Tuesday, January 30, 2018

Freezing the Winter Away

An edited reposting of an article from January 8, 2014.

During this frigid winter we can be thankful for our home heating, our layers of warm clothing, and most of all, our bodies’ abilities to generate heat. But it is times like these that make me wonder about our friends that live outside year-round… especially those that don’t generate most of their own body heat. How do they survive these periods of intense cold? There are several species of North American frogs that have an unusual trick up their sleeve: They freeze nearly solid and still live to see the next spring.

This picture of a wood frog is by Ontley at Wikimedia Commons.
Frogs are ectothermic, meaning they take on the temperature of their surroundings rather than generate their own body heat. This introduces some intriguing questions about how these species even exist in northern climates that experience freezing temperatures every year. When various North American frog species (including wood frogs, spring peepers, western chorus frogs, and a few gray tree frog species) take on freezing winter temperatures, they actually allow their bodies to freeze nearly solid. For most species, this would be a deadly approach: a frozen circulatory system would halt the delivery of oxygen to cells, which require oxygen to generate the energy they need to do just about everything a cell does. Furthermore, jagged ice crystal edges could rupture the cells they are inside. Dead cells lead to dead organs, which in turn lead to dead animals. These freezing frogs have found the secrets to freezing without killing their cells.

The first secret of the freezing frogs is to spend the winter snuggled in the leaf litter below the snow. This environment insulates and protects the frogs from the deadly wind chills we have been facing for the last several days.

The second secret of the freezing frogs is a creative use of colligative properties. Colligative properties are properties of solutions that depend on the ratio of the number of liquid molecules to the number of molecules of stuff dissolved in that liquid. One of those properties is called freezing point depression: The temperature at which a liquid will freeze can be lowered by adding particles to it. (This is why salt is spread on roads in the winter). A critical component of the freezing frog strategy is for the liver to produce massive amounts of glucose in response to the start of freezing. This glucose is pumped throughout the body, which lowers the freezing point of all of the organs.

A third secret of the freezing frogs is the use of ice nucleating agents: proteins that actually encourage freezing. This may seem counterintuitive, but remember that ice crystals inside cells can cause them physical damage. By having a high concentration of ice nucleating agents in the fluid between the cells, this ensures that ice first forms in the spaces surrounding the cells. When ice forms, the ice crystals are made of only water molecules, which draws water out of the solution and leaves behind a higher concentration of other stuff (like glucose) in between the cells. The high concentration of glucose between the cells draws water out of the cells and into that space. This additional water also freezes. In the end, the cells are chock-full of particles, lowering their freezing temperature, and are surrounded by ice, which insulates the cells. Thus, this process of ice formation around the cells prevents ice from forming inside the cells.

A fourth secret of the freezing frogs is a metabolic shift. Most animal cells rely on oxygen to produce the energy they need to support their demands. But cells have ways of producing energy without oxygen too. These ways are not very efficient, but are useful when there is not enough oxygen available to meet demand (such as when a seal dives or a cheetah reaches burst speed). When freezing frogs start to freeze and oxygen delivery to the cells slows and eventually stops, their cells shift from an oxygen-reliant system of energy creation to an oxygen-independent system of energy creation. Additionally, freezing organs do less and don’t require as much energy anyway, so they can continue functioning at low levels for a long time if the freezing spell is prolonged.

When the environment warms up (as forecasters promise will happen), the body temperatures of these frogs raise and body fluids slowly become liquid again. The heart starts to beat again within hours of the start of thawing and oxygen can again be delivered around the body. The delivery of oxygen-carrying blood helps the rest of the organs return to their normal functions.

There are still many secrets of these freezing frogs left to uncover. Maybe you’ll be the one to do it… once we thaw out a bit.

Want to know more? Check these out:

1. Storey, K.B. (2004). Strategies for exploration of freeze responsive gene expression: advances in vertebrate freeze tolerance Cryobiology, 48, 134-145 DOI: 10.1016/j.cryobiol.2003.10.008

2. Layne, J.R., & Lee, R.E. (1995). Adaptations of frogs to survive freezing Climate Research, 5, 53-59 DOI: 10.3354/cr005053

Tuesday, January 23, 2018

Body Clocks: What They Are and How They Work

Lately, with the new year, the #TimesUp movement, awaiting Disney’s movie A Wrinkle in Time based on one of my favorite childhood book series, and just watching my children grow faster than I thought possible, I have been thinking a lot about time. The continuous march forward, the constant rotation of the planet, and the revolution of the Earth around a distant star in its determined path all have far-reaching effects on our physiology and behavior. Our biological clocks affect everything from our sleep-wake cycles to our fertility to our mental and physical health. And it’s not just us that have them: Every living thing on Earth, including bacteria, protists, fungi, plants and animals, has them. But what do they do and how do they work?

A sleepy ferret minds his biological rhythms. Photo by Kimberly Tamkun at Wikimedia Commons.

Generally speaking, a biological clock is an organism’s inborn way of regulating its functions with respect to time. Many of these biological clocks follow circadian rhythms (changes that follow a 24-hour cycle). Vast portions of our planet have been exposed to dramatic but mostly predictable environmental changes on a 24-hour cycle since long before life existed, so it makes sense that us lifeforms have developed a means to make the best of those changes: sleeping when food is less available, having higher metabolisms when we are active, being more alert during times we are most likely to be interacting with the world.

Diagram of a human circadian rhythm by YassineMrabet at Wikimedia Commons.

Melatonin is a hormone widely known to synchronize circadian rhythms in vertebrates (animals with backbones) to the light-dark cycle of the day and night (or to an indoor room with a light timer). Melatonin is produced in response to darkness, and the longer the night, the more melatonin is produced. Rising and falling melatonin levels help determine sleep-wake cycles in animals. In animals that breed seasonally, the changing peaks of melatonin levels that correspond with dark nights getting longer or shorter stimulate the reproductive system to help synchronize breeding physiology and behavior with the seasons. Although we have known about melatonin and its effects for nearly a hundred years, we are now learning that it seems that all organisms, including bacteria, protists, fungi, plants and animals, make it. Whether it has the same effect in all organisms is yet to be determined.

In vertebrates, melatonin is produced by the pineal gland, a small structure in the center of the brain. In birds, reptiles, amphibians and fish, the pineal gland has light-sensitive cells that receive light as it passes directly through the skull and the brain! In mammals, the pineal gland receives a light signal through a more complicated pathway: Light is detected by light sensitive cells in the retinas of the eyes. They send this signal to the suprachiasmatic nucleus (SCN) in the brain, which relays it to other brain areas and then to the pineal gland. The SCN in mammals is commonly called “the master clock” due to its important role in synchronizing body rhythms with light cues.

Diagram of the human brain and the SCN by the
National Institute of General Medical Sciences at Wikimedia Commons.

Body rhythms are determined at the cellular level through the interaction of a small number of genes called clock genes. Clock genes have been found in every animal, plant and fungus studied so far. Originally, it was thought that in mammals, clock genes would only be found in the SCN. However, it now looks like clock genes are active in all cells and the SCN functions more like an orchestra conductor synchronizing the rhythms of the organs throughout the body.

Many clock genes have been discovered, and they all seem to work based on similar processes. Just last year, scientists Jeffrey Hall, Michael Rosbash, and Michael Young, were awarded the 2017 Nobel Prize in medicine for their research on clock genes in fruitflies. They found that biological clocks are self-regulated within the cell: Morning sunlight turns on a gene called the PERIOD gene, which starts to produce a protein called the Period protein. As long as there is light, Period protein accumulates to higher and higher levels. Another protein, named Timeless, shuttles Period proteins into the nucleus, where the DNA lives. The Period proteins shut down the activity of the PERIOD gene, while a third protein, called Doubletime, regulates the destruction of the excess Period proteins. The result of this process is that by nightfall, Period proteins have disappeared and sunlight is needed to start the cycle anew. This work by Hall, Rosbash and Young inspired a whole new field of molecular biology of circadian rhythms.

We have a lot more to learn about biological clocks and circadian rhythms, but what we do know is that their effects are wide-ranging. Whacky circadian rhythms have been implicated in sleep disorders, depression, bipolar disorder, cancer, obesity, and diabetes. And what else will we learn about them? Only time will tell.

Tuesday, January 16, 2018

The Bed Bug’s Piercing Penis (A Guest Post)

A reposting of an article by Rachael Pahl on January 26, 2015.

Sex is a dangerous, but necessary, part of life. Across the animal kingdom, there are a multitude of things that can go wrong. You could be injured in a fight by someone who wants to steal your mate, or maybe your partner eats you because you’re taking too long. Either way, nature must have a pretty good reason for the traumatizing effects of sex.

A male bed bug traumatically inseminates a female. Image by
Rickard Ignell at the Swedish University of Agricultural Sciences
posted at Wikimedia Commons.

Bed bugs have a particularly risky way of having sex. When a male bed bug wants to mate, he will pierce the female’s abdomen with his penis (called a lanceolate) and release sperm directly into her body cavity. Talk about forceful! This mode of reproduction in bed bugs is known as traumatic insemination; aptly named.

With what seems like a horrific way of reproducing, it’s hard to imagine that there are any benefits for the female. I’m sure you can come up with a plethora of things that could go wrong: infection, damage of major organs, bleeding, even death. Researchers Ted Morrow and Göran Arnqvist with Uppsala University in Sweden, argue that the female has a counter-adaptation to this antagonistic strategy. The area of the abdomen that the male pierces has been modified into a pocket lined with specialized tissues to prevent serious damage to the female. This area is termed the spermalege. Edward and Göran hypothesized that sex is not harmful to the female if the spermalege is punctured, but can be dangerous if any other area is pierced. They also hypothesized that more mating occurrences and improper punctures would reduce the lifespan of the female.

To test their hypotheses, Edward and Göran observed the number of times a female was inseminated and where she was pierced (on the spermalege or somewhere else). They had two set-ups to observe mating rate: (1) a female was placed with four males where lots of mating would take place and (2) a female was placed with four males, three of which had their penis glued to their abdomen so that they could not mate. These two set-ups allowed the researchers to observe the differences in female life span between those who had a high mating rate and those who had a low mating rate. Then, the researchers wanted to see where the female was being pierced and how that affected her life span. In addition to traumatic insemination by male bed bugs, the researchers used a pin to pierce the spermalege or an area outside the spermalege and then compared the damage.

The study produced two big results. First, females who mated more had a shorter lifespan than those who mated less. This was because the sperm and other fluids deposited caused an immune response as they were seen as foreign objects; too much of these foreign substances can have negative effects on the organism. Second, females that were pierced through the spermalege lived longer than those who were pierced outside the spermalege, suggesting that the spermalege functions to reduce damage and/or infection during insemination.

So what are the benefits of traumatic insemination and how does the spermalege reduce the costs to the female? Well, there is a lot of paternal ambiguity in the animal kingdom. The direct deposition of sperm into the abdomen may ensure paternity by getting the sperm as close to the ovaries as possible before another male bed bug can mate with her. This method also reduces courtship time and avoids female resistance, meaning that other males may not have the chance to steal the female away. The spermalege protects females from traumatic insemination by localizing damage to one area that can easily repair itself. Since the spermalege is lined with cuticle, it prevents the leakage of blood and sperm from the wound. The spermalege may also function to prevent entry of pathogens into the bloodstream. In the end, this traumatic insemination is no more dangerous than any other kind of sex, however painful and horrible it sounds. It may even be less risky if done correctly.

For more information, check out:

Morrow, E., & Arnqvist, G. (2003). Costly traumatic insemination and a female counter-adaptation in bed bugs Proceedings of the Royal Society B: Biological Sciences, 270 (1531), 2377-2381 DOI: 10.1098/rspb.2003.2514