even sacrifice their own cells just to make sure they kill the bacteria. It’s a jungle out there.

We don’t have the time nor the room to go into the thousands of ways that bacteria protect themselves from plant, invertebrate, and vertebrate immune attack, but we can give a few examples, like deception. Mimicry is when a bacterial antigen looks much like one of our molecules, so that the body is either fooled into not attacking, or tempers its attack.

Other bacteria change their clothes to remain hidden. Just when an immune system sees it and starts the attack, Neisseria gonorrhoeae changes its surface molecules and becomes invisible again. On the other hand, Yersinia pestis remains invisible by living inside macrophages.

Some bacteria stunt our antibody response. The best way to keep from being attacked is to not allow the host to recognize and identify you. The bacteria that cause TB inhibit our immune system from producing specific antibodies.

Some bacteria vary the antigens they show on

their surface in order to evade the immune system.

In this bacterium, the dark areas are stained for

one particular surface antigen. You can see that

some of the cells have none of that protein, some

have only that surface protein, and some have

discrete areas where that protein is expressed.

The defense is a good offense, so some bacteria attack. Pseudomonas strains kill the phagocytic cells that would try to eat them by releasing chemicals called aggressins. Staphylococcus aureus just confuses the phagocytes, producing toxins that stop their movement or make them move erratically.

These are but a few of the many bacterial defenses against our immune system. But they have evolved defenses against other threats as well, like our attempts to kill them with antibiotics.

We talked earlier about multidrug efflux pumps in bacteria that pump out the antibiotics with which we try to kill them. This is related to the stories in the media about antibiotic resistance in bacterial pathogens, but classic antibiotic resistance genes are often plasmid based defenses,as we have discussed. Recently, an additional defense against antibiotics has been recognized.

It seems most bacteria produce hydrogen sulfide (H₂S, smells like rotten eggs), which was previously thought to be only a metabolic byproduct. A late 2011 studyshows that H₂S is part of an integrated defense system used by almost all bacteria. The gas works to prevent oxidative damage. This is not unheard of since a few bacteria produce nitric oxide to do the same thing, but it is being recognized now that oxidative stress induction is a big part of how many antibiotics work. When the H₂S system was turned off in several pathogens, they became much more sensitive to antibiotics. Maybe this a lesson we can exploit in the future.

In addition to our attempts to kill them, the universe itself is a tough place to survive if you are a bacterium. They may end up in bright sunlight for long periods of time, or hurtling through space on a rocket or meteor. Bacteria have ways to protect themselves here as well. Ultraviolet radiation from the sun is a mutagen (causes mutations in DNA), but it also can break down cellular molecules to release oxygen radicals, like hydrogen peroxide or superoxide.

It has been known since the 1950’s that pyruvate and catalase, as well as the newly discovered H₂S discussed above, do some work in protecting the cell against oxidative damage, but a 2009 study described a whole new mechanism. It seems that E. coli has two proteins that seek out, identify, and repair oxygen radical-mediated damage to sulphur-containing cysteine amino acids within proteins.

Cysteine is the most reactive of the 20 common amino acids, which means that it are often located in the functional site of enzymes (where the enzyme reacts with the substrate). However, this reactivity also makes cysteine vulnerable to reaction with radicals, especially oxygen radicals, after which it becomes modified and non-functional.

Disulphide bonds are formed between adjacent cysteines on the

same peptide, far apart cysteines on the same peptides,

or between cysteines on different peptides. When

you (not me) get a permanent wave for your hair, the

disulphide bonds are broken or rearranged by a reducing agent.

To prevent this radical-mediated damage, cysteines often occur in pairs, where links between the sulphurs of the two cysteines help to prevent oxidation (called disulfide bonds, they also serve to link peptides together and give proteins their proper form). A 2008 study showed that this mechanism provides unusual oxidative stability to a cysteine-containing enzyme of the bacterium, Desulfovibrio africanus.

But there are exceptions; lone cysteines do occur, and these are the cysteines most vulnerable to oxidative damage. The DsbG and DsbC proteins of E. coli patrol the cytoplasm looking for oxidized cysteines to fix.

Here is how ingenious the system is – oxidizing a cysteine may or may not unfold the protein, so DSbG is charged and can interact with the still-folded proteins to correct the cysteine problem, but DsbC is uncharged, so it works better with proteins that have been unfolded. Amazing - and bacteria developed it all on their own – well, with the help of the evolutionary pressure of things trying to kill them.

I mentioned that radiation is also a DNA mutagen. The mutagenic properties of radiation affect bacteria just like they affect us; it is just that some bacteria can protect themselves better once their DNA is damaged. Follow me closely here - by using protein repair and protection systems, bacteria like E. coli, with its DsbG and C enzymes, can keep protein functions going when other organisms would break down and die. Some of these protein functions include DNA repair after mutagenesis. So - some bacteria don’t survive radiation because they protect their DNA better, they survive because they repair the damage better.

This is an overlap of different types of images of a

radiodurans bacterium. The circles of blue green and

pink show high concentrations of manganese, while

red is iron. The manganese is clustered around the

DNA and works to repair it after radiation damage.

Other bacteria have a different mechanism to maintain protein function. According to a 2010 study, a shield of manganese metal atoms and phosphates was found in D. radiodurans. It had been long known that manganese was present in very high levels in bacteria that are most resistant to radiation, but its function was unknown.

The recent study shows that these manganese complexes work together to protect proteins from radiation damage, but not DNA. The key for this system is to keep proteins functioning, which can then repair any radiation damage to the DNA. This mechanism allows D. radiodurans to withstand prolonged radiation that is 1000x stronger than that which would kill a human.

So, bacteria have defenses against immune and environmental attacks. Does anything else attack bacteria? How about other bacteria - it’s dog eat dog out there, competition for resources is brutal. Many bacteria have poisons (bacteriocins) that inhibit or kill bacteria that are distantly related (because related types of bacteria are likely to be in the same places looking for the same food).

One type of bacteriocin are the lantibiotics. These protein toxins contain a nonstandard amino acid, called lanthionine. We mentioned above that cysteines are very reactive; lanthionine is a modified circular (polycylic) cysteine that gives the toxin its reactivity. And because it is cyclic, it is much less vulnerable to oxidative damage itself – funny how bacteria seem to cover their bases so well.

This is so cool. Bacteria that are engineered to produce

light were injected into rats. The rat in the middle was

also given a bacterium producing a bacteriocin to the

light producing bacteria. The whole rat bodies were

imaged while they were still alive to see if the bacteria

were alive and reproducing. Live animal imaging is a

great tool that is becoming more popular. Image by S.

C. Corr and P. G. Casey.

Lantibioticscome in two types, they either form pores in Gram⁺ bacterial cell walls or inhibit the cell wall formation. Because they attack only specific types of bacteria, lantibiotics are useful in cheese-making; they allow some bacteria to grow and ripen the cheese, while killing those that would cause the cheese to spoil. One type B lantibiotic just came through its phase I clinical trial in July 2012 with flying colors (phase I trials are meant only to test safety, not effectiveness).

A recent discovery illustrates just how bacteriocins are delivered to the target organism. It seems that bacteria can build a spike and a spike launching system anywhere on their cell membrane. The spike is spring loaded in a tube just 80 atoms long, and is fired at the target cell. Then the bacteriocin is released at the end of the spike to do its damage.

The release of toxin was already known, called a type IV secretion system, but the CalTech study that identified the spring-loaded spike as the delivery system is very new. Once fired, the whole system is broken down, ready to be rebuilt somewhere else in the cell. Amazing. (click for video)

Of course, for every punch there is an evolutionary counterpunch, so there are bacteriocin resistance mechanisms as well. Nisin, a bacteriocin active against strains of listeria, is approved as a food preservative. But listeria can spontaneously develop resistance to nisin. It appears that some strains change their membrane chemistry in order to render nisin ineffective. Therefore resistance could be a problem if we pursue the use of bacteriocins as antibiotics; we might end up back in the same situation that we're in now.

Regardless of this possible downside, scientists have found a way to bring bacteriocins into the battle against antibiotic resistance. An E. coli has been engineered to contain the gene for pyocin, a bacteriocin that kills strains of Pseudomonas bacteria. E.coliand Pseudomonas are not closely related, so E. coli would not naturally possess this toxin, scientists added the gene to the E. coli.

This is schematic of the engineered bacteria to kill Pseudomonas.

P. aeruginosa make chemicals when their numbers reach a

certain density. These trigger pyocin production in the E. coli,

but also triggers the production of the protein that lyses the

E. coli. When lysed, the pyocin attacks the P. aeruginosa.

When the engineered bacteria encounters Pseudomonas, it does two things; it produces the pyocin toxin to kill the target cell, and the engineered E. coli commits suicide. No release system has been engineered into the E. coli, so the only way they get the pyocin to the target is to have the E. coli produce a lysin that destroys its own cell membrane.

This suicide accomplishes two things, it releases the pyocin to kill the target, and it prevents the engineered E. coli from hanging around forever, possibly trading genes with other bacteria or causing havoc in some unforeseen way.

So it looks like bacteria have it made. They can resist immune system attacks, some can resist environmental onslaughts, they even have ways to protect themselves against competition and threats from other bacteria. No wonder they have always been the predominate life form on Earth. But bacteria do have foes of considerable power – veritable “Micro-Hercules” – we will meet them after Thanksgiving.

Let’s take a couple weeks to talk about the biology of turkeys and the so-called “tryptophan nap.”

Basler, M., Pilhofer, M., Henderson, G., Jensen, G., & Mekalanos, J. (2012). Type VI secretion requires a dynamic contractile phage tail-like structure Nature, 483 (7388), 182-186 DOI: 10.1038/nature10846

Saeidi, N., Wong, C., Lo, T., Nguyen, H., Ling, H., Leong, S., Poh, C., & Chang, M. (2011). Engineering microbes to sense and eradicate Pseudomonas aeruginosa, a human pathogen Molecular Systems Biology, 7 DOI: 10.1038/msb.2011.55

For more information or classroom activities, see:

Bacterial defenses–

http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=1&ved=0CB8QFjAA&url=http%3A%2F%2Fwww.pct.edu%2Fdegreesthatwork%2Fdocs%2Fword%2F1_2-Science_Teacher_Series-Nanotechnology.doc&ei=kOFlUKW8OcjnyAHv8ICgAg&usg=AFQjCNFIooLBtpkA1vko0-lRwai7x7v1Zw

http://www.smallerquestions.org/blog/2012/5/21/from-soil-to-human-evolution-of-bacterial-immune-evasion-mec.html

http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=3&ved=0CC4QFjAC&url=http%3A%2F%2Fwww.educationscotland.gov.uk%2FImages%2FInfectiousDiseasesandImmunityTeachersNotes_tcm4-669755.doc&ei=o99lUJN5woXLAdeYgHg&usg=AFQjCNH-uSO824WJUdpVkxUg4xhP1C_fZA

http://crohn.ie/archive/primer/imunevad.htm

http://textbookofbacteriology.net/antiphago.html

http://textbookofbacteriology.net/antiimmuno.html

http://www.sciencedaily.com/releases/2010/04/100425151159.htm

http://faculty.ccbcmd.edu/courses/bio141/lecguide/unit2/bacpath/evade.html

http://www.ncbi.nlm.nih.gov/pubmed/15231256

http://www.sciencedaily.com/releases/2011/11/111117144009.htm

http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=2&ved=0CCoQFjAB&url=http%3A%2F%2Fassets.cambridge.org%2F97805218%2F01737%2Fsample%2F9780521801737ws.pdf&ei=_N5lUPu4D8-GyQGEy4GAAQ&usg=AFQjCNEKYTv8woZ0L40EEdezU3UKyIXmCA

http://phys.org/news193846665.html

Bacteriocins –

http://www.foodsafetynews.com/2011/09/a-lantibiotic-steps-up-to-kill-harmful-bacteria/#.UGXgahhf13I

http://www.sciencedirect.com/science/article/pii/S2211546312000034

see Pubmed (http://www.ncbi.nlm.nih.gov/pubmed) for more information on these defenses.

Immune To Evolution

Biology concepts – innate immunity, adaptive immunity, defense mechanisms, endotoxin

The Jardin des Tuileries is the setting for the

final scene of “The Happening.“ Located in

Paris between the Louvre and the Palace de

la Concorde, this garden was once a royal

promenade, but became public after the

revolution. The trees that line the walk are

chestnuts. Several species of Chestnut are

pollen sterile, meaning they don’t produce

pollen and must be cross pollinated from a

species that has pollen.

M. Night Shyamalan likes to make movies that have “hide in plain sight” twists: the psychologist is a ghost (The Sixth Sense); the villagers live in modern times (The Village); the mentor is the arch-villain (Unbreakable). In his movie, “The Happening,” mankind is under attack. Something is making us commit suicide in mass numbers. What is attacking us – or might something be defending itself from humans? If it is defensive, could be considered an immune response? If yes, then can we figure it out by deciding just who has immune responses?

Immune systems of defense can be very evolved, as in humans. Ours make use of two specific circulatory systems (blood and lymph), has organs designed to aid their generation and functions (lymph nodes, thymus, bone marrow, and spleen), and has mobile cells designed only to patrol and protect. These components function in both innate and adaptive immune cascades and webs.

Other organisms’ defense systems are not so intricately developed, but still deserve respect. Arthropods (insects, crustaceans and the like) have a highly developed innate immune system, with circulating immune cells of several types.

Mollusks (clams, octopods, and the like) also have an innate immune system with a few types of circulating immune cells. However, immune responses don’t have to be only from circulating cells. Sometimes they are proteins that kill bacteria, or merely surrounding the pathogen and keep it from the host cells. Many kinds of mollusks protect themselves by encapsulating invading parasites in a solid prison of shell-like material -we call them pearls! Any mollusk with a shell can make pearls – even snails.

Conch is a species of giant snail. It produces lovely

pearls, so pearls don’t just come from oysters. Any

shelled mollusk will react to a parasite that gets

through its shell by walling it off in layers of mother

of pearl (nacre). This is the very smooth material

that covers the inside of the shell.

Everyanimal has some sort of immune response built into its physiology, but supposedly only vertebrates have an adaptive immune system. Invertebrates have the older, innate system, but not the ability to adjust their recognition and response to particular pathogens like the adaptive system can. The specific, or adaptive immune system was believed to have arisen in the first of the jawed fishes (gnathostomes; gnath = jaw, and stoma = mouth), about 410 million years ago and been handed down and modified by mammals. But there are exceptions – there are always exceptions.

The Agnathans (jawless fishes, such as lampreys and hagfish) seem to have an adaptive system all their own. It has features similar to the adaptive system of jawed vertebrates, but the way that foreign antigens are recognized is completely different. The lampreys and similar organisms use a different kind of receptor molecule on immune cells. The receptors are variable, but not in the same manner as mammalian immunoglobulins. In jawed vertebrates, the antibody genes rearrange to form the basis of both circulating and receptor immunoglobulins.

This "similar but different" adaptive system would indicate that specific immune responses have sprung up at least twice in evolutionary history. I say at least twice because it is beginning to look like insects and worms may have a sort of adaptive system as well. Earthworms will reject grafts from other earthworms, and will reject a second graft faster than the first graft. So, we see that most organisms have elaborate ways to defend themselves.

This brings us back to “The Happening,” and the attack on the humans ---– it turns out that it was the trees trying to protect themselves from being overrun by mankind! Plants have defenses? Plants can sense attack and respond? Yep.

Plants don’t have immune cells, those that move around and whose job it is to protect and attack. But they do have immune defenses against pathogens, and pretty sophisticated ones at that.

This is a cartoon which shows plant immune response. First

a pathogen tries to gain entry and the plant recognizes its

surface molecules (PTI). Some pathogens survive the response

and emit effectors (ETS, effector-triggered susceptibility). The

effectors trigger ETI which increases the response proteins.

Some pathogens may survive and too much ETI and ETS

triggers the hypersensitive response. Image: Nature

444:323-329, 2006.

PlantPTI (Pattern Triggered Immunity) is similar to our innate immune system, just without the specific immune cells. In this system, plants recognize molecules that are common to microbes (MAMPS, microbe associated molecular patterns) using pattern recognizing receptors (PRRs).

This is similar to mammalian PRR systems for PAMPs (pathogen associated molecular patterns), the toll-like receptors for example. When triggered, resistance molecules and plant hormones are released to make the plant less appealing to the pathogen, or to interrupt the infection process. There are many of these resistance mechanisms, we can talk about a couple below and more in the future.

On the other hand, plant ETI (Effector Triggered Immunity) is signaled by the effector molecules released by the microbes that manage to set up shop inside plant cells or tissue. ETI is really just an increase in the amplitude of the same response molecules seen in PTI, plus another defense mechanism, called the hypersensitive response.

Some pathogens like the hypersensitive response.

Necrotrophic (necro = death, and troph= loving) fungi,

like Botrytis cinerea, or gray mold (the spots on the

leaves), must have dead tissue. They wait until some

thing else triggers the hypersensitive response, or they

trigger it themselves, and then feed of the dead plant tissue.

When a pathogen is successful at making entry into a plant at a specific site, the plant may respond by releasing oxygen and nitrogen radical compounds (those with free electrons that will attack dang near anything). This will kill the plant cell as well as the invader (hence the name “hypersensitive”), but it reduces the probability of infection by taking out everything in the area. It is a sacrifice of host cells that the plant is willing to make.

This response is much like the apoptosis (programmed cell death) that virally-infected animal cells may initiate. It is a small loss in order to protect the whole organism. Recent evidencesuggests a central role for S-nitrothiols (nitric oxide linking cysteines) in both turning on and limiting the hypersensitive response by controlling the amount of NADPH oxidase, an enzyme that produces reactive species. We will see next week that this suicide mechanism is very old.

Reactive species for cell suicide is cute, but plant responses get even cuter. When threatened by some herbivorous insects, 2012 research shows that plants can call in mercenaries to help. Members of the cabbage family are troubled by the larvae (caterpillars) of the large cabbage butterfly (Pieris brassicae). When this butterfly lays its eggs on a black mustard plant, the plant sends out a chemical signal that attracts two species of wasps (Trichogramma brassicae and Cotesia glomerata).

When the male cabbage butterfly fertilizes the female

and she lays her eggs on a brussel sprout plant, the

chemicals from the male semen will trigger the plant to

make a pheromone that attracts the Trichogramma

brassicae wasp. It lays its eggs INSIDE the butterfly

eggs (yellow cones) and they feed off the butterfly eggs

as larvae. Up to 50 wasps can come out of one butterfly

egg. Image:Nina E. Fatouros.

These wasps are natural enemies of the white cabbage butterfly and will attack its eggs and larvae. Voila, the plant stops the white cabbage caterpillar from eating its leaves even before the attack begins. Most amazing, the chemical signal isn’t triggered by other, less ravenous pests, so it is a specific response. That smells like an adaptive immune response to me. While many animals can’t specify a distinct response to a particular foreign organism, it looks like many plants can. Once again, plants show us how advanced they are.

Even more in support of the idea that plants have a form of adaptive response is the discovery that they have an immune memory of sorts. In 2009, researchers at the U. of Chicago found that when attacked by a certain bacterium, Arabidopsis plants (of the mustard family, a very common plant in research) make a chemical at the site of attack called azelaic acid.

The scientists found that this compound can stimulate a faster and stronger immune response when and if the plant was ever attacked again. Azelaic acid acts by stimulating salicylic acid (a compound very similar to aspirin) production in the plant directly, and by stimulating a newly discovered protein called AZ11. The increased salicylic acid then stimulates the defense mechanism.

More recent work (2012) in the same field has identified five additional compounds from Arabidopsis that also prime immune defenses. These new compounds work by inactivating enzymes that break down salicylic acid; the plant is therefore always ready to initiate a defense. These natural chemicals may be important for agriculture in that crops could be sprayed with a primer and be ready for a quick and strong response if they are ever attacked.

Priming is important for plant immunity. Priming can

induce production of more response proteins that may

be stored in vacuoles until needed. Priming can also lead

to modification of DNA regulators, so that more response

proteins can be made over time.

An important factor in this strategy is that the primers do not affect plant growth or seed/fruit production. Many plant defense mechanisms come with an energy or growth cost, the hypersensitive response for example. The time and ATP that a plant spends on defending itself ends up costing it in growth and flower/seed/fruit production. This is important when we are talking about cash crops that feed the world’s people. The newly discovered priming agents can stoke up a plant’s immune response with no loss of growth or productivity. It’s a win-win situation for plants and people.

So animals and plants have independently developed immune responses, including adaptive memory and host cell death mechanisms. Or have they been independent?

The S-nitrosylation regulatory step in the production of reactive species is conserved (the same function, in this case mediated by the same amino acids in similar proteins) in animals, so we and they have developed a similar control – is it conserved from an ancient time before plants and animals diverged? Has the same system developed independently two time – unlikely, many orthologous systems exist, but nature is hit and miss, it rarely twice stumbles upon exactly the same way to do something. The adaptive systems developed by the jawed and jawless fishes may be an example of this. They do much the same things, but through different mechanisms. Perhaps plants and animals shared information at some point in time – horizontal gene transfer, like we talked about a long time ago?

Plants and insects can protect themselves and can adapt to different pathogens, so we have learned not to assume humans are so special. How about if we take another step along this line next week? Can bacteria protect themselves? Do they need to?

Fatouros, N., Lucas-Barbosa, D., Weldegergis, B., Pashalidou, F., van Loon, J., Dicke, M., Harvey, J., Gols, R., & Huigens, M. (2012). Plant Volatiles Induced by Herbivore Egg Deposition Affect Insects of Different Trophic Levels PLoS ONE, 7 (8) DOI: 10.1371/journal.pone.0043607

Yun, B., Feechan, A., Yin, M., Saidi, N., Le Bihan, T., Yu, M., Moore, J., Kang, J., Kwon, E., Spoel, S., Pallas, J., & Loake, G. (2011). S-nitrosylation of NADPH oxidase regulates cell death in plant immunity Nature, 264-268 DOI: 10.1038/nature10427

For more information or classroom activities, see:

Invertebrate immune systems –

http://pulse.pharmacy.arizona.edu/10th_grade/disease_epidemics/science/pathogen.html

http://www.sciencedaily.com/releases/2007/06/070621102626.htm

http://www.ncbi.nlm.nih.gov/pubmed/15199951

http://www.reefs.org/library/aquarium_net/0498/0498_1.html

http://www.fu.uu.se/jamfys/jamimm3.html

http://www.sciencedaily.com/releases/2012/01/120105111946.htm

http://www.uwosh.edu/today/7365/scientists-study-insect-immune-systems/

pearl formation –

www.yvel.com/Assets/PearlGuide.pdf

http://marinelife.about.com/od/invertebrates/f/How-Do-Pearls-Form.htm