1 day-old chick

When people hear the name E. coli, even a passing familiarity brings about reactions of disgust and fear of food poisoning.  This outright hatred of the common bacteria is, perhaps, a bit unwarranted, considering there are many different types of Escherichia coli.  Not only are there harmful strains, but there are also many that are harmless to humans and some that are even helpful as well.  We actually have our own E. coli that live in our intestines, take some of our nutrients and make essential vitamin K₂ for us, which we cannot make for ourselves. Vitamin K is an important factor in blood coagulation.  So we have a good relationship with them, unless they are redistributed to the wrong places in our body where they can cause infection, illness and generally wreak havoc.  As many as 85% of urinary tract infections (UTI) are caused by E. coli, and most of these infections are thought to be linked to the native strain that lives in our intestines.⁽¹⁾  Now there is a new suspect to the crime, chickens.

A group of scientists from McGill University, led by Amee R. Manges, compared the DNA of common human UTI bacteria to samples of bacterial strains found in beef, pork, and chicken.  Strains from beef and pork turned out to be less genetically related to UTI strains than samples collected from chicken, which seem to be very closely related.⁽²⁾  To add to the intrigue, this is a strain found on the actual animal, and is not connected with contamination from meat production plants.

So, does this mean we have to stop eating chicken?  Absolutely not, in fact, in my small family it is an essential staple.  Imagine a world with no chicken nuggets!  There are many things that the average consumer can do to reduce the chance of E. coli infection.  The proper handling and cooking  of raw material will adequately kill most of the bacteria.  Careful sterilization of the area exposed to any raw meat will usually take care of the rest. 

However, the responsibility should not rest only on the shoulders of consumers.  Manufacturers can play a big role in the reduction of disease-causing E. coli.  One factor that makes chickens vulnerable to the contagion is their proximity to one another.  When their living quarters are too tight, then they share all of their nasty pathogens as well as their food and water.  Giving them more space in a cleaner environment would immediately ease the spread of E. coli. 

Antibiotics have often been used by livestock owners to kill bacterial infections.  This can be effective, but overuse has been proven to produce antibiotic resistant bacteria.  The transmission of resistant bacteria to humans has been seriously complicating treatment of infections, even in UTI. 

References

1.  http://www.kcbd.com/story/16942940/e-coli-in-chicken-linked-to-urinary-tract-infections: E. coli in Chicken Linked to Urinary Tract Infections
2. http://www.gazettenet.com/2012/02/18/bc-med-utila-national-itop-300-words0326-urinary-tract-infections-linked-to-contaminated-chicken: Urinary tract infections linked to contaminated chicken

Recent studies have shown that plants seem to respond to other neighboring plants, and will alter their growth patterns accordingly.  At McMaster University, Ontario Canada, Susan Dudley and Amanda File have demonstrated that plants grown near their siblings are less competitive than when they are grown near unrelated “strangers” of the same plant.  The response of plants to competition in their environment has been well documented.  They are known to sprout deeper roots for water and nutrients.  However, recognition of their own genetic kin has never been seen before. 

In their experiment, Dudley and File grew batches of Cakile edentula (the Great Lakes Sea Rocket) together in pots of four.  Some were paired with members of the same maternal family and others were paired with unrelated families.  Considering that the plants were of the same species, the growth of their root masses were expected to be the same.  Surprisingly, a greater mass of roots were grown when plant “strangers” were grown next to each other, while less root mass was ass

Cakile edentula (the Great Lakes Sea Rocket)

ociated with tandem plants of the same maternal line, thus indicating a sharing of resources as opposed to competing for them.  The mechanism behind plant kin recognition is still a mystery. 

For Agriculture, competition has been known to reduce yields.  However these recent findings suggest that kin planted with kin work better together and may produce a more prosperous harvest.  

Considering their lack of neurons, any communication between plants is hard to conceptualize.  Perhaps more research in this avenue will bring us closer to understanding more beyond our limited  “animal scope.”

 http://news.nationalgeographic.com/news/pf/858755.html

Normal and Sickled Red Blood Cells

While scientists have long known that carriers for Sickle Cell Trait are more resistant to Malaria infection, the mechanism by which protection is conferred has not been well understood—until now.  Scientists at Heidelberg University used an electron microscope to observe what happens when the parasite that causes Malaria in humans, Plasmodium falciparum, infects red blood cells containing both healthy and mutant hemoglobin.

Scientists noticed that in red blood cells with healthy hemoglobin, the parasite hijacks the actin cytoskeleton to transport its own “adhesin” protein to the cell membrane.  The adhesin, also called Plasmodium falciparum Erythrocyte Membrane Protein 1 (PfEMP1), causes the red blood cells to adhere to each other and to the walls of small blood vessels so that the infected cells don’t circulate through the spleen, where they would otherwise be destroyed.   The parasite continues to reproduce within the infected cells and causes cell lysis, destroying the red blood cells and releasing more Plasmodium into the blood stream.  As a result, Malaria patients become severely anemic and suffer from symptoms related to insufficient oxygen delivery.

While mutant hemoglobin polymerizes into long rods and causes red blood cells to sickle dangerously in low oxygen conditions, it appears that in sufficient oxygen conditions the mutant protein prevents Plasmodium from borrowing the actin cytoskeleton to ferry adhesin to the cell surface.  Without knobs of adhesin protein, infected cells travel to and are destroyed in the spleen so that patients do not suffer Malaria symptoms.

Each individual carries two copies of the information needed to make a protein.  People with two mutated hemoglobin genes may be highly resistant to Malaria infection, but they also suffer from Sickle Cell Disease, in which abnormally shaped red blood cells clog blood vessels and cut off the blood supply to organs.  People with one copy of the mutant hemoglobin gene, however, make both enough healthy protein to maintain red blood cell shape and enough mutant protein to interfere with Malaria infection.

Pony with Pangare markings

Before the dawn of the written language, prehistoric humans began recording events from their daily lives and environment on the walls of their local caves.  Now many of these cave paintings are treasured, priceless works of ancient history and art.  Many different animals are represented in these paintings and about a third of them are horses. ^[1] 

There has been much speculation about exactly which horse breeds existed when the painting of cave walls began about 25,000 years ago.  Some of the types predicted included bays, grays and horses with dun colored coats with pangaré markings (tan coat with white around the muzzle, belly and eyes-pictured above).   

Typical horse breeds represented in cave paintings

Discovered in the Peche-Merle caves in the Midi-Pyrénées region of France, was an illustration of a “horse of a different color”, white with black spots.   Some archaeologists doubted the accuracy of the painting, believing that this spotted variety post-dated the period in which the paintings were created.  They supposed that ancient cave art might be more symbolic than realistic.  A DNA analysis conducted on nearly 90 ancient horses dating from 12,000 to 1,000 years ago seemed to support this theory.  Out of the 90 samples, there were many examples of bay and black breeds, but no evidence of the spotted variety. ^[1]  

The team decided to expand their analysis by selecting 31 pre-domestic horse samples (involving bones and teeth), dating back as far as 35,000 years ago from Siberia, Eastern and Western Europe and the Iberian Peninsula.^[2] The results of the analysis revealed 18 bays (reddish to reddish brown), 7 horses with black coats, and, surprisingly, 6 samples had the genetic marker for spots, also known as “LP” for leopard-like spotting.  This was the first evidence for the white spotted phenotypes in pre-domestic horses, and therefore suggested that our ancestors were accurately depicting their life and times, not formulating fantasy. ^[2] 

So, this begs the question, why would spotted horses be more abundant 14,000 or more years ago only to thin their numbers after?  The answer was most likely “Darwinian,” and based on natural selection.  During the Ice Age, white spotted horses would have the advantage of better camouflage in snow conditions, leaving them less visible to predators.  However, the genetics behind the gene had a disadvantage.  In modern horses, if two copies of the “LP” gene are inherited (one from Mom, one from Dad), these horses have “night blindness”.  This handicap would leave spotted horses susceptible to any nocturnal predators hungry for a big meal.  As the Ice receded, it is believable that the spotted horses would appear less in the gene pool and may have disappeared entirely if not for humans.  After humans began to domesticate horses, breeding them for aesthetic value became common.  The rare spotted horses were likely bred for their visual appeal.  

Citations:

1.  http://www.wired.com/wiredscience/2011/11/cave-painting-colors/: Cave Paintings Showed True Colors of Stone Age Horses
2. http://www.biologynews.net/archives/2011/11/07/ancient_dna_provides_new_insights_into_cave_paintings_of_horses.html: Ancient DNA Provides New Insights into Cave Paintings of Horses

So why have they not succumbed to the pressures of natural selection?  They are much tougher than they appear.  Butterflies have three dominant defense mechanisms that have kept them safe for approximately 50 million years (the earliest butterfly fossil dated back to the Eocene Epoch): camouflage (they blend in with their environment, some even look like flowers), “warning” coloration (bright colors that indicate to predators that the butterfly is poisonous or has a fowl taste), and mimicry, which involves non-poisonous, non-fowl tasting butterflies that imitate genuine warning coloration.

Recent studies have shed light on the relationship between warning coloration and mimicry.  Originally, mimicry was thought to only be beneficial to the “copy” organism because predators would have to eat more of the distasteful or poisonous butterflies to learn to stay away.  A behavioral study conducted in Liverpool put this theory to the test.  An experiment was conducted to use artificial “butterflies” filled with food (some were tainted with a fowl tasting non-toxic chemical, some less fowl and some not tainted).  The birds preyed upon both nasty-tasting and normal alike, until they learned to give up both species altogether to avoid mistakenly eating bad tasting specimens.  This indicated that the warning coloration was beneficial to both the poisonous butterflies and their mimics.^[1]

So how do these mimics get their similar characteristics?  If they can’t paint themselves, how do they copy their nasty-tasting cousins?  Recent studies on the genetics behind these colorful traits shine new light on this evolutionary puzzle.  Genetic conservation is the key.  Many of the genes we have are conserved from past generations and related species.  In this case, the genes responsible for making a fruit fly’s eyes red have evolved to produce the red wing patterns in the Heliconius butterflies from South and Central America and many other varieties of passion vine butterfly species.^[2,3]  In  other words, changes in a single gene, called “optix,” which makes the red pigment, can result in changes in gene expression.  This gene is conserved and drives wing pattern evolution across remotely related butterflies.^[3]    

It has always been challenging explain how convergent evolution actually happens and it has been a bit of a mystery for a long time.  But by studying the genetics of an organism we have a better understanding that genes are conserved across all living organisms.  Just a little tweak here and a tweak there and you can change a feature or a function.  DNA has revealed to us an interesting reality.  Nature seeks not to re-invent, but to alter and re-use what is already there.

Here is a little “mimicry” challenge:

Monarch (left)                    Viceroy (right)

The Monarch is considered unpalatable to predators and the Viceroy is also toxic but more tolerable.

Can you tell the difference?  If you were the predator, which one would you eat?

1. http://www.sciencedaily.com/releases/2007/07/070705101502.htm: “Mimicry: Research Ends Debate Over benefits of Butterfly Defenses”
2. http://www.physorg.com/news112537321.html: “New Study Uncovers Secrets Behind Butterfly Wing Patterns”
3. http://www.physorg.com/news/2011-07-butterfly-convergent-evolution.html: “Butterfly Study Sheds Light on Convergent Evolution”
4. All pictures were found on Wikipedia.

HIV infects white blood cells by latching onto two protein receptors, CD4 and CCR5.  Scientists noticed that people with a defect in the CCR5 gene (a 32-bp deletion) are incapable of making the CCR5 receptor and are highly resistant to HIV infection.  Unlike with other genetic defects, these people appear otherwise healthy.  If an HIV patient’s own white blood cells could be removed, their CCR5 genes mutated, and the cells returned to the body, then the patient would be protected from further infection.  The virus would not be eradicated from the patient’s body, but the HIV would be unable to attack more white blood cells so that the patient’s immune system would remain intact to fight off other infections.

The primary problem with such a technique, however, has been an issue of gene targeting: how do you inactivate the CCR5 gene without disrupting the rest of the genome?  Scientists have found  a pair of proteins that can help them do just that.  Zinc finger proteins are exceptionally good at binding to DNA.  In addition, they can be designed to bind to very specific sequences of DNA.  A type of enzyme, called a restriction endonuclease, can cut DNA.  Scientists have hitched these two protein types together to create the molecular equivalent of a heat-seeking missile:  the zinc fingers home in on and attach to a sequence in the CCR5 gene while the restriction enzyme damages the DNA in that gene only.  Cells come armed with machinery for patching damaged DNA, but the repair process eliminates some of the information needed to make the CCR5 protein.  The end result is a shorter, defective CCR5 protein which cannot guide HIV into the cell.

Scientists at Sangamo BioSciences have used this approach to inactivate the CCR5 gene in a type of differentiated white blood cell called a T cell.  The company has progressed to clinical trials with HIV patients and has so far found that the genetically altered T cells survive and function normally while the amount of virus detected in patients decreases.  Because T cells eventually die, however, the company is also in the process of modifying blood stem cells, called Hematopoietic Stem Cells (HSCs), in much the same way.  If the company succeeds in modifying HSCs, then any new white blood cell made in a patient’s body would be immune to attack—the treatment would need to occur only once for life-long protection to be realized.

Martin Chalfie began attaching GFP to gene promoters, hoping that GFP would be produced whenever the gene was activated.  After successful experiments, his group published a paper in Sciencein 1994. During this time, scientist Roger Tsien wanted to better understand how GFP worked.  So his team cloned, mutated and picked at the protein’s DNA and discovered that they could create new colors!  These three scientists won the Nobel Prize for their achievements in 2008.

The discovery and development of GFP has been an essential driving force for genetic engineering and has brought this technology to new levels of complexity in the 21st century.  Today, making domestic animals glow or lighting up neurons with many fluorescent colors (this project is called “Brainbow”) is almost “standard operating procedure.”  This has revolutionized many aspects of research, especially regarding disease.

Recently, they have decided to produce GFP felines, or cats that “glow in the dark.”  Although these cats might make interesting house-mates, the purpose was to create animals with specific disease resistance.  Occasionally cats suffer from a virus called the Feline Immunodeficiency virus (FIV).  It is a virus that resembles HIV (Human Immunodeficiency Virus), but is not always fatal in cats.  An antiviral gene that produces a protein that can block the AIDS virus was discovered in a rhesus macaque.  This gene was found to work in other animals as well. 

This is  very exciting, but how would you know that it is actually working? Is the cat’s immune system really producing the antibodies?  To answer this question, scientists decided to use GFP as a marker.  They attached the GFP DNA sequence to the gene that makes the FIV antibodies.  Every time an antibody is produced, GFP proteins are made as well.  Therefore, cats producing the genetically engineered antibodies for FIV would also fluoresce under UV light.  In other words, a glowing green cat indicates FIV resistance.  This may seem like a breakthrough only for feline health, but scientists are hoping this will give us insight into fighting the human version as well. 

GFP Cat image

http://www.sciencenews.org/view/generic/id/334271/description/Cats_engineered_for_disease_resistance

Glowing C. elegans

http://www1.ucsc.edu/oncampus/currents/97-10-13/worms.photo.htm

All other photos are from Wikipedia (public forum)

I happen to work at an institution where evolution is revered as the underlying theme that explains life and all of its processes.  For a biology teacher it’s a comfortable place to be.  I suppose I am spoiled. When I travel to schools, I am on occasion told by teachers how happy they are that I am presenting evolution for them.  It is a required part of the New York State science curriculum, but some of the teachers who are supposed to teach it, don’t want to.   It makes me wonder.  Are they uncomfortable with the science?  Are they afraid of parents or students lashing out at them?  Does the scientific theory of evolution somehow conflict with their religious beliefs?   I don’t know the answer.  I’m sure it’s a combination of several factors. 

My gut feeling is that most teacher reticence is due to lack of understanding.   I would feel very uncomfortable if asked to teach a topic I didn’t fully understand, and unfortunately this is what’s happening.   I think we need better teacher training, especially for elementary teachers who receive very little training in science.  Everyone who receives a degree in general education or in science education should have to complete a course in basic genetics and/or evolution.   This would significantly reduce the negativity associated with teaching evolution, and could help produce much happier teachers!

Clostridium sporogenes are anaerobic soil dwellers which cannot survive in the presence of oxygen.   Researchers have genetically modified these bacteria so that they produce an enzyme that activates a cancer drug.  It turns out that the centers of solid cancer tumors contain very little oxygen.  Researchers hope to inject cancer patients’ tumors with the engineered Clostridium spores, which would not survive in the rest of the oxygen-rich body.   After a tumor is infected with the Clostridium, a patient would also be injected with a cancer drug.  The drug would circulate throughout the body in an inactive, “pro-drug” form, and would become active only inside of the tumor.  This would allow for targeted attack of the tumor with fewer healthy cell casualties than conventional chemotherapy.  If successful, this treatment would be especially useful for hard to reach tumors, such as in the brain.

One of the scientists involved in the research, Professor Nigel Minton, explains, “Clostridia are an ancient group of bacteria that evolved on the planet before it had an oxygen-rich atmosphere and so they thrive in low oxygen conditions. When Clostridia spores are injected into a cancer patient, they will only grow in oxygen-depleted environments, i.e. the centre of solid tumours. This is a totally natural phenomenon, which requires no fundamental alterations and is exquisitely specific. We can exploit this specificity to kill tumour cells but leave healthy tissue unscathed.”

The bacteria are slotted to be tested in clinical trials starting in 2013.

While the genetic modification of plants for human consumption is common in the United States (think corn and soybeans), genetically modified (GM) animals have yet to be approved.  But now, a Massachusetts-based company, AquaBounty, is petitioning the FDA to sell genetically modified Atlantic Salmon to consumers.

Thanks to some genetic mix and match, the salmon, dubbed AquAdvantage, reach full size faster and with less food than non-modified salmon.  Typically, Atlantic Salmon produce growth hormone during warm months only.  AquaBounty scientists borrowed a growth hormone gene from another salmon species, the Chinook, and hitched it to a molecular “on switch,” called a promoter, from the eel-like ocean pout.  Combined, these additions to the Atlantic Salmon genome allow the creatures to produce growth hormone year-round, shortening maturation time from three years to two while reducing feed consumption by 10%.  The genetic manipulation is essentially analogous to feeding cows and poultry growth hormones, a regular American farming practice.

AquaBounty insists that the GM fish are identical in composition and taste to their non-modified counterparts, making them safe for human consumption.  The reduced maturation time would ostensibly protect wild fish stocks and stabilize the salmon supply as seafood demand rises with the awakening of the American health conscience.  AquaBounty’s assurances haven’t, however, prevented consumer advocacy groups from maligning the product as a repulsive “Frankenfish” whose approval would open a Pandora’s Box of genetic misfits that would make it onto our dinner tables.

Dear reader, you likely already consume GM crops; would it bother you to eat genetically modified animals too?