Mutations in numerous pathways need to accumulate for cancer to progress. Given the ability of transposons to cause mutation and the role of mutation in cancer, it seemed likely that transposons would play a role in cancer. A few years ago, Iskow and colleagues showed that transposons jump in some lung tumors, suggesting a link to cancer progression. They also showed that methylation levels are often lower in lung cancers. Methylation is important for transposons silencing, so they hypothesized that lowered methylation in cancer could lead to more transposon jumps. This would “destabilize” the genome, allowing more mutations to accumulate, and accelerating cancer progression.

However, very little evidence of this connection existed until recently. With the advent of high-throughput sequencing, it is becoming possible to examine changes in the genomes of cancer cells. Lee and colleagues report on one such study. They decided to look at the effect of retrotransposons by comparing the location of these jumping genes in normal and cancer cells. Retrotransposons copy their sequence from one location to another by going through an RNA intermediate that is read “backwards” from RNA to DNA.

In their study, they had to overcome a problem: because transposons are found throughout the genome and are mostly the same in different individuals, it is hard to figure out exactly where new transposons are located. To sort this out, they developed a bioinformatics tool that could align sequence to a reference genome and identify new transposon sequence associated with this sequence. They then used normal tissue and cancer tissue from the same individual to identify transposition events in cancer cells.

Interestingly, different cancer types had different numbers of transposon jumps. Brain and blood cancers did not have many transposon-induced mutations, while epithelial cancers had frequent insertions. These jumping-gene insertions are probably important for cancer, as many of the insertions occur within genes known to affect cancer biology.

If these jumping genes cause mutations and promote cancer, why are they there? It’s still an area of contention, but all that jumping around helps provide diversity in our genomes. Sometimes that will prove to be bad, but it also allows natural selection to act on the diversity, allowing new, helpful innovations in our DNA power evolution.

Iskow el al, 2010. Natural mutagenesis of human genomes by endogenous retrotransposons. Cell. 141(7):1253-61.

Lee et. al, 2012. Landscape of Somatic Retrotransposition in Human Cancers. Science. 337(6097): 967-971.

Biologists would like to understand how a bear, who eats continuously throughout the summer to lay down fat reserves for the winter, can have cholesterol levels that would be high for a human, but not suffer the hardening of arteries that one might expect. And what about the bone loss one would expect from months of inactivity?  Humans on bed rest can lose 3-4% of their hip bone minerals from lack of weight bearing exercise.  Bears show no signs of bone loss or osteoporosis as a result of their long rests.  It is likely that the genes involved exist in our cells too, but they just aren’t being used in the same way.

We clearly have a lot to learn from our hibernating friends. Teams of researchers in Sweden have actually been studying Brown bears to learn about these interesting phenomena.  How do you study wild Brown bears you ask?  You tranquilize them while they are hibernating, collect as many samples as you can, and get out before they wake up!  For the full story on hibernation, go to: http://www.sciencenews.org/view/feature/id/338318/title/Lessons_from_the_Torpid.

For most of the year, deciduous trees are green because of chlorophyll in the chloroplasts.  This pigment helps harness energy from the sun to fuel photosynthesis, or food production.  In the fall, days become shorter and sunlight more sparse, so plants begin to prepare for the winter – a period during which they rely on stored nutrients.   Nutrients are stored and superfluous leaves are shed , but before that, the chlorophyll begins to disappear, revealing other pigments such as yellow and orange that weren’t visible before.  Sometimes during this process, new pigments (such as reds) are produced as well.

This is controlled by up to 35 genes that can turn on and off in response to the reduction of sunlight hours.  It is a great example of the interaction between an organism’s DNA and its environment, a phenomenon many people are unaware of.  The traits and characteristics of all living things are the result of a combination of its genetic makeup and its physical and chemical surroundings.  To learn more about this type of interaction, go to chapter 35, “DNA responds to signals from outside the cell.”

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!

One of the cooking tips that I have picked up from all of the foodie shows I watch is to use fresh herbs, whenever possible.  Believe it or not, that green spring of parsley on my plate at restaurants that used to repulse me, has actually become a part of my regular cooking repertoire.  Turkey meatloaf just wouldn’t be the same without it!  My homemade pizza now seems bland without fresh basil.

The one herb that I just can’t get cozy with is Cilantro.   It turns out that I’m not the only one.  There are lots of people who also dislike the flavor of these green leaves, as well as their seeds (aka. Coriander).  The plant produces molecules called aldehydes, that determine its scent and taste.  It turns out that aldehydes are also found in soaps and lotions, hence the soapy taste that some report.

It is known that genes play an important role in taste, but there isn’t sufficient data in this field to pinpoint specific genes or gene variants to explain the Cilantro phenomenon.  It is also known, that the evolution of taste and smell has played an important role in our survival.  It’s possible that the cilantrophobe’s distaste is a result of the choice some of our European ancestors made when they turned their noses up at the herb, hundreds of years ago.

In the article, “Cilantro Haters, It’s Not Your Fault” by Harold McGee of the New York Times (http://www.nytimes.com/2010/04/14/dining/14curious.html?partner=rss&emc=rss?)  cilantrophobia can be overcome, through association of the flavor with positive experiences.  Makes sense, but I’m not sure I’m even willing to try!

One very amazing example of this is the Widowbirds that live in the grasslands of southern and eastern Africa.  During the non-mating season, the males and females look very similar to one another.  Once breeding season begins, the males molt and produce long black feathers, some that can be up to half a meter in length.  Studies have been done where feathers have been glued on to some males, and females chose these males over others with shorter tails.  You also have to wonder why the tails don’t get even longer.  That even though females desire very long tails, if they get too long, they could hinder the flight of the birds, which would decrease their fitness.

Other examples that might be more familiar to you are the elaborate feathers of male peacocks, and the beautiful plumage of male birds.

Once upon a time, in a forest with leaves and soil on the ground, there is a family of rabbits. Many animals live in this forest, including several predators for the rabbits. The mom and dad are both brown rabbits and most of their rabbit children are also brown. One of the children was born with all white fur due to a mutation in the gene for fur color. The mutation was a random mutation that occurred in the egg cell before conception even occurred. In their current environment, which of rabbits will be more likely to survive (brown or white)?

The brown rabbits are more likely to survive because they can blend in with their environment. If a predator walks by they will probably see the white rabbit before the brown ones. Unfortunately this means the white rabbit has a greater chance of dying early.

The question that stirs up confusion is: Can an organism change in response to their environment?

I would first answer this by saying that the cells of an organism can respond to changes in their environment. In fact, this flexibility allows organisms to live. Does this mean that the white rabbit will adapt to its environment and become brown? No.

Adaptation in relation to evolution refers to the population as a whole. If a member of the population has a trait that provides an advantage for survival, it is likely that the trait will be passed on to future generations. Eventually, the trait can be seen in greater numbers and even throughout the population.

Although an organism may produce different proteins under different conditions, the DNA of the individual organism will not change because there is a need for a different trait.

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…

Ida was a lemur-like mammal that roamed central Europe about 47 million years ago. She died at a relatively young age of 9 months, on the banks of the volcanic Lake Messel in modern-day Germany. The circumstances of her death play a large part in her current fame – researchers involved in the find speculate that Ida was overwhelmed by a belch of carbon dioxide gas from the lake, causing her to slip into the oxygen-deprived lake. The unique concoction of Messel’s volcanic water coupled with the lack of trauma to her body meant that Ida’s corpse was preserved almost perfectly preserved within the lake bed, gradually fossilizing over millions of years. In 1983, Ida’s fossilized remains were resurrected but the significance of this find only came to light in the past week.

Ida is remarkable because her fossilized skeleton is almost 95% complete. It includes almost every bone, fur, and even Ida’s final meal – fruit and leaves. In the past, similar fossils have been found but none so exquisitely preserved. Ida’s almost fully intact frame allows researchers to address questions that have frustrated them for decades.

In particular, it offers some intriguing clues to human origins. She dates from a time when primates split into two branches – anthropoids, whose descendants include humans, apes, and monkeys, and prosimians, whose descendants include lemurs. Ida has characteristics of both groups, and may hold the key to a shared lineage.

A commonly-held view among paleontologists is that anthropoids (and therefore humans) evolved from Eosimias, whose fossilized remains have been dated to 45 million years ago.

Jørn Hurum of the Natural History Museum of the University of Oslo and Philip Gingerich of the University of Michigan, Ann Arbor, the main players in the Ida discovery, do not agree. Hurum and Gingerich believe that anthropoids arose from a more primitive group of primates called adapids.

Ida has a number of features not found in lemurs – namely a grooming claw on her second toe and front teeth arranged into a toothcomb. Furthermore, Ida’s front teeth and ankle resemble the anthropoid branch of primates. Together, these features suggest that adapids link primitive primates and anthropoids, and therefore the lineage leading to humans.

Many paleontologists are skeptical, however. Science magazine points out that Hurum and Gingerich’s analysis examined only 30 traits, where standard practice is to compare 200 to 400 traits. They quote Richard Kay, of Duke University, who says “There is no phylogenetic analysis to support the claims, and the data is cherry-picked.

Many in the science community have rolled their eyes at the manner of the announcement, which included an international press conference, publication of a book, and exclusive prime-time television special documentary. Hurum’s suggestion that “Any pop band is doing the same thing” did little to allay the criticism.

Ultimately, Ida is an important fossil and will doubtless shed considerable light on human origins. At the same time, the media blitz that accompanied the announcement seems to have tainted its significance and put critics on the offensive. Ida has changed some things – namely the debate about whether anthropoids come from the suborder strepsirrhinae or the suborder haplorrhinae. The “scientific find that will change everything”? Possibly not.