As Many Exceptions As Rules: parasite

Showing posts with label parasite. Show all posts

Thursday, December 14, 2017

It’s A Plant World, We’re Just Living In It

Biology concepts – cell walls, chloroplasts, myco-heterotrophs, holoparasites,

Life on Earth is easy. It can be boiled down to three sentences. “The mitochondria and the chloroplasts are, in a fundamental sense, the most important things on Earth. Between them, they produce oxygen and arrange for its use. In effect, they run the place.” Lewis Thomas wrote this in his award winning book, The Lives Of The Cell: Notes Of A Biology Watcher, in 1975.

Nature’s carbon recycling center. The sun’s energy is used to
polymerize carbon (CO₂) into carbohydrates (CHO) and releases
oxygen (O₂). Then the mitochondria use the O₂ to break down
the CHO, resulting in chemical energy (ATP) and carbons (CO₂)
ready to be polymerized again.

He was so right - for the organisms that use them. I guess he didn't consider the exceptions. These two organelles mesh seamlessly in their functions. One produces carbohydrate and oxygen, while consuming carbon dioxide. The other consumes carbohydrate and oxygen and produces carbon dioxide. The ultimate recyclers.

If these two organelles are the most important things for life, then doesn’t that make plants the kings of life on Earth, since they have both chloroplasts and mitochondria? Makes you feel a bit more humble now about your place in world, doesn't it.

However, this brings up an essential question – and the main focus of today’s topic and exceptions. What makes a plant cell a plant cell? Green algae have chloroplasts and mitochondria, but they aren’t plants, they belong to the kingdom Protista. We have discussed the sea slug, E. chlorotica, and its ability to photosynthesize – it is certainly not a plant. So what makes a cell a plant cell?

Leaving the chloroplast out of the equation for a minute, you could argue that a plant cell is one with a cell wall and cell membrane. That surely separates them from animal cells, since animal cells only have the cell membrane. But many bacteria, archaea, fungi, and algae have cell walls. If the argument is refined to define a plant as having a certain kind of cell wall, then we must look a little closer. Many cell walls are made of sugars, but are plant cell walls unique in their constituents?

True bacteria have two large groupings, Gram+ and Gram -,

based on their cell wall structures. The gram stain sticks to

the peptidoglycan layer, so the thick layer on G+ bacteria make

them stain deeply. The lipopolysaccharide (LPS) layer of the G-

species keeps them from staining, and is highly toxic.
Endotoxin (LPS) and causes about 70% of septic shock cases.

Bacteria cell walls are made of peptioglycan (peptido = amino acid containing, and glycan = polymer of two sugars). One of the two components is always N-acetylmuramic acid, and the other is often poly-N-acetylglucosamine, but other things can be included as well. The exception is the Mycoplasma, a group of small bacteria that don’t have a cell wall at all. Since many antibiotics function by disabling the bacterial cell wall or preventing its formation, they don’t work against mycoplasma infections like M. genitalium, which a 2011 study linked to pelvic inflammatory disease in women.

Fungal cell walls are also made of a polysaccharide (poly = many, and saccharide = sugar), in a polymer called chitin. Chitin is also the rigid polymer that makes so many insects crunch when you step on them. Chitin cell walls are defining for fungi, as many cellulose containing cell wall fungi have been moved out of the kingdom of Fungi. But this still doesn’t tell us what is unique to plant cell walls.

Plant cell walls contain cellulose, and is complex. Plant cell walls can contain up to three layers, with different sugars involved, including cellulose, hemicellulose, and pectin, and lignin. Lignin is a more rigid polysaccharide that gives strength. It is what makes bark hard, protective, and water resistant.

If the hydrogens (H) bound to the #1 and #4 carbons

up on the same side, the polymer is starch. If they

are on different sides, the polymer is cellulose.

We can digest starch: we can’t digest cellulose.

Plants make both – the part we can’t digest we call

dietary fiber.

Cellulose is made of a chain of glucoses, yet we can’t digest it. The number one carbon in glucose has an –H that is sticking up or down. If the –H sticks “down”, then it is an alpha glucose. If it sticks “up”, then it is a beta-glucose. Cellulose is linked chains of beta-glucose. Starch is linked chains and branches of alpha-glucose. Just that difference in –H position determines if it is food for us or not. Herbivores have the enzymes (and bacteria) to digest cellulose, but not us.

So is it the inclusion of cellulose that makes a plant cell wall unique? Well, no. Algal cells also use cellulose in their cell walls. You might try to argue that algae are plants, since many of them also have chloroplasts and are primary producers – but you would be wrong. Algae can be unicellular (although they can also be multicellular) while plants are all multicellular. Algae don’t have specialized reproductive cells or parts like plants do; algae reproduce by spore or from broken parts of themselves. Finally, DNA analysis shows that while plants and algae are monophyletic (one ancestor), they diverged from one another long ago.

Then there is the issue that not every plant cell has a cell wall. In angiosperms (angio = chest or vessel, and sperm = seed; plants with enclosed seeds and flowers), the gamete (sex) cells of the male in the pollen and the gamete cells of the female in the ovary do not have cell walls, at least not on all sides. The ovary contains the ovules (latin for small egg), and the pollen contains the sperm cells and the tube cell, that forms the pollen tube and delivers the sperms cells to the ovules.

After the ovules are fertilized by the sperm cells of the pollen, the ovules form the seeds, and the ovary forms the fruit. From here on in, all the daughter cells will have cell walls. For fertilization, it would make sense that the involved cells would not have a cell wall that would just get in the way of love.

The Sago Palm isn’t a palm, but is one of the most

primitive plants that reproduces with seeds. It

presents a problem to pet owners because every part

is toxic to pets, but it tastes good to them. They don’t

know not to eat it; then they bleed to death.

And even weirder, not all plants use just this strategy. Cycads (like the sago palm, which isn’t really a palm at all), and gingko biloba plants have sperm cells with flagella, long projections that whip and move them along, hopefully toward an egg cell. They don’t use a tube cell or pollen tube; these plant cells without cell walls swim. Plant cells that move, now there is an exception worth noting! Some more primitive bryophyte plants (liverworts, mosses) also have motile sperm, but the cycads and gingko are the only examples of seed plants with motile cells.

So cell walls aren’t a defining characteristic of plant cells either. Maybe it is the chloroplast that defines a plant cell --- maybe not.

As you can guess, there are exceptions going both ways. There are organisms that have chloroplasts that aren’t plants, namely the algae. But a more interesting exception are many of the protozoan Euglenids. Euglena gracilis is a prototypical euglenid that can produce carbohydrate by photosynthesis. However, most euglenids can also eat things, which makes them both autotrophic and heterotrophic.

As for the other direction, there are many plants that don’t have chloroplasts. Of the roughly 350,000 different species of plants on earth, almost 3000 of them are non-photosynthetic. Therefore, the most common characteristic that people use to tell a plant from a non-plant (photosynthesis by chlorolplasts) isn’t true for almost 1% of the species on Earth. That is a pretty big exception. That would be like saying 1% of people on earth don’t have a brain! O.K., maybe that's a bad example.

Indian Pipe is Monotropa Uniflora. Monotropa means

one turn, and uniflora means one flower. The plant is

called the ghost plant – obvious, or the corpse plant –

because it turns black as it matures. This naming thing

is easy!

Indian pipe (Montropa uniflora, or ghost plant) is one such plant. Related to the blueberry of all things, the ghost plant has gone its own way and become parasitic. It garners its nutrients and energy from the tissue of another plant. The roots of the Indian pipe penetrate the rhizoids (root-like projections) of certain types of fungi and sponge off their hard work. In fact, the fungi themselves are symbiotic, having invaded the roots of certain pine tree species.

The fungus and tree live together in a mutualistic relationship, making the fungus a mycorrhizal (myco = fungus and rrhizal = root) variety. The tree supplies the fungus with carbohydrate, and fungus supplies the tree with mineral nutrients. However, Indian pipe does not respect this mutualism and is a parasite of the fungus, taking some of the carbohydrate supplied by the tree. This makes the Indian pipe a myco-heterotrophic parasite.

Other plants without chloroplasts are holoparasitic (gain nutrients only by parasitism). These would include the rafflesia species of the Indonesian rainforests. These plants are know for having the largest single flowers in the world, some the size of car tires! The plant doesn’t have a stem or root or leaf, it is a vine that grows inside another type of vine. Only when it is ready to flower does it bud out from the bark of the host. The flower takes nine moths to develop, and then smells like rotting flesh in order to attract fly pollinators.

Rafflesia is also known as the corpse flower, as opposed

to the corpse plant (Indian pipe). This is because it

smells like a corpse in order to attract the flies that

pollinate it. This young man is either holding his breath,

has no sense of smell, or is just really odd.

In addition to holoparasitic plants, plant cells without chloroplasts would include those same gamete cells we discussed above as not having cell walls. And neither to do most root cells. However, there are exceptions, like many of the orchids. The ghost orchid has photosynthetic roots, which is a good idea, since they grow directly on other plants; their roots are not buried in the dirt.

Maybe it is not a single characteristic that makes a plant cell a plant cell, or a plant a plant. Maybe it is the combination of cells with cell walls, central vacuoles and in most cases, chloroplasts that make it a plant. I guess it is like beauty; you can’t define it, but you know it when you see it.

Next week we will take another shot at finding a defining characteristic of plant cells, namely the plastid, the mother of all chloroplasts – might there be an exception?

Mizukami I, & Gall J (1966). Centriole replication. II. Sperm formation in the fern, Marsilea, and the cycad, Zamia. The Journal of cell biology, 29 (1), 97-111 PMID: 5950730

Nikolov LA, Tomlinson PB, Manickam S, Endress PK, Kramer EM, & Davis CC (2014). Holoparasitic Rafflesiaceae possess the most reduced endophytes and yet give rise to the world's largest flowers. Annals of botany, 114 (2), 233-42 PMID: 24942001

For more information and classroom activities on cell walls or parasitic plants, see:

Cell walls –

http://www.biology4kids.com/files/cell_wall.html

http://www.scienceprofonline.com/microbiology/bacterial-cell-wall-structure-gram-positive-negative.html

http://library.thinkquest.org/C004535/cell_wall.html

http://www.ccrc.uga.edu/~mao/intro/ouline.htm

http://micro.magnet.fsu.edu/cells/plants/cellwall.html

http://www.cellsalive.com/cells/cellwall.htm

http://faculty.ccbcmd.edu/courses/bio141/lecguide/unit1/prostruct/cw.html

http://employees.csbsju.edu/ssaupe/biol327/lecture/cell-wall.htm

http://www.biologie.uni-hamburg.de/b-online/e26/26.htm

http://www.answers.com/topic/how-does-a-primary-cell-wall-differ-from-a-secondary-cell-wall

www.umsl.edu/~microbes/introductiontobacteria.pdf

http://www.scienceprofonline.org/microbiology/gram-negative-bacteria-cell-wall.html

http://tami-port.suite101.com/how-do-antibiotics-work-to-kill-bacteria-a74616

Parasitic plants -

http://waynesword.palomar.edu/plnov99.htm

http://www.botany.org/parasitic_plants/Hydnora_africana.php

http://www.teachervision.fen.com/dk/science/encyclopedia/parasitic-plants.html

http://www.bbc.co.uk/learningzone/clips/parasitic-plant/12796.html

http://www.ehow.com/info_8575832_two-rain-forest-illustrate-parasitism.html

http://www.moreheadplanetarium.org/index.cfm?fuseaction=page&filename=science360_flowerpower_videouse.html&print=1

http://www.montgomeryadvertiser.com/article/20120427/LIFESTYLE/304270006/Parasitic-field-dodder-very-hard-control

http://www.parasiticplants.siu.edu/

http://parasiticplants.blogspot.com/

http://www.apsnet.org/edcenter/intropp/pathogengroups/pages/parasiticplants.aspx

http://www.forestpathology.org/mistle.html

http://www.gardenbuildingsdirect.co.uk/Article/parasitic-plants

Wednesday, May 4, 2016

Feelin' Hot Hot Hot!

Biology concepts – fever, infectious disease, sexually transmitted disease, innate immune system

Would you be willing to be a human guinea pig, to

see if one disease might stop another? The term

“human guinea pig” refers to the fact that from the 1890’s

to the 1920’s guinea pigs were a major model for medical

research. Later replaced by rats and mice that could be

bred faster, guinea pigs were used to develop the first

diphtheria antitoxins, which subsequently saved

millions of lives.

Would you be willing to let a doctor give you a disease? What if that might save you from another disease? You suppose this might be O.K., if the disease you were being given on purpose wasn’t too nasty.

What if the disease you're to be given as treatment is a form of the infection that kills a million people each year, the second most of any infection? Now you're thinking the disease you already have must be pretty horrible if this is the best idea for a cure. Let’s investigate and see if it might be worth it to save you from.... neurosyphilis.

Syphilis is a sexually transmitted disease that has distinct stages. The primary infection is marked by a lesion on those parts of your body that are most at play in the contracting of a sexually transmitted disease. It is amazing that some scientists believe that sexually transmitted diseases such as syphilis, in their primary stages, actually make sexual relations feel better. The organism (Treponema pallidum) benefits from this because the infected individuals might be more likely to have sex more often and this is an opportunity for the organism to be transmitted to additional hosts. Called “host manipulation” this is an evolutionary process that is just now gaining more attention, and will be something we will talk a lot more about in this blog in the near future.

The gumma lesions (left side) of secondary syphilis are not

meant for polite society. It's no wonder the Elizabethans

opted for the ruff collar (right side).

The second stage of syphilis is marked by lesions, called gumma, on many parts of your body. You know those huge collars that the Elizabethans wore in 1500-1600 England? (see picture) As the story goes, the collars actually came into fashion as an attempt to keep syphilitic gummas out of sight. Syphilis ran roughshod through the English royal families at the time. Whatever the royals did everyone else wanted to do, so the collars became a fashion hit.

The tertiary (3^rd) stage of syphilis is much more likely to be fatal. Appearing anywhere from 3-15 years after the primary lesion, tertiary syphilis attacks the brain, heart, liver, or bone tissues of the victim. Neurosyphilis can bring dementia, hallucinations, psychosis, as well as unsteady gait and movements (ataxia or paresis). While only a quarter of the patients reach this stage, it is a nasty way to go.

Do you agree that being purposefully infected with one disease to avoid the ravages of neurosyphilis might be worth considering? Even if the doctors were going to give you....... malaria?

This is the spirochete bacterium Treponema pallidum,

the causative organism of syphilis. Recent evidence

suggests that the bacterium is flatter and less like a

corkscrew than previously thought. They don’t look like

they have a flagella to move around, but they do. It is

located INSIDE the cell, which makes the whole cell

whip back and forth, not just the tail.

In the modern day, the treatment for syphilis is antibiotics; penicillin G can easily kill T. pallidum in the primary and secondary stages. However, antibiotics do not cross the blood brain barrier very easily (this barrier is made by very tight junctions between the cells and reduced movement of molecules through the cells, in order to protect your brain from toxins and infectious agents). Very high doses of drugs must be used to treat neurosyphilis. They may not work at all and might bring side effects.

But in the days before antibiotics, other treatments had to be sought. In the state of Indiana, USA, just as in all states and countries at the turn of the 20^th century, syphilis was rampant in mental hospitals. This was both the cause and effect for some of the incarcerations, and was a source of constant battle in the institutions.

For better or worse, these patients were a stable population for the testing of different therapies for neurosyphilis, and Walter Bruetsch at the Central State Hospital in Indiana was a leading American researcher on the use of malaria to combat neurosyphilis.

Originally developed by Professor Julius Wagner-Jauregg of Vienna, Austria, the “malaria cure” was used to originally to treat paresis (very unsteady) and general paralysis patients; he suggested that fevers were helpful in paresis and tertiary syphilis.

Wagner-Jauregg had noted as early as 1887 that in the tropics, both malaria and syphilis were common, but those with syphilis rarely progressed to the tertiary stage, with the paresis that if often brought. In 1917, he treated nine paretic patients with good results, so other institutions expanded the study of this treatment. In Indiana, several decades of work were summarized in a series of papers in the 1940’s, making Indiana the prime American spot for “malaria cure work.”

The female Anopheles mosquito can take in quite a bit

of blood in just a short time. Take too long and they

could get squished.....but take hot blood in too fast

and they roast. That drop of fluid at the end of their

abdomen evaporates and helps cool their body as they

suck up the 37˚C blood, according to a 2011 study.

So how might malaria help in the treatment of syphilis? To discuss this, we have to know a few things about malaria. It is an infectious disease caused by an apicomplexan parasite called Plasmodium falciparum, although early hypotheses implicated bad air in the disease – hence the name; mal = bad, and airia = air. This organism has a complex life cycle, part of which occurs in the gut and salivary glands of the Anopheles mosquito and part of which occurs in human liver and then red blood cells (erythrocytes, RBCs).

There are five species of malaria parasites; P. falciparum is the one that causes the most severe disease. Other species include P. vivax and P. malariae, which are dangerous but do not cause as many deaths. They are also the prevalent species outside of Africa.

The merozoite (meros = portion, and zoo = animal, so like half an animal) stage of the organism invades the RBC’s and reproduces asexually. Periodically the merozoites burst out of the depleted erythrocytes and look for new blood cells to infect. These periodic bursts are timed differently in the different species, from every 48 hours for P. falciparum, or every 36 hours for P. vivax. When they break the RBCs and escape into the bloodstream, an immune reaction is stimulated by the broken cells, including a very high fever, from 103-110˚F!

The fever itself may be lethal, but there other factors, such as the fact that infected cells have parasite proteins on their surface that makes them sticky. The infected RBC's don't pass through the entire circulation and can block circulation in the brain or spleen and cause other problems. So which part of the infection was helpful in tertiary syphilis?

The consensus idea was that the malarial fever killed the T. pallidum of syphilis. Microorganisms like to live inside us because we provide them with something they need, and they have evolved to live best at our temperature. A fever is one way your body tries to make you a bad host for the organism. A high fever, induced by malaria, would make you a very inhospitable host for T. pallidum, and could be lethal to the organism.

Think about this the next time you want to take an Advil or Tylenol for that low grade fever. By medicating yourself, you are preventing your body from using one of its natural defenses against infectious agents. But high fevers cause damage on their own, so declining an anti-febrile (anti-fever) drug when your temperature is 100˚F is much different that counting on your body alone when the fever is 105˚F and you're having convulsions.

Here is a macrophage (false color image) ingesting

bacteria. The macrophage is part of the innate

immune system, it can phagocytose (eat) many

different foreign invaders. One macrophage can

take up and destroy hundreds of bacteria. They

stick to tissue culture plates not because they are

sticky, but because they're trying to eat the plate!

Work done by Dr. Walter Bruetsch at Central State Hospital during the 1940’s questioned whether it was the high temperature of the fever that stimulated T. pallidum destruction. Artificial fevers were not as effective as malarial fever in treating neurosyphilis; Bruetsch suggested that malarial fever and the RBC destruction it brought stimulated innate immune macrophage activity, while artificial fever stimulated only adaptive immune lymphocytes and resulted in lowered Ab concentrations (called titers) at the same time, making the adaptive response less effective. Bruetsch concluded that it was the activation of the innate system that produced results in treating general paralysis and neurosyphilitic paresis. The obvious answer isn't always the complete answer.

In later years, antibiotics took over as the major treatment for syphilis, and only rarely does the infection progress to the tertiary stage. However, proponents of fever therapy have, over the years, suggested that malaria as a treatment could be used for a variety of infections, from lyme disease to HIV.

The primary cheerleader for using malaria to treat HIV infection was none other that Henry Heimlich, inventor of the Heimlich maneuver. In the late 1990’s and early 2000’s Heimlich carried out a series of highly questionablestudies on malaria fever in HIV infection. It is not altogether clear whether proper informed consent was used, and the results of the studies have been universally discounted. But that is not where HIV and malaria part company.

A schematic cartoon shows how HIV replicates. It

first attaches and uncoats. The RNA is reverse transcribed

and then transcribed and translated into protein.

When the new virus assembles itself, the coat proteins

have to be chopped up into usable pieces. This is the

job of the HIV protease. Protease inhibitors stop this

and prevent virus maturation.

It turns out that protease inhibitors used to treat HIV infection may be potent inhibitors of P. falciparum as well. HIV takes over a cell and forces it to produce the proteins and RNA to form new HIV particles. Many of the proteins must have portions cut off to make them functional; this is the job of the protease (prote = protein, and ase = cut). Protease inhibitors prevent this cleavage and therefore stop the formation of new viral particles.

It turns out that malaria parasites use proteases very similar to those of HIV, and preliminary studies indicate that these drugs can prevent reproduction of the organisms. As hard as it has been to come up with useful malaria drugs, here’s hoping that human studies are successful.

Finally, there is some speculation that malaria and HIV are linked. The dangerous P. falciparum was not used to induce fevers in syphilis patients; doctors used less virulent Plasmodium species, such as P. malariae or P. vivax. Charles Gilks, in a 2001 paper in Philosophical Transactions of the Royal Society, suggests that some primate strains of malaria were also used, wherein infected monkey blood was injected directly into the syphilis patients. Gilks wonders if this is where a simian immunodeficiency virus made the jump to mankind. I think that is an extremely long leap.

Next week let’s work the other side of the street; do some diseases keep you from getting malaria? Yes, and there are more than you might have guessed.

C. Gilks (2001). Man, monkeys, and malaria Philos Trans R Soc Lond B Biol Sci DOI: 10.1098/rstb.2001.0880

For more information and classroom activities, see:

Syphilis –

http://www.metapathogen.com/syphilis/#biology

http://www.news-medical.net/health/Syphilis-History.aspx

http://microbewiki.kenyon.edu/index.php/Treponema_pallidum

http://www.microbiologybytes.com/video/Tpallidum.html

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

http://www.biomeds.eu/cms/show_article/30007.html

http://www.cdc.gov/osels/ph_surveillance/nndss/casedef/syphiliscurrent.htm

http://www.slideshare.net/shahparind/syphilis-and-neurosyphilis-101

Malariotherapy in syphilis and other infectious diseases –

http://www.cdc.gov/mmwr/preview/mmwrhtml/00001850.htm

http://books.google.com/books?id=d3wdy3b9VUkC&pg=PA72&lpg=PA72&dq=malariotherapy+syphilis&source=bl&ots=CvlucP551q&sig=6-whBW3Z4lsumtrhTq9aOdFKJt8&hl=en#v=onepage&q=malariotherapy%20syphilis&f=false

http://www.foxnews.com/health/2012/02/07/malaria-cure-claim-sparks-vienna-probe/

http://triviaextreme.com/technology/malaria_cures_syphilis.php

http://scientopia.org/blogs/whitecoatunderground/2010/09/14/syphilis-malaria-and-other-oddities/

http://www.nobelprize.org/nobel_prizes/medicine/laureates/1927/wagner-jauregg-lecture.html

Malariotherapy in HIV –

http://www.ncbi.nlm.nih.gov/pubmed/9089572

http://www.circare.org/malariotherapy.htm

http://www.lightparty.com/Health/MalarioTherapy.html

http://www.thelancet.com/journals/laninf/article/PIIS1473-3099%2803%2900642-X/fulltext

Protease inhibitors-

http://www.aidsmeds.com/archive/PIs_1068.shtml

http://biosingularity.com/2007/07/04/super-3d-animation-that-shows-the-mode-of-action-of-an-hiv-drug/

http://faculty.ccbcmd.edu/courses/bio141/lecguide/unit3/viruses/pianim.html

http://www.hhmi.org/biointeractive/disease/protease_inhibitor.html

http://www.cellsalive.com/hiv4.htm

www.hhmi.org/.../guides/.../HHMI_AP_%20Biology_%20Guide.pdf

www.biotechinstitute.org/sites/default/files/publications/yw92tg.pdf

http://inventors.about.com/library/inventors/bl_protease_inhibitors.htm

http://www.thebody.com/content/art12606.html

Wednesday, February 10, 2016

Form Follows Function - It’s About Time

Biology concepts – circadian rhythm, vision sense, adaptation, parasitism, form follows function

The sun and the moon are symbols of different

activity cycles. As with everything else, we have to give

them human characteristics (anthropomorphism).

Many animals are active in the day or the night, but not both. So what are humans, diurnal (active in the daytime), nocturnal (active in the nighttime), or something else?

Maybe humans are two species, because I know folks who can’t accomplish anything before noon, and do their best work after 11:00 pm, whereas I get up around 5:00 am and am pretty much useless after 8:00 pm.

Whether diurnal or nocturnal, organisms are physically and behaviorally adapted to their activity pattern. This includes the way they sense their environments. Diurnal animals are more likely to have color vision, while nocturnal animals may only see in black and white. The upside for nocturnal animals is greater visual sensitivity, so they can see better than diurnal animals in low light conditions.

The reasons for these different visual talents lies in the types of light receptors on the retina. Rods sense light, but only its presence or absence (white/black). Different receptors, called cones, detect various wavelengths of light (colors). Diurnal animals have about 5-10 times more cones than nocturnal animals (3 types, one for yellow, one for green to violet, and one for red to orange), but they only function in higher levels of light. Therefore, the greater number of rods in nocturnal animals allow for more sensitive night vision, a good thing to have if you are active after sundown.

Rods (yellowish) and cones (blue) are different light receptors located on the retina. Rods are more numerous and detect low levels of light. Cones are less numerous and sense colors of light, but require more light. As shown in the middle image, the tapetum is located beneath the retina in some animals, and can bounce light back to the retina. This bouncing around is responsible for animals glowing eyes at night.

Many nocturnal species have an additional adaptation to improve their night vision. Their retina has an iridescent layer called the tapetum lucidum that bounces the available light around so it may hit more rods. This improves sensitivity, but at a cost to acuity (the image gets a little fuzzier). When you shine a flashlight in the woods at night, the little pairs of reflections you see are the tapetum lucida of the animals looking back at you. The light bounces around inside the eye and some escapes back out through their pupils and that is what you see. Some look at your flashlight to see if you are a predator, others look to see if you are worth eating.

But not every animal with a tapetum lucidem is necessarily nocturnal. An interesting new study has looked at the visual system of the Peter’s elephant nose fish (Gnathonemus petersii). This weakly electric fish has a long nose-like appendage that was thought to mediate location and communication through electrical pulses. But scientists at the University of Cambridge have found that this fish has surprisingly good vision to go along with electrical impulse usage.

The elephant nose fish lives in the dark, murky waters of Central Africa. For this low light environment, it has evolved a unique retinal arrangement for its rods and cones. The cones are arranged in discrete packets, each housed in a cup lined with a tapetum lucidem. Behind these cones are the rods that work in lower level light. In this way, the visual field can respond with cones and rods at the same time. It is believed that this gives the elephant nose fish the ability to pick out predators moving quickly through its visual field.

Humans don’t have a tapetum lucidum, so when reflected light bounces off our retinas and back out the pupils, they appear red like the retinal blood vessels and tissues. This is the eerie red eye effect on some flash photography. I always thought it was a sign of vampirism!

Other nocturnal animals, like many owls, rely on hearing and smell more than vision. They are adapted to maximize these senses. We have discussed previously the changes in owl anatomy (Do You Have To Be Ugly To Hear Well) as examples of form following function to improve hearing. Other animals, like raccoons, have a heightened sense of touch. Their paws have elongated sensor pads, and thousands of touch receptors. With these, raccoons can differentiate textures well enough to tell if a fruit is ripe or not, even in the darkest night.

Raccoons have a strong sense of touch for moving around in the dark.

Their elongated paws have thousands of touch receptors to increase the

sensitivity of this sense. On the dorsal (back) side of the raccoon’s paw,

whiskers (vibrissae) on the ends of their digits heighten the sense of touch.

Raccoons don’t even have to touch something to sense it; they have vibrissae (whiskers) on the ends of their digits, above their claws. Whiskers in general are a potent aid to nocturnal animals, whether located on faces, paws, or bodies (remember the naked mole rat’s whiskers on its torso in Take Off Your Coat And Stay A While).

Even plants can be adapted for nocturnal activity. Moonflowers, night-blooming philodendrons, and other flowers that rely on nocturnal pollinators tend to be white (since their pollinators most likely can’t sense color), and strong smelling. Indeed, the increased temperature of the P. selloum spadix (Is It Hot In Here Or Is It Just My Philodendron) is an adaptation to nocturnality.

So why be nocturnal? Anyone who has tried to negotiate an unfamiliar room in the dark knows that being active in the dark brings certain obstacles that must be overcome. There must be distinct advantages to it or needs for it, or else nature wouldn’t go to the trouble of adapting. Some scientists believe that nocturnality arose from originally diurnal organisms taking advantage of an underused ecological niche. Being active at night can be a form of crypsis (hiding), either to make them better hunters, or to avoid being hunted.

Nocturnality can also reduce the amount of water lost to the environment, and can lower the thermal stress on certain species of animals. For example, many frogs lose water through their skin, so daylight and higher temperatures can dehydrate them quickly.

That doesn’t mean that certain species won’t be exceptions. Moths are all nocturnal, except for the polka-dotted wasp moth, that is. There are four species of wasp moths, all diurnal, but the polka-dot is the prettiest, so we will fall into that old trap and give the pretty one all the attention. Diurnally active, this moth has abandoned many of the nocturnal adaptations of its brethren.

The polka dot moth has color and patterns that might be useful

for mating or for warding off other animals, but they would

be wasted if the animal was nocturnal.

For instance, it is beautifully colorful - usually a no-no for nocturnal moths. Since color doesn’t show up at night, moths are generally white, tan, or grey. Second, the coloration, especially the bright rump, mimics a wasp (hence the name) and warns of a toxic mouthful if consumed. This defense is called aposematism (apo = away from, and soma = body, basically, keep away from me). Many brightly colored insects will make predators sick, purely a diurnal method of survival, as the warning colors would be of no use at night.

Just as this moth species is diurnal when its close relatives are nocturnal, there is a single genus of primate that has chosen to be nocturnal when all others, including humans, are diurnal. Owl monkeys (8 species) live in Central and South America, and leave their sleeping sites about 15 minutes after sunset each day. They forage for fruits and the odd flower or insect until just before sunrise, then retreat to a hollow tree or within dense foliage to sleep away the day.

Owl monkeys adopted a nocturnal pattern after millions of years being diurnal, so it must have afforded them some advantage or was an answer to some overwhelming stressor. They have adapted by developing larger eyes, with more rods and fewer cones. They still see color, but less so than other monkeys.

The owl monkey is nocturnal, so it needs to have more sensitive vision.

For this reason, it eyes (and eye sockets) are huge! Compare the eye

size and skull morphology in the diurnal capuchian monkey. Form of

the skull follows the functional capacity of the eye.

Owl monkeys are interesting to science for being the source of another exception, as they are the only primates susceptible to the human form of malaria. In The Perils of Plant Monogamy, we used malaria in chimps and humans as an example of divergent evolution; malaria developed into species-specific forms. But the owl monkey is susceptible to both the primate and human species, so they can substitute for humans in malaria research.

Malaria is caused by a parasite, and as such, depends on its host organism for nutrition. The rule is that parasites are active when their host is active (feeding). A good example is the intestinal parasite of the surgeonfish, E. fishelsoni (Of Fish Guts And Cancer).

As I am sure you have committed to memory and made a part of your life, E. fishelsoni grows to an amazing size and replicates its DNA thousands of times before it divides into two or three progeny organisms. It takes tremendous energy for a bacterium to grow 80 fold and produce 85,000 copies of its DNA in one day, so it must occur when nutrients and carbohydrates are plentiful - during the day when the fish is feeding. Although it is a stretch, I guess you could call E. fishelsoni a diurnal parasite.

The malaria parasite, Plasmodium falciparum, has chosen a different path. P. falciparum’s host is man, and man is diurnal (teenagers and third shift workers excepted), but the parasite works to produce many progeny (gametophytes) and have them mature in the nighttime. The reason is simple; malaria has two hosts.

Plasmodium falciparum needs two hosts to complete its life

cycle. One immature form (sporozoite from oocyst) grows

only in the mosquito, while another (gametocyte) forms only

from mature sporozoites in the human red blood cells.

While one stage of the organism grows in the human, another needs to be inside a mosquito in order to complete its life cycle. After finishing its development, it is ready to be injected into another human when the mosquito feeds again. The key is that the mosquito is nocturnal and the gametophyte is short-lived. The gametophyte must be produced and mature just in time to be sucked and deposited into the mosquito gut. P. falciparum has been pressured to conform to the activity of one host while it is inside a host with the opposite activity pattern.

It is common that most species within a group will have similar activity patterns, since they are derived from common ancestors and therefore many characteristics are similar, including those that determine fitness for day life or nightlife. But there are exceptions. For instance, most rodents are nocturnal, but we see squirrels all day long - they are diurnal. Also, we mentioned above that most primates are diurnal, but the owl monkeys are nocturnal.

But there are bigger exceptions, organisms that aren’t diurnal or nocturnal. Ants, primates, and cats have species that are all over the place; some are nocturnal, some are diurnal and some are neither. It is the in-betweeners and the neithers that we will talk about next time.

Kreysing, M., Pusch, R., Haverkate, D., Landsberger, M., Engelmann, J., Ruiter, J., Mora-Ferrer, C., Ulbricht, E., Grosche, J., Franze, K., Streif, S., Schumacher, S., Makarov, F., Kacza, J., Guck, J., Wolburg, H., Bowmaker, J., von der Emde, G., Schuster, S., Wagner, H., Reichenbach, A., & Francke, M. (2012). Photonic Crystal Light Collectors in Fish Retina Improve Vision in Turbid Water Science, 336 (6089), 1700-1703 DOI: 10.1126/science.1218072

For more information or classroom activities on activity cycles, night vision or adaptation, see:

diurnal/nocturnal –

http://zoogirl-zootopia.blogspot.com/2010/08/nocturnal-diurnal-and-crepuscular.html

http://www.desertmuseum.org/kids/oz/long-fact-sheets/Title%20Page.php

http://www.bigfoothunting.com/info/bigfoot_nocturnal.shtml

http://www.mesacc.edu/dept/d10/asb/origins/primates/day_night.html

http://www.bbc.co.uk/learningzone/clips/different-adaptations-between-nocturnal-and-diurnal-animals/12644.html

http://www.brighthub.com/education/k-12/articles/58019.aspx

www.cal.org/siop/pdfs/nocturnal-vs-diurnal-animals-lesson.pdf

http://library.thinkquest.org/25553/english/interact/lessons/noctlp.shtml

www.seaworld.org/just-for-teachers/lsa/i-014/pdf/9-12.pdf

night vision –

http://www.pbs.org/wgbh/nova/kalahari/nightvision.html

http://dmohankumar.wordpress.com/2010/04/12/night-vision-in-animals/

http://www.news-medical.net/news/2009/04/16/48432.aspx

http://www.webexhibits.org/causesofcolor/17.html

http://www.bigbridge.org/BB14/NIGHT.HTM

http://animal.discovery.com/tv/night/

www.bouldercounty.org/play/recreation/naturedetectives/2004c.pdf

http://www.aoa.org/x6046.xml

http://www.aoa.org/x6035.xml

adaptation –

http://evolution.berkeley.edu/evosite/evo101/IIIE5Adaptation.shtml

https://notes.utk.edu/bio/greenberg.nsf/0/3ee9cccd7c64bffd85256cff0061f4d7?OpenDocument

http://www.nyu.edu/projects/fitch/courses/evolution/html/adaptation.html

http://news.nationalgeographic.com/news/2002/01/0110_020110TVfinches.html

http://www.pbs.org/wgbh/nova/teachers/resources/subj_06_03.html

http://www.nclark.net/Evolution

http://evolution.berkeley.edu/evolibrary/article/evo_31

http://ethemes.missouri.edu/themes/905

http://www.windows2universe.org/teacher_resources/teach_beaks.html

http://serc.carleton.edu/sp/mnstep/activities/35021.html

http://www.teachersdomain.org/resource/tdc02.sci.life.evo.lp_humanevo/

http://www.hhmi.org/biointeractive/activities/pocketmouse.html

http://www.teach-nology.com/teachers/lesson_plans/science/biology/evolution/

http://www.nationalgeographic.com/xpeditions/lessons/17/g35/smcreatecreature.html

Wednesday, March 5, 2014

Taste And Be Tasted – Fair Is Fair

Biology concepts – metamerism, tagmentizaton, taste, arthropods, receptor, parasitism

Carbonated sodas come in all flavors, but across all cultures, it is

the carbonation that is the same. Mauby is a tree bark flavored

soda sold in the West Indies islands of Bermuda, Trinidad and the

like. On the left is a bird’s nest/white fungus soda sold in Vietnam.

I don’t think it includes the bird.

There is no doubt that humans love the taste of carbonated sodas. There are as many flavors as you can imagine, but the common element among them is the infusion of carbon dioxide (CO₂). Do you taste the carbon dioxide or is it important for some other reason?

Many insects will tell you that it’s the CO₂ that makes the difference. Fruit flies, mosquitoes, ticks and other insects can taste CO₂ on surfaces and in the air. For mosquitoes and ticks, tasting CO₂ helps them find food. These are hematophagous (blood-eating) organisms, and they find their victims by flying upstream along their exhaled CO₂ and the CO₂ that is exuded from their skin.

Even more amazing, fruit flies and other insects taste the increased CO₂ that stressed (injured, diseased) flies emit. They may avoid other insects that are dying so they won’t be near disease or danger. In other insects, they may follow it to animal carcasses - their buffets. In either case, the insects can actually taste death.

But are they tasting CO₂? It’s a gas, and we have said that gases are detected and perceived by smell, not taste (except for us and DMS). It turns out that CO₂ sensation is really an exception. A 2007 paper from John Carlson’s group showed that the receptor heterodimer (hetero = different, and dimer = two different proteins) is made of GR21a and GR63a, two gustatory proteins (hence the GR in the name).

However, the two taste receptors are located on olfactory neurons. The signal is detected by taste signaling on a smell neuron, and the signals are then sent to the smell portion of the brain! This may be one of the biggest exceptions in all of taste science, and it’s the insects that have it and use it.

For insects to accomplish many different tasks with taste, it helps to have the taste receptors in specific places. Catfish had them all over their body, but that’s not very specific. In insects they are found in distinct places, and may have distinct functions.

The shrimp is a good example to show metamerism in arthropods.

All the parts are just reiterations of the same subunit. Some kept

their appendages, and some changed them into something else.

Tagmentization is the result of modifications so that some of the

somites act together as the cephalothorax, and others

from the abdomen.

Many arthropods have taste receptor sensilla on exterior mouthparts, on their legs, on their antennae, and even on their wings. These may seem like a lot of work to develop them on so many different structures, but maybe not. Metamerism is at work.

Metamerism (meta = subsequent, and mer = unit) is a biology concept for efficient addition of complexity in an animal. Over time and evolution, certain specific structures and functions may develop in response to pressures. It is much more efficient to just create another unit using the same blue prints instead of creating a new part from scratch. The repeat is metamerism; the specialization over time of the different mers is called tagmatization.

You can see metamerism and tagmentization at work in arthropods and annelids (worms) by looking for repeating units. Millipedes and centipedes are great examples. Their bodies are made from many copies of the same basic unit. In many animals, repetition of units allows for drift over time and slow changes in structure and function, even grouping of different mers together for special function (tagmatization).

Mers (or somites) in insects include appendages like legs. But over time, many of the appendages evolved into other structures, like mouthparts, antennae, and egg-laying apparatus. Some characteristics are retained, others are dropped or altered, and some new characteristics appear.

Feel like your being stared at? The left picture is good for showing

the mouthparts of a grasshopper. Every one is a remnant of an

appendage. The mostly come in pairs, one from each modified

appendage. On the right, the cartoon shows the different

mouthparts, the labrum (lr) and hypopharynx/labium (hp/lb)

have fused to form just one piece. md = mandible, mx = maxilla

In terms of taste, the appendages seem to have been a seat of gustatory receptor sensilla. When several appendages evolved into mouthparts, the taste receptors were there. When some appendages developed in antennae, the taste receptors were there. But there is still the chicken and the egg question - did taste receptors on mouthparts result from them being derived from appendages, or did taste receptors on legs and other appendages come from early appendages being used as mouthparts?

A run down of tasting anatomy is hard for insects as a whole, because different arthropods taste with different parts, but some structures are more common. Mouthparts seem to be a favorite, and that makes sense. Flies taste with their probsocises (am I making up the plural?), but they also taste with the ends of their legs. Arthropod legs come in segments, and the last segments are called the tarsi.

Flies can taste food with their tarsi just by landing on it, but the also have taste receptors higher on their legs as well. Honeybees taste primarily with their antennae, but other flying insects can actually taste things with their wings! Wing tasters include fruit flies and mosquitoes, and they are more of an exception than you might think. We talked above about how tasting with different parts isn’t so crazy, since metamerism is just the modification of similar starting parts. But wings are not modified appendages.

Wings actually evolved from abdominal gills, and most insects have either given up these early structures and those that have them don’t taste with them. It may be that taste receptors on wings developed on their own, or that taste is older than metamerism. We don’t know their function yet – you work on that one.

Drosophila is the quintessential research model. The left

cartoon shows the olfactory and gustatory receptors. Notice

how many taste receptors are around the proboscis. On the

right, the red dots show all the different places gustatory

receptors are found. Wing margins, legs, tarsi, and mouthparts

all have taste receptors.

We have introduced mosquitoes and taste when we talked about CO₂ above, but they come into play again here, according to a 2010 study. They taste with wings, and this may have something to do with how we can keep mosquitoes away from us. The two main chemical deterrents to mosquitoes are DEET and citronella candles. And they work differently.

Citronellal is only smelled by mosquitoes; the active molecule triggers only olfactory receptors. But DEET triggers both olfactory and gustatory receptors, it is smelled and tasted. Both senses stimulate avoidance responses in insects, so even if a mosquito lands on you, the DEET you put on will be tasted and may keep it from biting.

So some insects taste with wings - is that as weird as it gets? Nope, some females taste with their ovipositors (ovi = egg, and posit = laying). Ovipositors are a result of metamerism, they are modified appendages. The females of many species can taste the plants or places they land to determine if they are a suitable place to lay eggs.

The ovipositors most likely have rare taste receptors, applied to only to this one specific task. For example, there are two subspecies of a particular fruit fly called a goldenrod gall fly (Eurosta solidaginis). The females look for specific plants, and then for buds of the right age in which to insert their eggs. The growing larvae then feed on the bud, and cause a tumor (gall) to form.

The ovipositor of a female wasp or fruit fly is also a modified

appendage. In the wasp on top has a rigid ovipositor that may

be used to inject eggs into a caterpillar larva. On the fruit fly

ovipositor below, you can almost see the sensillae that

contain the taste receptors.

The interesting point is that there are two different kinds of goldenrod and two different kinds of flies. One type of fly will never pick the other type of goldenrod to lay it eggs on. The slightly different plants must have slightly different tastes, and the two subspecies of flies have evolved to react favorably to only one of the two tastes.

Obviously, some insects pick their plants very carefully. Let me give you an example that really knocks this point home. Tiger moth (Grammia incorrupta) caterpillars are sometimes parasitized by flies or wasps that lay their eggs inside the wooly bear (tiger moth caterpillar). A 2009 paper shows that when this occurs, the caterpillars switch the kind of plant food they eat, opting for poisonous plants that contain pyrrolizidine alkaloids (PA).

The PA-rich food is much less nutritious than the caterpillar’s regular food, so it definitely costs the caterpillar in terms of grown and health, but the PA is toxic to the parasites. The food choice sometimes depends on the number of parasitic eggs laid in one individual caterpillar. Just one egg – a caterpillar may eat some PA-rich plant material and let its immune system do the rest of the work. But with more eggs, the woolly bear will consume PA-rich plants exclusively – hoping to kill off all the eggs. The caterpillars are self-medicating, tasting their way back to health.

Turnabout is fair play – we haven’t discussed the plants that are being eaten by all these insects. In some cases, it turns out that the plants are tasting them right back, and even tasting each others' messages.

You can see the parasitic wasp injecting eggs into the

caterpillar. When the eggs hatch, they will feed on the

caterpillar through their larval stage. Two things may

happen. The caterpillar may switch plants (based on taste)

to try and poison the parasites. Second, the plant they are on

now may have called in the wasps to kill the caterpillar using

volatile chemicals, and the toxic plant that the caterpillar

switches to may do it again.

Corn plants (maize) get munched on by caterpillars. In response, they produce chemicals to attract predators of the caterpillars. This has been known for a while. But a 2000 study showed that the plants respond to the caterpillars saliva; the maize tastes it (contact chemosensation) and starts to send out the volatile chemicals that will attract parasitic wasps looking to lay eggs in the caterpillars. A more recent study shows that the caterpillars play an even bigger role in their own demise.

The volatile chemical that maize uses comes in two forms; it’s the switch from primarily one form to the other that attracts the wasps. But even before the plant starts to produce the attractive form, the caterpillar’s saliva converts the inactive form to the attractive form. The attractive message starts about a day before the plant starts to make the attractive form. The maize molecule has evolved to make the caterpillar call the cops on itself.

What is more, plants can send taste messages to nearby plants through the dirt. In a 2011 study, researchers induced drought like conditions on one row of plants. In less than an hour, plants five rows away started to close their stomata (pores in leaves) to conserve water for an impending drought. Plants that were just as close, but planted in a different container did not prepare for drought, so the message had to be traveling through the soil. I leave it to you to decide if this is really a taste sense.

So - if you’re a raw food enthusiast, you might be being tasted back. And maybe your food is spreading the word about you to his neighbors. Next week – why do we call spicy food "hot?"

Falik O, Mordoch Y, Quansah L, Fait A, Novoplansky A (2011). Rumor Has It…: Relay Communication of Stress Cues in Plants. PLoS ONE, 6 (11)

Lee Y, Kim SH, & Montell C (2010). Avoiding DEET through insect gustatory receptors. Neuron, 67 (4), 555-61 PMID: 20797533

Singer, M., Mace, K., & Bernays, E. (2009). Self-Medication as Adaptive Plasticity: Increased Ingestion of Plant Toxins by Parasitized Caterpillars PLoS ONE, 4 (3) DOI: 10.1371/journal.pone.0004796

Allmann S, & Baldwin IT (2010). Insects betray themselves in nature to predators by rapid isomerization of green leaf volatiles. Science (New York, N.Y.), 329 (5995), 1075-8 PMID: 20798319

Kwon JY, Dahanukar A, Weiss LA, & Carlson JR (2007). The molecular basis of CO2 reception in Drosophila. Proceedings of the National Academy of Sciences of the United States of America, 104 (9), 3574-8 PMID: 17360684

For more information or classroom activities, see:

Carbon dioxide taste in insects –

http://www.webmd.com/allergies/features/are-you-mosquito-magnet

http://science.howstuffworks.com/zoology/insects-arachnids/mosquito.htm

http://labs.russell.wisc.edu/mosquitosite/carbon-dioxide-baited-mosquito-traps/

http://pestcontrol.about.com/od/bitinginsectprofiles/a/Why-Are-Mosquitoes-Attracted-To-Some-People.htm

http://www.universityherald.com/articles/6037/20131206/mosquitoes-are-attracted-to-the-smell-of-carbon-dioxide-exhaled.htm

http://www.nytimes.com/2010/06/15/health/15real.html

http://www.utsandiego.com/news/2013/Dec/05/ray-riverside-mosquito-neuron-skin-carbon-dioxide/

http://jeb.biologists.org/content/216/12/vi.short

http://www.nature.com/nature/journal/v461/n7261/edsumm/e090910-12.html

http://ndri.com/news/fruit_fly_has_opened_new_era_of_taste_behavior-367.html