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

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.

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)

One Scientist from Baylor College of Medicine in Houston Texas, Richard A. Gibbs, decided to test whole genome sequencing on his colleague, a medical geneticist, Dr. James R. Lupski, who suffers from a rare genetic disorder known as Charcot-Marie-Tooth Neuropathy (this disease damages nerves to the hands and feet and causes muscle weakness). As it turns out, this disease is caused by a single mutation in any of 39 genes. Dr. Lupski’s mutation turned out to be in a gene called SH3TC2. He inherited the mutated variant from both parents; however, the mutations were in different sites within the gene in each parent. His father had an error on one site, his mother in another. These mutations were also passed on to three of his seven siblings.

The second team, run by Leroy Hood and David J. Galas at the Institute for Systems Biology in Seattle WA, also decided to use Whole Genome Sequencing. They sequenced the genomes of a family of four, where two children each inherited rare, single gene diseases known as Miller Syndrome (this can cause malformation of facial features and limb development, but does not affect intelligence) and ciliary dyskinesia (this impairs the development of cilia in the respiratory tract and the fallopian tubes, which can lead to difficulties expelling mucus). The completed sequencing allowed the researchers to identify the genes causing these diseases.

Today, the cost of sequencing an entire genome has gone down quite a bit, from approximately $500 million to about $50,000. This technique has also allowed the Seattle scientists to estimate the number of mutations passed from mother to child, which turned out to be less than expected.

There are many diseases that are caused by a single, rare mutation in a gene. However, common diseases, such as cancer, may have mutations in many genes. This is what prompted the beginning of the Human Genome Project in 1987 at the cost of about $3 billion dollars.

After the project’s completion in 2003, scientists created a $100 million project called HapMap, which identified common mutations among human populations. This was meant to be a “short cut” to finding disease causing genes. As it turned out, about 2000 of these sites were linked to assorted diseases, but many more did not appear in working genes, implying that HapMap was somehow missing some of the connections between these mutations and diseases among individuals. Too much money was being spent, but not enough answers were being found.

Now some scientists lean toward the belief that common diseases do not have common mutations, but actually have rare mutations in multiple sites. Whole genome sequencing seems to be the “way to go” for gene and mutation analysis of diseases. The price for this type of sequencing is dropping as technology advances. In the near future, sequencing companies are hoping to get the price down to a $5000 genome.

Information for this blog was taken from:  http://www.nytimes.com/2010/03/11/health/research/11gene.html?hp

Only recently has science began to unveil some of the mysteries of these behemoths. For decades it was believed that ancient DNA, proteins, and soft tissue could not be preserved over millions of years. Now, during the last 2 years, soft tissue was discovered deep inside the thigh bones of T-Rex.

There are times that inspiration for truth comes from science fiction, such as the best selling novel and blockbuster film, “Jurassic Park.” The film took some artistic liberty with their dinosaurian profiles. One of the most noticed was giving a carnivorous dinosaur known as Dilophosaurus a special skill – the ability to spit toxic venom.

According to their fossils, there was no evidence for venom production in this type of dinosaur. In fact to most paleontologists this idea was laughable. Today venomous dinosaurs might not be so funny.

A fossil of a small dinosaur called sinornithosaurus (a chicken-sized dinosaur) was discovered in China about 9 years ago. This species existed in the mid-Jurassic (about 124 million years ago). This find caused a sensation because it had clear evidence of feathering. In 2009 a research team studied the skull of this animal intensively and made an interesting discovery. They found mysterious air pockets located above many of the teeth. These “pockets” connected to grooves in the dinosaurs teeth that spanned from the base of the tooth to the tip. This would be the perfect mechanism for a venomous bite. Even though this new theory is controversial, it is a logical explanation.

If these little dinosaurs were poisonous, it may be impossible to tell anything about the venom itself. There would be no trace of it left after about 124 million years. The answer lies within their DNA. There is an unbearably slim chance of finding any soft tissue remaining in such a small fossil. This is always the problem for every paleontologist, we just have to take what we can get, and go as far as we can go – and hope for answers along the way.

For more information on this new discovery go to:

http://www.sciencenews.org/view/generic/id/51402/title/Groovy_teeth_suggest_dinosaur_was_venomous

Cancer cells have mutations in their genes that render them unable to respond to signals that regulate cell division. These cells grow uncontrollably and can invade normal tissue in other locations of the body and cause disrupted functions of major organs. This is why cancer is so deadly.

A mutagen is a physical or chemical substance that can alter genetic material in cells. DNA can be damaged or changed (mutated). Cancer cells have changes in the genes themselves. These changes can include mutations , deletions of part or whole genes or even the addition of extra copies of genes.

There are many mutagens that can cause cancer in cells. These are called carcinogens. Two of the most common and most deadly cancers, lung and skin are caused by two well known carcinogens, cigarette smoke and sunlight. Some studies suggest when 15 cigarettes are smoked, an error in DNA occurs.

Now the UK’s Wellcome Trust Sanger Institute has cracked the code for the mutations within DNA that can cause tumors that lead to these two devastating types of cancers.

This new information can open the door to major advancements in treatment, medication and maybe even cures in the future of skin and lung cancers.

Affectionately known as “Ardi”, some of her features were distinctive. Due to her location in the ancient Ethiopian strata, she was dated to 4.4 million years ago, pre-dating “Lucy” (Australopithecus afarensis) by over a million years. Her brain size was much smaller than Lucy’s but was similar to that of a modern chimpanzee.  According to the form of her limbs and pelvis, she was able to walk upright, yet she had a grasping hallux (big toe) on each foot, which suggests that she had an arboreal lifestyle.  This theory was supported by the fossils discovered locally near Ardi’s resting place.  This “woodland” lifestyle came as a surprise to scientists because Ardi’s descendant, Australopithecus afarensis (“Lucy”), lived on the savannah.  Now thoughts on the evolution of bipedalism must be re-threaded.  

To date, Ardi (Ardipithecus ramidus) has replaced Lucy (Australopithecus afarensis) as the oldest hominid fossil.  Genetically, the common ancestor between humans and chimps was estimated to exist 6 million years ago.  “Ardi” takes us one step closer to that ancestor.

For more on Ardi, see our interview with researcher, Tim White, at the DNALC website here.

Ardi sketch redirected from The Guardian.

In 2007, they were able to identify and compare seven protein sequences.  Three of these proteins seemed to be closely related to chickens.  Two others resembled frog and newt sequences.

Although tempting to contemplate, this does not indicate that T Rex was really a “Chikafrogonewtasaurus.”  This information simply provides us with tools to better understand the relationships between extinct and extant animals.

Who knows, maybe we are getting closer and closer to a new “Jurassic Park” reality show…