Many of us are familiar with hurricanes and the disaster they cause. This last season brought some of the worst storms ever seen, and the trend indicates more will be coming.
Not only should we be concerned with the devastation this will have on the human population, but we must turn our attention to other species as well.
So when you see this video, don’t be so surprised.
Yes, that’s right. For the sole purpose of science, researchers put lizards on a leaf blower and tried to kick them off. Turns out they are pretty good at riding along.
But, why would scientists torture innocent lizards?
Well, they really didn’t. As it seems, lizards are remarkably talented at staying put when necessary, even during high force wind events, such as a hurricane. Scientists had an incredibly hard time knocking the lizards off (and if they did fall off, there was padding in place to keep them safe).
Biologist Colin Donihue, after recently visiting small islands in the Caribbean and studying the anole lizard, was given a remarkable opportunity.
Not long after his team’s departure, two hurricanes hit the islands, both with wind speeds clocked above 200 kilometers per hour.
The team returned as soon as the coast was clear, and examined the lizards present immediately after the devastating storms.
What they found was interesting. After a quick examination, it was noted that the lizards most present after the storm had larger toepads, longer forelimbs, and shorter hind limbs than what was measured before the storm.
This gave the team from Harvard an idea. Could they replicate a hurricane like experience under a controlled setting and actually show if these traits are favorable? Since I have already shown you the video…. the answer is yes, they could.
It is thought that these traits allow lizards who live in such a climate to latch onto branches in small bushes and hold on for dear life until the storm has passed.
What makes this particular study so unique, is the chance to study a population before a large event, and immediately after. The scientists were able to directly measure the difference between the species and discover what sort of traits enhanced survival. This allows a direct measurement of natural selection, the idea of how evolution works.
While there many other possibilities besides a hurricane that could drive a lizard to have larger toepads or shorter hind limbs, the natural selection process is still present.
More importantly, this small study could provide a glance into how climate change affects species. With the heating of the oceans due to astronomically high temperatures, weather patterns change dramatically. This includes the frequency of large scale storms such as hurricanes.
With hurricanes becoming more common in the tropical areas, such as the Caribbean, this forces animals such as the anol lizard to either adapt or suffer. While it seems this remarkable lizard has developed a method to out ride the storms, and probably give them a severe advantage at rodeos if given the chance, much yet is to be discovered as to how well species adapt with the increasing temperatures, ocean acidification, and frequency of severe weather patterns.
Thank you for reading this fun, quick blog!
If you have any questions, comments, concerns, or suggestions, please email us directly or post a comment below. You can also reach out to us on Facebook and Twitter.
For centuries, one of the biggest mysteries of the human race as been aging. Through science and medicine, we have been able to increase the quality and longevity of life, but at some point we all reach an age where our body stops working and we die.
A few decades ago, scientists came across a structure within cells that appears to contribute to aging, called telomeres. Today, I want to spend time discussing what they are and the pseudo-scientific claims associated with them.
The Discovery of Telomeres:
I find the discovery of telomeres a remarkable achievement of women in science, and I want to spend a few moments discussing the brilliant scientists responsible.
In 1933, Barbara McClintock, and American biologist focusing on chromosomes and their role in the life of the cell, discovered that when the very tips of chromosomes were missing, they became “sticky” and formed with other parts of the chromosome. This phenomenon is called ring chromosomes From this work she hypothesized that there must be a structure responsible for protecting the ends of chromosomes and named them telomeres. These telomere structures would be non-coding regions of DNA that if lost, would not directly harm the cell.
Barbara McClintock later became a well renowned biologist, contributing to the understand of meiosis (division of cells producing the two sex cells, sperm and eggs), mitosis (normal cellular division) and other cellular processes. She eventually went on to earn the Nobel Prize in Physiology or Medicine in 1983 for discovering transposable elements, segments of DNA that jump from one chromosome to another. She remains to this day the only woman to receive this award unshared.
Fast forwarding to the 1970’s a man named Alexey Olovnikov learned through experimentation that DNA replication, a process necessary before a cell splits into two, occurs with an error. After each division, the telomeres cannot be fully replicated, and a small segment of telomere DNA is lost. Dr. Olovnikov further suggested that after a certain amount of cell divisions, the telomeres are lost and the cell dies.
After discovering this phenomenon, Olovnikov predicted that there should exist an enzyme responsible for correcting this mistake and re-lengthening the telomeres. He dubbed it telomerase.
Sure enough, a few years later, Elizabeth Blackburn discovered telomerase and showed it did indeed restore the length of telomeres. From this work, Blackburn received her Nobel Prize in 2009, along with Carol W. Greider and Jack W. Szostak.
With all of this research compiled together, it shows that shortening of telomeres is at least in part contributing to the aging process
How Telomeres and Telomerase Work:
The structure of telomeres is relatively unique, but simplistic in its own way. Telomeric DNA, at the very ends of chromosomes, consist of long sections of repeating nucleotide sequences. Remember, the four “letters” of DNA are A,T,C,G. In species, telomeric DNA all have repetitive sequences, but they differ slightly depending on the organism.
Most vertebrates (including humans) for example have the sequence TTAGGG. Some plants have TTTTTTAGGG.And yeast have TCTGGGTG.But all are relatively similar to each other and are repetitive.
In addition to DNA, there are also proteins involved in creating the structure of the telomere. Certain proteins bind to the telomere section of the chromosome, and provide structural support, and even wrap the DNA like a knot on the end of the rope. This complex structure thus prevents any damage that could occur from the cell (think of the aglets on the end of your shoelaces).
However, as previously mentioned, during DNA replication a small portion of telomeric DNA is lost. Once the telomeres are gone, important genomic DNA is damaged and the cell recognizes it’s time to die.
But that is not always the truth. In certain cells, telomerase is expressed to re-lengthen telomeric DNA.
Telomerase is a special type of enzyme that is made up of protein and RNA. The RNA included into the protein section will recognize the repetitive sequence, and the enzyme can then replace the missing sequences left during DNA replication.
After the discovery of telomerase, many people were interested in discovering how to use telomerase as a molecular fountain of youth. However, it was quickly realized to be quite dangerous.
Normal adult cells have low expression of the telomerase enzyme, providing a natural end point when the cell must die. Cancer cells however, need to grow without being hindered by the natural fuse telomeres provide. Therefore, they express telomerase in abundance. It is reported that 85-90% of cancers have overexpression of telomerase. This suggests that having telomerase active and available for cells may give them a predisposition to cancer, which of course would not be favorable.
Much work has been done to develop a method of lengthening telomeres including drugs, and genetic modification, with little success. Therefore, scientists have been trying to understand how environment and other events can shorten telomeres, and thus shorten our lifespan.
The Not-So Scientific Claims of Lengthening Telomeres:
For the past few years, there has been much work done trying to understand if shortening of telomeres is caused not only by regular aging, but also by stress or other life events. And so far, the data has been inconclusive.
Part of the problem is finding trends involving telomeres. There is a wide diversity of telomere length among human individuals, which it makes it difficult to study.
In turn, modelling stress is challenging, and very little work has been done to suggest telomere length is actually affected by stress. The only meta-analysis provided on stress-induced telomere shortening showed a very small decrease in telomere length with higher stress. However, there are so few studies, there appears to be publication bias. Once the bias is corrected, the trend dissapears.
This however, has not stopped the pseudo-scientific community for jumping on the bandwagon.
Hundreds of articles and pseudo-scientific experts claim that decreasing stress, changing diet, meditation, exercising, vitamins and antioxidants, herbal supplements, essential oils, and many other things can lengthen your telomeres and give you longer life.
Even Elizabeth Blackburn, the woman who discovered the enzyme telomerase, claims in her book The Telomere Effect: A Revolutionary Approach to Living Younger, Healthier, Longer that changing your lifestyle has a profound effect on lengthening telomeres and promoting longer life.
“One study has found that people who tend to focus their minds more on what they are currently doing have longer telomeres than people whose minds tend to wander more. Other studies find that taking a class that offers training in mindfulness or meditation is linked to improved telomere maintenance.”
–Elizabeth Blackburn, The Telomere Effect: A Revolutionary Approach to Living Younger, Healthier, Longer
Unfortunately, there is no evidence to support these claims.
In fact, while it seems that telomeres do in fact play a role in the aging process, we have no idea how large of a role it plays. Even if we can lengthen our telomeres back to normal levels, would it make a huge difference? Probably not as big as we think. Would there be another factor that contributes to aging once we solve the telomere problem? I/ guessing yes.
The truth is, aging is a complicated process and likely is a result of multiple factors. Telomeres do seem to be one of those factors, but only lengthening telomeres may not be enough to significantly lengthen your lifespan.
The science of telomeres is a beautifully example of science and pseudo-science. Hard work and many years have discovered a novel section of chromosomes, and has given us a deeper understanding of how cellular death occurs. Pseudo-science has then taken up the information, and twisted it to sell snake oil. So the next time someone tries to tell you about this magical product that lengthens telomeres and prevents aging, be sure to set them straight.
With that said however, I look forward to the discovering more about telomeres and their contribution to aging. It’s always nice to discover one piece of the puzzle, no matter how big or small it is. I suspect in the next few years, an update will be added to this post, it just won’t be on how to lengthen telomeres with yoga or diet.
Thanks for reading!
If you have questions, comments, concerns, or suggestions please do not hesitate to leave a comment or contact us via email at firstname.lastname@example.org.
Many of us are aware of DNA, the molecule often nicknamed our “genomic book”. Ever since the structure of DNA has been revealed, scientists have been working 24/7 to understand how it works, and how we can manipulate it.
With today’s technology, more than 60 years after revealing the structure and composition of DNA, we can mutate, add on, or take off sections of our genome and utilize it to our benefit.
Now after years of research, scientists from California have been able to take it one step further by adding letters to the book.
Before we dive into our news item, let’s take a few minutes for some background. If you have knowledge about DNA and how it encodes protein, you can skip this section:
Imagine if you will, the english alphabet (A-Z). Twenty-six letters mixed together can create millions of words. These words then come together to create stories…or blog posts.
Our genomic alphabet is comparatively small. In fact, it only has four letters; A, T, C, and G. Each “letter” is a symbol for molecules. A is Adenine, T is Thymine, C is Cytosine, and G is Guanine (note: RNA replaces thymine with uracil (U), we will not discuss this today). These molecules are commonly called bases.
These molecules pair up together to make the double stranded DNA helix we all know and love today. The two strands are bound together by bonds between these four bases. A will bind with T, and G will bind with C
These molecules make up your genes. Each gene is a long strand of the four bases, and thus affect the functionality of your gene.
Some of you may be asking, how exactly a gene works. Well, here is a quick introduction.
Take for example a sample gene we have created below
This gene is one DNA strand that will eventually turn into a protein. It is proteins that then travel throughout the cell and perform various functions that we think of as genes (eye color, hair color, etc..)
In order for DNA to create a protein, it must first be converted into RNA. RNA is very similar to DNA, with only slight differences between the two. RNA is single stranded rather than double stranded, and rather than having thymine as one of the “letters” it has uracil (U). Thus in RNA, A will bind to U. RNA is made from the template DNA strand and is complementary.
So taking our example,
The complementary RNA strand would look like this,
Once the RNA strand has been synthesized, it will be used as template to make proteins. In order to make proteins, RNA is read by another molecule (called the ribosome) that will make “words” out of the letters of RNA.
Our example RNA molecule will be read three letters at a time (commonly called codons)
UAA CAA GCC CUA AGA AGC UUU ACC
These codons then are used as a guide to make protein. Every protein is made up of 20 components called amino acids. The 3 letter words above will thus code for an amino acid to make protein (note; there have been a few other amino acids discovered, but are extremely rare and will not be discussed today). These 20 amino acids will then fold together to make complex and specific protein structures.
UAA CAA GCC CUA AGA AGC UUU ACC
Looking at the example above, we see that there are 2 codons that encode for the same amino acid. This is due to the amount of possible codons and amino acids. As mentioned, there are 20 different amino acids. With the four letters of DNA and RNA, there are 64 possible codons. Thus, multiple codons can correlate to the same amino acid in the code.
Now to our news item!
Scientists have recently been able to add two more letters into the genetic code.
Why would it be beneficial to add letters to the genetic alphabet? Going back to our book analogy, imagine if the english alphabet received an additional two letters. These letters can in turn add thousands and thousands of word to our language. These words in turn can be used in stories you read….or blog posts.
In the genetic book, adding new bases allows us to incorporate synthetic amino acids (not found in nature). Now rather than being stuck with 64 different codons, with two more bases, we now have 216 (over 3 times the amount) of codons to work with, each being able to potentially incorporate new amino acids.
This will allow us to change the structure of proteins and how they function, and thus change gene expression.
The research done by these scientists included modifying a famous protein, dubbed green fluorescent protein (GFP for short), a protein that glows a bright green color.
While the alterations made to the gene did not directly affect the function of the protein, this is just the beginning of altering our code in a new way to fight diseases and unlock more clues about the evolution of life.
It is very exciting to be at the forefront of this research. We are sure that in the upcoming months more will be revealed and utilized with this technique.The Copernicus Called crew is excited to read and share more as the research is expanded.
Callaway, Ewen. ‘”Alien’ DNA makes proteins in living cells for the first time.” Nature News. Online. https://www.nature.com/news/alien-dna-makes-proteins-in-living-cells-for-the-first-time-1.23040?WT.ec_id=NEWSDAILY-20171130&utm_source=briefing&utm_medium=email&utm_campaign=20171130
I’m sure that many of our readers know (or at least you will in a few moments) that I am a cancer researcher. It of course makes sense then that one of my first blog posts is on cancer. I also happen to study prostate cancer. This article came across my desk recently and I could not help but share it with the Copernicus Called Family.
Cancer is by far one of the largest threats that currently looming over societies head.Prostate cancer is especially worrisome, being the third leading cause of cancer deaths in the United States for males; behind lung and colorectal (colon) cancer 
That being said, being diagnosed with prostate cancer does not necessarily indicate a painful or tragic death. In fact, a recent article in The New England Journal of Medicine sought out to study exactly when treatments are necessary for prostate cancer patients……and when watching without conventional treatment may be the best option.
Although prostate cancer still is high on the list for mortality in men, many patients are diagnosed at a very early stage. Currently Stage 1 and stage 2 prostate cancer (tumor contained within the prostate, no lymph node metastasis, no metastasis to other organs) has a 5 year survival rate of 99%. That’s pretty great. And later stages of prostate cancer have a high survival rate (nearly 100%) even though the cancer has potentially spread to nearby areas (regional lymph nodes)
So, I mean, this is all pretty good news right? The only downside is of course cancer that has spread to distant areas of the body (brain, liver, bones), which has a survival rate of 29%. Not the best. 
But, fortunately many men who are diagnosed usually fall into the Stage 1 to Stage 2 category. About 4 out of 5 cases actually. 
Therefore, medical doctors are faced with the question on how to treat early stage prostate cancer.
Back in the good ole’ days, prostate cancer was considered a major issue, even at Stage 1.
Men would get checked, blood and pee would be analyzed, and then prostates would be cut. Pretty routine procedure that did indeed prevent cancer. The official term is radical prostatectomy (removing the whole prostate and neighboring tissues). There are various methods for surgery. If you would like to read more about the subject, please follow this link.
But…there’s a small problem. Side effects from a radical prostatectomy aren’t the best. These include incontinence (leaking of urine from the urethra) and incompetence (do I need to explain this one?). For a man potentially in his 40’s, the downsides of surgery are just a little bit daunting.
The best way to determine whether or not surgery should be performed regardless of the consequences, is to study whether or not it has a major effect on survival for patients.
Turns out… for the early stages of prostate cancer, we may want to hold the scalpel.
The study previously mentioned supports the hypothesis that a radical prostatectomy is just a bit overkill.
At this time it’s important to note that this study is not the only one to propose this idea. In fact, the authors of this current study published something similar four years ago.
And there have been a few other sources that favor this hypothesis.
Let’s get into this study.
731 lucky patients with localized prostate cancer were divided into 2 groups. One group received radical prostatectomy surgery, and the other received nothing but observation (medical doctors call this active surveillance or watchful waiting).
Now you may be wondering how long the study lasted. 5 years? 10 years? Well in reality, it was more like 15-16 years. Patients were randomly assigned from 1994-2002 (do not confuse this with the length of the study, this is how long they were selecting patients), and then all patients were observed until August of 2014. Quite a long time.
Well, after the study, 64% of the men had died. This may sound devastating, but we must remember that the majority of males diagnosed with prostate cancer are older, and this study has the average age at 67 years. Not spring chickens.
The researchers address this by determining the “all cause mortality” or in layman’s terms, dying from anything. What they found is that there was no significant difference in those who received treatment, and those who did not. Note: Statistical significance is extremely important in research, and this will be discussed more thoroughly in another blog.
Another powerful piece of data is the comparison of those who died due to prostate cancer rather than non-related deaths. Death by cancer occurred in 69 men, or 9.4% of those in the study. 65 deaths were attributed to prostate cancer and 4 to treatment complications.
Death due to prostate cancer occurred in 7.4% of those in the surgery group, and 11.4% in the observation group. Again the differences between the two groups are not significantly different.
Another aspect of this study that is interesting, is what the patients thought of different treatment conditions. Subjects were asked to fill out a Medical Outcomes Study 12-Item Short-Form General Health Survey (from what I can gather it’s just a fancy name for a survey to asks how patients feel about their treatment).
Overall, worry about health did not differ between groups. But, the interesting fact is that men who received surgery reported more complications due to prostate cancer or treatment, physical discomfort, and limitations to daily activities. Incontinence also was an issue with those who underwent surgery, and erectile dysfunction occurred in a significant portion of those who visited the surgeon’s table.
There is a touch more to the study, but we will not cover those in the blog today. If you are interested, and want learn more, follow the link to the study.
Now, so far I have talked about this study as if it’s the finality of the topic, but really it’s not.
One of the main issues I have with this study is the statistical significance. As mentioned above, we will discuss this in much more detail at a later time, but I can’t help but get this off of my chest now.
Officially, a set of data is considered significant if the p value is at or below 0.05. In our context, this number would suggest that the probability that those treated with surgery and those not will have different outcomes (i.e beneficial to have surgery). This suggests that there is a 5% chance that the surgery is actually beneficial to patients.
If the p value is higher than 0.05, let’s just take a hypothetical number, 0.45. This hypothetical value suggests that 45% chance that the surgery is beneficial to patients. So at that point, is it worth having the surgery, if it means that your sexual function is eliminated, or if you are forced to wear a pad due to a leaky urethra?
The p values for the study are just barely over the line of significance. For the overall mortality rates, and the prostate related deaths examined in this study, the p values were 0.06. So 6% of patients who receive treatment will have no difference in outcome based off their treatments.
Technically… by standards set, 0.06 is not a statistical significance. But it’s pretty damn close.
Let me be as clear as I can. I am not trying to change the way science works, or how statisticians evaluate data, and I am not trying to knock what the study suggests here.
But I do want our readers to be thinking. “Is this study really the final word?” I will let you, as the reader make the final decision.
That being said, I do not oppose the active surveillance treatment method. I think it’s a perfectly valid method for prostate cancer patients who are in the early stages. As more studies are performed, researchers and clinicians will be able to make the best decisions for their patients.
Thank you all for reading! I have just a few notes to add to today’s blog:
If you happen to be reading this, and you have prostate cancer or have recently been diagnosed, please do not take this blog post as medical advice. I will always recommend that you speak to your medical team and discuss the best options for your specific case. If you are seeking answers to questions, I would ask that you visit cancer.org. This website run by the American Cancer Society has fantastic information on all types of cancers (and was a great source for me writing this blog) and can direct you to assistance you may need.
And finally, since I am already on my soap box, I would like to remind everyone who is at the age for testing (whether it be prostate, breast, colorectal, or any other type) of various cancers. Please go. It is worth it. A small amount of discomfort now can prevent a lifetime of suffering. Testing is the best way to detect cancer early.
Wilt TJ, Jones KM, Barry MJ, Andriole GL, Culkin D, Wheeler T, Aronson WJ, Brawer MK. “Follow-up of Prostatectomy versus Observation for Early Prostate Cancer.” New England Journal of Medicine. 377:132-142. July 13 2017. DOI:10.1056/NEJMoa1615869. http://www.nejm.org/doi/full/10.1056/NEJMoa1615869
Featured image credit-http://www.globalpatientservice.com/prosatate-cancer.php
Most everyone has probably seen at least one installment of the Jurassic Park series. For those of you in the small population, the main plot of each movie is running away from a ferocious predator, usually a Tyrannosaurus Rex or some similar carnivorous dinosaur. The protagonist typically has the job of running, driving, or otherwise hiding to avoid being eaten alive.
Much like in the movies, the world of dinosaurs, at least in the research of dinosaurs, has thought that a T-Rex had the capability to run and catch fast prey.
Certain research articles suggest that dinosaurs like a T-Rex could run upwards to 50-60 kilometers per hour, or about 37 miles per hour(Paul, 1998). That’s pretty damn fast.
However, a recent study published in Peer J suggests that a T-Rex was actually incapable of running. In this particular study, running was defined as a gait that would be running without having both feet off of the ground at the same time, for example a horse gallop.
So with Velociraptors being the actual size of our modern turkey, and a T-Rex being unable to run, Jurassic Park may not be such a bad idea after all….Just kidding.
But how in the world can a T-Rex be incapable of running?
The study that previously mentioned a high speed for the T-Rex suggested so due to their long and strong legs and specialized hip structure. This new study indicates that the legs of a T-Rex was actually the reason why they couldn’t run. In fact, their top speed reached about 12 mph.
How can two studies contradict each other when they are looking at the exact same information?
The answer of course, is in the details.
If you get a chance to read the Peer J article (which I always recommend), the introduction focuses on previous studies and the various mechanisms used to determine speed. While we don’t have enough time to go over all of them, I figured one may be beneficial to our readers.
Gregory S. Paul published an article in 1998 suggesting that a T-Rex, with its specialized pelvis and leg structures being similar to modern tetrapods (four legged creatures), would be able to run at a reasonable pace. In case you are unfamiliar with the running patterns of different species (which I was until researching for this article), it’s important to note that a Rhinoceros, having a similar pelvic and leg structure is able to run at a reasonable pace. They are also quite large. Meanwhile, an elephant, which is more comparable in weight to a large T-Rex has a very different bone structure and is designed specifically for walking (see figure above). Elephants also have an ankle that prevents mobility (which differs from ours, a Rhino’s, and a T-Rex) and have a “flat” pelvis more similar to humans. In addition, examining the shape and orientation of the hip bones of Tyrannosaurus suggests that it is better suited to maintain the weight of its owner and can give it the ability of running.
Paul continues to discuss the correlations of femur bone length and speed where there appears to be a positive correlation between speed and the length of your thigh bone. He also goes on to discuss how bone shapes and certain structures can suggest how fast an animal is able to run.
He then focuses on other studies that suggest a T-Rex is unable to run. One in particular highlights the frailty of the leg bone, and how running could not be possible with the average weight of these gigantic creatures. Paul points out that the femur of a T-Rex may be able to support more weight than expected with these models, largely due to the thicker walls of the femur. He also mentioned discrepancies with the weight they predicted and the fossils analyzed have damage that would confound the data.
As I am sure you have noticed by now, there appears to be a slight conflict in regard to the speed of our beloved dinosaur.
So what does this new study have to say?
The Paul study we just previously mentioned, and other studies that conflict with it all have one thing in common. The research is focused only on bone morphology. All of these scientists spent time studying fossil structures and comparing them to bones of modern animals to “tweak out” clues of what life being a T-Rex was like.
But there is one aspect missing; the tissue.
Bone alone cannot work to move our limbs. Soft tissues like muscles are needed to let our bodies twist and turn. And these soft tissues can have an impact of how we can move.
Recent advances in technology have given scientists the opportunity to estimate how muscles connected to bone, and how they affected movement in extinct species. This technique is what the Peer J article primarily utilizes.
The figure above shows an estimation of various muscle structures and limb interactions might have been like for the T-Rex. By scanning the bones and calculating joint positions and range of motion, muscle structure could then be predicted.
After this, computer models can be simulated. The output from the computer simulations were able to give a maximum velocity. The answer? Eh, about 8 meters per second. The data also calculated the estimated stride of the dinosaur (at its peak about 8 meters), and the Froude number (used to compare speeds with other animals) that suggested a T-Rex can only reach a walking stride.
Additional data that focuses on the change in kinetic and gravitational potential energy also confirms that a T-Rex could not gain the energy differences to achieve a running speed.
While I think this study makes valid points, and uses technology that can estimate at a much higher efficiency than previous analyses, there is still much to weed out. Unfortunately, soft tissue does not preserve well and we most likely will not find a perfectly preserved T-Rex. However as technology increases in power, and as we work to understand how other tissues might have impacted the movement of the large dinosaurs, much more is left to be discovered. I do think this study is moving in the right direction, and gives us more information than we had previously. If you are interested in either of the articles I discussed today, the links are below. Attached here is also a link to videos the scientists produced with their program of the simulated T-Rex walking!
If you have any questions, or comments about this article or others, please do not hesitate to email us directly at email@example.com. You can also reach us through social media, at our Facebook and Twitter pages.
Plants, like many other life forms, have to adapt in order to combat the many predators that threaten their existence. Several varieties of plants have developed various techniques to prevent becoming insect feces. A brief communication published in Nature Ecology & Evolution highlights a….. unique way plants evolve to fight their little enemies.
Although most people are fascinated by plants, many are unaware of just how amazing they really are. Many plants are able to halt insects and other potential predators by developing weapons to prevent or delay consumption.
There are several types of mechanisms plants have developed, but here are a two quick examples:
Mechanical defenses– Plants utilize this mechanism by producing thorns, needles, or perhaps other other specialized structures such as waxy resins to make feeding difficult. I am sure most of you are thinking of plants like a cactus, or perhaps a thorny rose bush. Mechanical defenses are the most common type of herbivore defenses among plants
Chemical Defenses– Another technique for defense is chemical warfare. Literally. Many plants have developed complicated chemicals with complicated names (such as terpenoids, phenolics, and nitrogen compounds like alkaloids, benzoxazinoids, and many others) that specialize in destroying/inhibiting potential threats.
These molecules work to either deter the insect from eating (like inhibiting enzymes important for digestion, making consumption extremely difficult) or can possibly destroy DNA repair mechanisms in these little buggers and render them completely helpless (aka death from weird insect cancer).
Obviously, some of these chemicals are dangerous to ingest, but there are quite a few that have inserted themselves into our everyday culture, and are relatively harmless. Caffeine, morphine, cocaine (okay, cocaine isn’t exactly harmless), and nicotine all fall into this category.
Biologists call these defense mechanisms Host-Plant-Resistance or HRP for short.
Note: There are other mechanisms of defense considered in the HRP category that we will not be discussing today.
So..let’s get back to the current article. Recently scientists at the University of Wisconsin in Madison have discovered a completely novel HRP in Solanum lycopersicum or better known as the tomato plant.
In short, when the plant was exposed to a chemical secreted normally by plants in distress (yes, they can indeed “warn each other” so to speak), and then exposed to an arch nemesis, the small mottled willow moth, they found that plants who were exposed to the warning chemical had overall more biomass compared to the control plants or those who were not “cued” as well.
Plant biomass is a fancy way biologists explain how badly plants were eaten. The research team measured biomass by clipping the visible part of the plant (aka without the roots) and weighed the shrubs to compare biomass. Plants who received the highest dose of the “warning” chemical had as much as 5x the biomass compared to the non treated plants.
This data suggests that those plants who get warned properly have a mechanism to ward of those evil moths. So what exactly did the plants do?`
In case you happened to miss the title, the team in Wisconsin determined that cannibalism was at play.
Further experimentation is used to highlight the relationship between plant and insect.
Tomato plants were once again warned with the various concentrations of the chemical (or not at all), but this time they removed the leaves and fed them to the caterpillars. The team noticed that those insects fed with warned plants tended to eat dead larvae planted inside their containers sooner than the control plants.
It is important to mention at this point, that herbivores such as the lovely small mottled willow moth, will eventually eat their friends if food becomes scarce. It really is a moth-eat-moth world. But for the first time, scientists are actually seeing that plants have the possibility to trick the caterpillars into eating themselves even when they have an abundance of food.
Now, many of you may be wondering; “Why don’t all plants have a defense mechanism such as this?”
The short answer is that it’s not as easy as it seems.
Although plants may benefit from this chemical defense system, HRP mechanisms are extremely costly for vegetation. It takes a ton of energy for plants to make molecules strong enough to make fellow caterpillars look delicious. There are many plants on our planet that lack defense mechanisms. They may be potentially more exposed, but they are able to allocate energy to other important mechanisms (photosynthesis, water uptake, etc..)
As of right now specifics on the properties of these cannibal inducing molecules, and how they actually work towards influencing caterpillars to eat dead comrades is vague, at least from the news article published on Nature.com. It’s also worth mentioning that brief communications piece is not a full-fledged article. The information has not been peer reviewed and there is much left to do to piece out the details of how these species co-exist.
To wrap up: The article mentioned highlights a novel defense mechanism for plants that has previously been undiscovered by biologists. While this article is not the final word on the issue, it does create an interesting starting point for scientists to weed out specifics and potentially (a long time from now) morph this information and create potential pesticide treatments.
But let’s not get ahead of ourselves.
THANKS for reading our humble blog! Please feel free to email the crew at firstname.lastname@example.org if you have any questions about this article, previous articles, or anything you may have heard in your own travels.