By Natalie Rossington Have you ever been tricked by a plant? Played by a less complex organism? Ha. No, of course not you are thinking, as you munch on your tasty apple or your juicy tomato. Wrong. We’ve been tricked by that little innocent apple tree or tomato plant for thousands of years. It seduced us by producing something tasty, so we took it out of the harsh wild environment where it faced competition for water, light, nutrients, space and lovingly planted it where we could irrigate it and give it fertilizer. It’s living the good life now. Soon enough, we were planting whole fields of these things, spreading their seeds around the world, and making reproduction a walk in the park. Sound familiar? If you lean real close you can hear these cultivated plants snickering or quietly (yet evilly) laughing at you.
Keanu just realized what's really going on.
Now, I know you feel a bit embarrassed because you never quite realized what’s really going on in the relationship between you and agriculture, but I guarantee you are not as embarrassed as the insect pollinators of the orchid genus Ophrys. They are duped in a completely different way. This little orchid flower produces a powerful concoction of chemicals that exactly replicate female pollinator sex pheromones. These pheromones secreted by the orchid combined with some modified floral hairs and blue-colored patch on the fused flower petals (or labellum) create a sex-driven craze among male pollinators. In their valiant attempts to mate with the flower (aptly called “pseudocopulation”), the males are doused in orchid pollen (Schiestl et al., 1999). And because the insect is not so smart, it flies off to have sex with another flower and has now effectively pollinated the orchid. Those sneaky devils. As the second largest plant family in the world with about 22,075 species, the diversity within Orchidaceae is astounding. This diversity is maintained by pollinator specificity among the orchids. This means each orchid species is pollinated by a different species of insect (Mant et al., 2005). Species in the genus Ophrys produce chemical compounds to attract male pollinators and each orchid produces a different combination of chemical compounds to attract a specific insect (Schiestl et al., 2000). This kind of relationship creates incredible floral diversity - take a look at the images below. If you squint your eyes or take off your glasses, even to us these flowers look like wasps or bees.
You don't even have to squint to see the "insects" in some of these flowers, amazing! From left to right: O. speculum, O. umbilicata, O. insectivfera, O. fuciflora, and O. apifera.
Why do these orchids do it? What kinds of chemicals do they secrete? How do the chemicals trick these horny pollinators? We will address and answer these three questions about these special little flowers.
Whoa guys, wait your turn.
Why do they do it?The fundamental reason these orchids (and plants in general) seem so sneaky (yet so crafty) is they can not move. How do you have sex if you can’t move? You must reward or trick someone to do it for you. Some plants provide a sugary nectar to reward pollinators such as birds, bats, and butterflies. Others, like Ophrys, found a more efficient way that secreting costly nectar to attract pollinators and simply swindle pollinators into doing their dirty work.
What kinds of chemicals do the orchids secrete? In order to elicit the "pseudocopulation" response from male pollinators, the orchids secrete electrophysiologically active chemical compounds from their flowers and, to a lesser extent, their leaves.These active compounds, or pheromones, are volatile and change the behavior of the pollinators. To compare bouquet of compounds produced by female pollinators and orchids,researchers used gas chromatography to create a kind of chemical fingerprint of compounds present. These two fingerprints are remarkably similar in both type and quantity of the compounds. The fingerprints also showed the compounds consist of a variety of hydrocarbons like docasene and farenosol (Schiestl et al., 2000). Some orchids produce up to 100 different compounds to attract male pollinators (Ayasse et al., 2001)!
Chemical fingerprints of pheromones present on female
pollinators (a) and Ophrys (b) are remarkably similar.
Adapted from Schiestl et al., 2000.
How do the chemically active compounds trick these horny pollinators? Insects such as bees and wasps detect pheromones through pheromone receptors in their antennae. The detection of pheromones causes an electrical signal that is relayed to the insect’s brain. The electrical signal due to the reception of the pheromone elicits a sex-crazed response among male pollinators and pseudocopulation ensues (Ayasse et al. 2001; Schiestl et al., 2000).
I hope you have gained an appreciation for the amazing creativity and problem solving skills present in the plant world, especially amongst the orchids. I leave you, again, with a video narrated by the great Sir David Attenborough who has led us around the world (in the same light blue shirt and khakis) to explore the awesomeness and oddities present on our Earth. He, of course, tells the story of Ophrys better than me and uses awesome words like “bamboozle” to describe the relationship between orchid and male pollinator.
References:
Ayasse, M., R.J. Paxton, and J. Tengo. 2001. Mating behavior and chemical communication in the order Hymenoptera. Annual Review of Entomology 46: 31-78.
Mant, J., R. Peakall, and F.P. Schiestl. 2005. Does selection on floral odor promote differentiation among populations and species of the sexually deceptive orchid genus Ophrys?. Evolution 59: 1449-1463.
Schiestl, F., M. Ayasse, H.F. Paulus, C. Lofstedt, B.S. Hansson, F. Ibarra, and W. Francke. 1999. Orchid pollination by sexual swindle. Nature 399: 421-422.
Schiestl, F., M. Ayasse, H.F. Paulus, C. Lofstedt, B.S. Hansson, F. Ibarra, and W. Francke. 1999. Sex pheromone mimicry in the early spider orchid (Ophrys sphegodes): Patterns of hydrocarbons as the key mechanism for pollination by sexual deception. Journal of Comparative Physiology 186: 567-574.
Time to explore the
eye; not the senses, but rather something deeper. Class, today we’re going into
the tear ducts to explore how and why we cry.
-Miss. Frizzle
Heat pulsating, heart rate accelerating, chest tightening, throat
clenching, nose burning, eyes watering. “Don’t cry. Only babies cry,” you scold
yourself. A nearly silent sob seeps out—then the waterworks come like a dam
broken causing an uncontrollable flood. Many of us have been there…embarrassingly
crying over something we look back on (sometimes defensively) as “not a big
deal” and wonder why we cried about it. Whether it is the puppy and horse Budweiser commercial or the end of
Toy Story 3, or on a more serious
note at the loss of a loved one, some things just pull on our heart-strings more
than others. We also may be extremely stressed with
cortisol furiously pumping through our veins. Or we may have been
sleep deprived. The list goes on...
The act of crying is not just for sissies; tears serve a multitude of functions. There are three types of tears:
1.Basal
tears act as a protective lubricant
by preventing desiccation so the eye and eyelids can move.
2.Reflex
tears occur an involuntary response to an irritant such as the chemicals
released into the air from slicing those pesky onions. A signal is sent to the
brain which allows the tear duct response of releasing tears to clean the eye.
3.Emotional
tears of sadness or joy can signal to others to elucidate our true feelings
and sincerity.
(aside from fake crying of course). The signal is one of need, appeasement, or
attachment. It shows our vulnerability and lets others know our emotions are
overwhelming us so much that they are literally flowing out of our body. Wait,
WHAT?!?
While reflex tears have been shown to be composed of mostly
water, emotional tears have high levels of adrenocorticotropic hormone (ACTH)
which is a hormone or chemical messenger that is linked to high stress
levels. So when a person consoling you says “let it all out,” there may be
some justification to this if we do indeed 'cry out' our stress, but little is
known about release theory.
But Miss. Frizzle,
where do tears come from? And why do we sometimes laugh when we’re happy?
Formation of Tears
The hypothalamus, important for bodily functions
like sleep regulation, appetite, and reproduction, is incapable of distinguishing
whether we are feeling happy, sad, overwhelmed, or stressed when it receives a
strong signal from the amygdala. The amygdala then activates the autonomic
nervous system (ANS), which results in involuntary body functions that we have
no conscious control over. As you probably know, the ANS is composed of the
sympathetic ("fight-or-flight") and parasympathetic
("rest-and-digest") sectors. In the sympathetic response, the
hypothalamus activates the body during times of stress (e.g. release of glucose
into the bloodstream, increased heart rate, etc.). The parasympathetic nervous
system (PSNS), on the other hand, has a calming effect and is connected to our
lacrimal glands, or tear ducts. When the neurotransmitter acetylcholine binds to
receptors and activates the PSNS, one response is tear production.
Additionally, the reason for a runny nose while crying is that tears flow
through canals that drain into the nose. Here is a zoomed in view of the
lacrimal gland:
a. tear gland / lacrimal gland
b. superior lacrimal punctum
c. superior lacrimal canal
d. tear sac / lacrimal sac
e. inferior lacrimal punctum
f. inferior lacrimal canal
g. nasolacrimal canal
Crying as
Communication
Mothers, for instance, penguin mamas
can pick out the vocal signature cry (a call rather than emotional tears, which are only produced by humans) of
their offspring from great distances. This ability has the important
evolutionary purpose of allowing the mother to nurture its own young. This gives the baby the greatest likelihood of survival to
thereby improve the mother and child’s fitness. Tears are also used to signal
to others to show vulnerability, solicit sympathy, and advertise trust and
need for attachment. We often cry when
we feel powerless and that we can’t change the circumstances of a bad
situation. In essence, crying increases communication effectiveness and
also our chance of survival. For instance, looks of sadness without tears could
be confused with looks of awe or puzzlement, as shown in a study when
participants looked at photos of real people crying with the tears digitally
removed (thanks Photoshop!).
Who would have thought crying could actually sometimes
increase fitness rather than merely be a sign of weakness? The trade-off,
however, is that crying blurs our vision and often leaves us in an
unaggressive, helpless state. Conversely, tears of joy often during extreme
bouts of laughter act as social signals to strengthen bonds with people close
to us.
Males &
Females: A Disparity in Crying
Crying is a gendered activity; women generally cry more often than men. Social
constructs deem women allowed to cry, especially during that time of the month, and deem men less masculine and mentally
weak when they cry. Countless studies have shown that men and women perceive, process, express, and experience
emotions differently. Of note, there
is fMRI (functional Magnetic Resonance Imaging that uses strong magnetic fields and radio waves to form
images of the body and brain)
evidence that women’s neural hardwiring predisposes them to effectively process
infant laughter and crying.
Other findings show that women are more empathetic, sensitive, and inclined to express their own emotions to conspecifics, or those of the same species. Furthermore, women often are better at understanding non-verbal indicators of emotions (e.g. facial expressions). Evolutionarily speaking, this motherly wiring is vital for parental care because it gives moms the edge when it comes to recognizing and then comforting their offspring or others in times of need.
And what about those
days when everything seems to set us off as if our eyes are leaky faucets
(girls, you likely know what I’m talking about)? Blame it on the hormones! Increased
crying could coincide with higher levels of the ovarian steroid hormones, progesterone and estradiol.
These steroid sex hormones are implicated to exacerbate PD, or Premenstrual Distress
associated with loneliness, crying, and skin blemishes. In a study conducted by
Stoddard and colleagues, women who exercised moderately reported lower pain
symptoms, and had lower peak estradiol and progesterone levels than did
sedentary women—just another reason why exercise is so important.
Case Study:
Pathological Laughing & Crying
Some people have a neurodegenerative disease called amyotrophic lateral sclerosis (ALS or Lou Gehrig's Diseasenamed after the Yankees baseball player). ALS can involves pathological (caused by
disease; extreme
in a way that is not normal or that shows an illness or mental problem) laughing and crying due to a dramatic
disorder of voluntary emotion regulation. The terms in the acronym ALS can be broken down into “no muscle
nourishment”+ “at the sides ” (referring to areas in a person's spinal cord where portions of the motor neurons that
signal and control the muscles are located) + “hardening of tissue.” Simply, ALS is a motor neuron disease that is a disruption of brain systems involved in
generating and/or regulating emotions via neurological injury, yet the exact
mechanism is not fully understood. Symptoms include uncontrollable outbursts of
crying and/or laughing among other things such as increasing muscle weakness, especially
involving the arms and legs, speech, swallowing, or breathing. Muscles stop
receiving messages from motor neurons and begin to atrophy, or shrink.
Olney and colleagues studied patients with pathological laughing and crying due to ALS and
those with ALS but no pathological laughing or crying. They quantified emotion
with self-reported emotions, video recordings of facial reactivity, and
peripheral physiological responses (skin conductance, heart rate, and somatic
activity). These outburstswere shown to be much more normal than
often portrayed in previous literature, although the ability to stop during an
episode is sometimes inhibited. Can you imagine the embarrassment you would
experience if you could not help laughing at a funeral? How terrible! They proposed that this disorder may be
due to dysfunction in frontal neural systems that support voluntary regulation
of emotion. In sum, we cry for many reasons. There is more research to be done on how we cry, especially on how stress influences crying behavior. Thanks for reading!
WOW! Crying is way more complicated than I thought. Now I feel like I know a
lot more about different types of tears, hormonal and neuronal crying control, and even evolutionary reasons for crying. THANKS MISS. FRIZZLE!!
References
ALS Association.
2010. http://www.alsa.org/about-als/what-is-als.html Hasson,
O. 2009. Emotional tears as biological signals. Evolutionary Psychology
7:363-370. Olney, N.T., M.S. Goodkind, C. Lomen-Hoerth, P.K. Whalen, C. A.
Williamson, D.E. Holley, A. Verstaen, L.M. Brown, B.L. Miller, J. Kornak, R.W.
Levenson, and H.J. Rosen. 2011. Behaviour, physiology and experience of
pathological laughing and crying in amyotrophic lateral sclerosis. Brain 134:3458–3469. Proverbio, A.M., A. Zani, and R. Adorni. 2008. Neural markers of a greater female responsiveness to social stimuli. BMC Neuroscience 9:56-65.
Romans, S.E. and R.F. Clarkson. 2008. Crying as a gendered indicator of
depression. Journal of Nervous & Mental Disease 196:237-243.
Searby, A. and J. Pierre. 2005. The double vocal
signature of crested penguins: is the identity coding system of rockhopper
penguins Eudyptes chrysocome due to
phylogeny or ecology? Journal of Avian Biology 36:449-460.
Stoddard, J.L., C.W. Dent, L. Shames,
and L. Bernstein. 2007. Exercise training effects on premenstrual distress and
ovarian steroid hormones. European Journal of Applied Physiology 99:27–37.
Some people say that runners who seek out ultramarathons are crazy.
They insist that it’s a form of masochism where mentally deficient athletes go
to destroy their bodies. The physical toll of exerting oneself over 30, 50, 60,
100 miles at a time is enormous. Consider the energetic demands: a
study on energy expenditure during the grueling Western States 100-mile
Endurance Run in California (originally designed as a horse race over big
mountains, occasional snow, rivers, hot valleys, etc.) found that the race
required over…drumroll please…13,000 kCal!
Obviously, energetic demands are not the layman’s only deterrent from
ultramarathons. A long-term monitoring project, known as the Ultrarunners
Longitudinal TRAcking (ULTRA, but they’re reaching on that one) study, has been
following approximately 3,000 volunteers for the past few years and found some
interesting results. (The use of the prefix “ultra” gets some flak due to the
notion that these runners are in some way above and beyond normal runners. I
will use it because it is convenient.) Some basic findings are that injuries were
common (about 77% of participants), especially stress fractures and knee
problems, and silly young runners got the majority of the injuries. There were
also many reasons why these ultrarunners ended up in the hospital after events, including
dehydration, heat exhaustion, skin lesions, fractures, and concussions. So, why
do it?
I would join the camp of people who insist that it is more about
strategy, like a game of chess: figure out what your body really needs and what
it thinks it needs, then coax it further with mental games. This is
based on the theory that we unconsciously hold back during exercise to prevent
fatigue and physical harm. Athletes are realizing more and more that with a
calculated approach to figuring out what the body really needs and when you
can keep it satisfied and draw the most potential from its obstinate frame.
Doctors have done a wonderful job finding out what endurance athletes
really need. Volunteers have been stopping occasionally to donate some blood to
science whilst casually jogging or biking for 24 hours at a time, allowing us
to see in real time the measures our body takes to preserve itself. First of
all, our metabolism goes through certain shifts in fuel sources during the
prolonged exercise. The initial energy source is stored in our muscles as
creatine phosphate. This gets broken down quite rapidly, acting as more of a jump starter
than a battery. At the right pace, our bodies shift into aerobic metabolism
where we require oxygen to break down carbohydrates like glucose and glycogen, our
primary energy storage molecules. Without constant supplementation, we will
deplete these stores in about two hours. This would be okay if we were world-class
marathon runners. And if we were only talking about marathon distances.
(http://tinyurl.com/kpvlxxb) Marathon world record
holder William Kipsang at the Berlin Marathon. No, not the fool in the fluorescent
shirt. The other guy.
Studies show that around this time our fats start to kick in. These
hold quite a bit of energy, but not as much as carbohydrates and they require
us to slow down to much lower exercise intensities. However, they are extremely
important for keeping blood glucose concentrations relatively stable. Then
what? Of the major macromolecules, we’re still missing nucleotides (nope, ATP burns up lickety split) and…protein! Protein metabolism has actually been shown to offer
only a small amount to our energy budget, partly because proteins are important
to every other function and their loss affects us in a multitude of ways.
(Immediate body mass loss is one of these losses, but over 100 miles, who
wouldn’t want to be a bit lighter on their feet? I call that a win.) In fact, a
reliance on protein breakdown puts recovering ultrarunners in a negative energy
balance for several days following an event while a disappointed body cleans up
the mess. Any decent endurance athlete understands that the only way to stave off this process is to take in the right combination of nutrients while on the move.
Exercise physiologists also point to other signals of bodily stress
over the course of ultra-endurance events. As I mentioned before, the Western
States race ranges from freezing temperatures to 100oF while runners
contend with a combined elevation gain of approximately 17,000 feet. As if
running 100 miles on flat ground wasn’t hard enough.
(http://www.wser.org/course/maps/) Western States Endurance Race elevation profile. Meh. Looks like a lot of downhill to me...
Now picture yourself sweating throughout this event. Depending on
intensity and ambient conditions, the rate of sweating would be between 1 and
2.5 liters per hour. If this race takes you 24 hours (you actually get a
special prize if you do in this race…a belt buckle) that means you’ve sweat
between 24 and 60 liters. Losing this kind of fluid without replacement can
lead to fatal dehydration, but misjudging the ratio of water to electrolytes
(sodium, potassium, magnesium, etc.) can also lead to potentially fatal
hyponatremia. This makes calculated rehydration a tricky, but vital, business
over the race duration.
(http://tinyurl.com/aoykums)Yeah.
Other signs of the grueling physical effects include the inflammatory
response. Skeletal muscle damage from the excessive weight-bearing muscle
contraction does not go unnoticed in the body, and boy is there a lot of it. Creatine
Kinase (CK) in blood plasma is the most direct measurement of muscle damage,
and a recent study during a 24-hour race showed up to a 70-fold increase in CK
activity in their participants. (Melodramatic people like to compare the amount
of CK triggered by these endurance events to that spurred by a severe heart
attack, though this is flawed since the heart contains its own specific subset
of CK.) This kind of damage incurs quite an immune response. These participants
doubled their white blood cell count, likely stimulated by the 30-fold increase
in the inflammatory mediator interleukin-6 (IL-6). While IL-6 increased during
the race and stabilized, one of its functions is to induce high-sensitivity
C-reactive protein (hsCRP), which induces anti-inflammatory cytokines and
recognizes damaged cells for removal. How much did hsCRP increase? Well, after
showing up around marathon-distance, it increased exponentially to over 20
times its original amount by the end of the 24-hour race.
Even before reading this, many people would agree that ultrarunners
are completely mental. In some respects, they’re right. We all experience
mental fatigue. Consider your exhaustion after a long drive during which,
physically, you’re really just sitting in one spot. The reality is that fatigue
from mental exertion activates the anterior cingulate cortex (ACC) of your
brain, which just so happens to also be related to the perception of effort
during exercise, even enough to affect autonomic body systems—ones which we
don’t consciously control—like respiration and heart rate. This means that both
the physical and mental effort involved in endurance events (most people get
mentally fatigued just trying to stay awake for 24 hours!) recruit brain
signals that influence your decisions about whether to keep moving or not. This
contradicts the previously held notion that fatigue sets in only when the
muscles’ demands for oxygen and fuel can no longer be met. In reality, you unconsciously guard your body to ensure that when you reach
that finish line you don't actually give 100%, keel over, and Rest In Peace.
(http://tinyurl.com/kmpqzja) RMT device. What’s wrong with a straw?
So, with an event like the Western States 100, why doesn’t our brain
want us to stop earlier? Well, it does. But you want that post-race barbeque, beer, and belt buckle.This is where strategy becomes crucial.
The numerous studies on physiological changes during endurance events provides
a list of carefully calculated ins & outs to prevent dehydration,
hyponatremia, renal failure, etc. and cope with the stress. However, the mind
needs some tricking. A new hype is Respiratory Muscle Training (RMT), using a device which was supposed to increase oxygen capacity but didn’t really work that
way. Instead, researchers found that the training reduced perception of effort during
exercise without any significant physiological changes, suggesting that there
may have been a desensitization of the brain’s feedback mechanism, thus
prolonging high-intensity exercise.
Other studies have attempted to separate the sensations that alert the
brain to physiological effort from the psychological effort required to fight
back and drag on for another mile. They found that the brain’s dorsal posterior
insula may be the receptor for the body’s afferent alerts, which then will be
processed into the overwhelming sense of fatigue that we feel in the right
anterior insula. Don’t worry: all of these parts of the brain will come together
soon.
In practice, ultrarunners don’t care where the signals are, just that
they’re there. They try mental workouts to strengthen their resistance to
mental fatigue, all-nighters and sauna workouts to simulate race conditions,
preparatory workouts on courses to improve their task familiarity, Zen
practices for improved mind control, and, of course, the carefully calculated
cocktails of fluids to keep the brain working smoothly. In general, training is
the most reliable way to improve endurance. Just like the RMT (um…breathing
practice) the brain will become accommodated to long, stressful workouts as it
realizes “Hey, I didn’t die!” Beyond this training, we are pushing into the realm where the mind can also be tricked. In 2009, Chambers et al. showed
that simply swishing some liquid with carbohydrates, sweet or not, and then spitting it out stimulated areas of the brain involved in the reward and regulation of physical
activity, including both the insula and the anterior cingulate cortex that we saw earlier! Furthermore, they gave
some athletes a placebo and others carbohydrates, and those swishing the
carbohydrates (not even swallowing them) completed a timed course significantly
faster than those with the placebo.
Take one look at the video below and you'll see that there's very little that endurance athletes want to stop for. This research makes the prospect of tricking the brain
into allowing increasingly more hazardous endurance events a reality. For
athletes who constantly want to push the fringes of what the body is capable
of, that is an extremely exciting opportunity. After all, what possibilities open up without the brain's panicked signals to slow, be careful, or stop?
References:
Chambers,
E. S., M. W. Bridge, and D.A. Jones. 2009. Carbohydrate sensing in the
human mouth: effects on exercise performance and brain activity. The Journal of Physiology 587:1779–1794.
Dumke
C.L., L. Shooter, R.H. Lind, and D.C. Nieman. 2006. Indirect calorimetry during ultradistance
running-a case report. Journal of Sports Science and Medicine:692-698.
Edwards,
A. M. 2013. Respiratory muscle training extends exercise tolerance without
concomitant change to peak oxygen uptake: Physiological, performance and
perceptual responses derived from the same incremental exercise test:
Respiratory muscle training efficacy. Respirology18:1022–1027.
Hoffman,
M. D., and E.Krishnan. 2014. Health and exercise-related medical issues
among 1,212 ultramarathon runners: baseline findings from the Ultrarunners
Longitudinal TRAcking (ULTRA) study. PLoS
ONE 9:e83867.
Kreider,
R. B. 1991. Physiological considerations of ultraendurance performance. Integrative Journal of Sport Nutrition, 1:3–27.
Marcora,
S. M., W. Staiano, and V.Manning. 2009. Mental fatigue impairs physical
performance in humans. Journal of Applied
Physiology 106:857–864.
Noakes,
T. D. 2012. The central governor model in 2012: Eight new papers deepen our
understanding of the regulation of human exercise performance. British Journal of Sports Medicine 46:1–3.
Noakes,
T. D., J. E. Peltonen, and H. K.Rusko. 2001. Evidence that a central
governor regulates exercise performance during acute hypoxia and hyperoxia. Journal of Experimental Biology 204:3225–3234.
Waskiewicz,
Z., B. Klapcinska, E. Sadowska-Krepa, M. Czuba, K. Kempa, E. Kimsa, and D. Gerasimuk. 2012. Acute metabolic responses to a 24-h ultra-marathon race
in male amateur runners. European Journal
of Applied Physiology 112:1679–1688.
If you haven’t had a chance to
visit the monarch butterflies clustered on the trees in Pismo Beach, now is the
time. Monarchs cannot survive cold winter temperatures so they
migrate to warmer areas. From October to late February, all monarchs east of
the Rocky Mountains migrate to Mexico and those west of the Rockies spend the
cooler months clustered by the hundreds and thousands in groves of trees. As of
February 4th, the current population count for the Pismo beach
population was estimated to be around 20,000.At some point in your youth you learned about the butterfly life cycle and the
amazing process of metamorphosis. But did you ever think about what actually
happens during the process of metamorphosis? I bet you just think that the
caterpillar wraps itself in a cocoon and wakes up as a butterfly. Although that
is partially true, the actually mechanisms that take place before the butterfly
emerges from its pupa is complex, mystical, and not very well understood.
First, let’s take a
look at the 4 basic stages of the butterfly life cycle.Adult female butterflies (in this case
we’ll look at the Monarch, Danaus
plexippus) lay eggs on the underside of a milkweed plant. A
monarch butterfly egg is the size of a pinhead and the caterpillar that hatches
from this tiny egg isn't much bigger but it will grow up to 2 inches in
several weeks. They eat the leaves of the milkweed plant and split their skin,
or molt, many times as they grow. Once the caterpillar is full-grown it stops
eating and pupates. There is a common misconception that caterpillars crawl into or surround themselves with the chrysalis but that is not the case. As
their final molting stage, caterpillars grow the chrysalis beneath their wormy
skin and molt not into a bigger caterpillar, but into a chrysalis. The
chrysalis that comes out from under the skin is soft and wet, but hardens over
a few hours. The third stage is the transition
stage and lasts for about 7-10 days (Oberhauser & Solensky, 2004). In the
case of monarchs the pupa, or chrysalis, is suspended under a branch or leaf. It
may look like nothing is going on but big changes are happening inside. Special
cells that were present in the larva are now growing rapidly. They will become
the legs, wings, eyes and other parts of the adult butterfly. Many of the
original larva cells will provide energy for these growing adult cells. When
the adult butterfly emerges from the pupa it enters into the fourth and final reproductive
stage. The adult stage is what most people think of when they see a butterfly. They no longer have tiny eyes and stubby legs but instead have
long slender legs, compound eyes and the ability to fly.
I want to
focus on some of the amazing discoveries that occur during stage three of
metamorphosis, the pupa. This is the most complicated stage of metamorphosis
and little is known about the process by which a caterpillar emerges as a
butterfly. The word metamorphosis is a Greek word meaning transformation or change in shape. Insects
have two common types of metamorphosis. Grasshoppers, crickets, dragonflies,
and cockroaches have incomplete metamorphosis. The
young (called a nymph) usually look like small adults but without the wings
(Baluch 2011). Butterflies, moths, beetles, flies and bees have complete
metamorphosis. The young (called a larva instead of a nymph) is very
different from the adults (Baluch). Massive structural development occurs
during complete (Pelling, et al., 2009) metamorphosis.
As I
mentioned before, metamorphosis is a bit of a mystery but all you really need
to know is that there is a lot of GOO. Dr. Lincoln Brower at Sweet Briar
College studies the overwintering, migration and conservation biology of the
monarch butterfly. He explains that enzymes are being released that digest all
the caterpillar tissue, so that the caterpillar is being converted into a rich
culture medium (i.e. goo). “During the first 3-4 days, the pupa is literally a
bag of rich fluid media that cells are growing. Inside the caterpillar are
several sets of little cells that are in different parts of the body and
they're called imaginal disks. These are really like little groups of embryonic
cells that start growing like crazy. There are imaginal disks that form the wings,
legs, the antennae and all the organs of the adult butterfly” (Brower, 2000). Simply put, the
caterpillar forms a chrysalis, dissolves into goo, reforms, and emerges as a
butterfly. But how much of butterfly resembles its larval stages cellularly
speaking?
Metamorphosis has been studied in
Monarch butterflies as early as 1904. Two studies: Bauei, 1904 and Tiegs, 1922,
suggest that all larval neurons are destroyed and that the adult brain is an
entirely new structure. For those of you in Biology 502, it shouldn’t be too
much of a surprise that people were already beginning to debate the destruction
and regrowth of new neurons 100 years ago! But what does this mean for the butterfly? Are the
larval and reproductive stages representative of the death of one species and the
resurrection of another? Bernd Heinrich, Ph.D is a professor emeritus at the
biology department at the university of Vermont and a prominent entomologist in
his field. He suggests that the “radical change that occurs does indeed arguably
involve death followed by reincarnation." For more on this debate I
suggest you check out Robert Krulwich’s blog post on this exact question: http://www.npr.org/blogs/krulwich.
Using radioautography, a study conducted by Ruth Nordlander and John Edwards in
1969 found that the majority of larval brain cells are incorporated into the
adult brain.
(Pelling et al., 2009)
Moving on to
the heart of a metamorphosing butterfly, a study from 2009 used a novel
ultra-sensitive detection method, optical beam deflection, and measured the
mini motions of the pupae during transitional stage. The contractions that they
were able to record were occurring at regular intervals, which they attributed
to the mechanical function of the heart (Pelling et al., 2009). They concluded
that the heart organ remains intact throughout metamorphosis but undergoes
morphological changes. It’s hard to imagine that any animal can sequester
enough time and energy in such a short life to facilitate actual changes in a
necessary organ. Human hearts grow and experience some changes during embryo
development but it is rare to see a natural progression as complicated as what
happens during metamorphosis of a butterfly.
In
researching this post, I came across endless papers that use moths and
butterflies as models for development, neuron generation, hormonal maturations,
evolutionary arms races, and more!!! A study published in PNAS in 2013 uncovered
an unknown developmental timer in the tobacco hornworm, which determines the
time to metamorphosis and ensures that each individual reaches sexual maturity
even in the face of adverse environmental conditions (Suzuki et al., 2013). But
I saved the most radical study for the end (also the namesake of this
blogpost). Martha Weiss is an associate professor of biology at Georgetown
University. She conducted an experiment with her lab where she put a caterpillar in a large
box and gassed it with a foul smelling odor. When they could smell the odor she
gave them a 10-second zap so they would learn to hate the smell and repeated
this so-called torture over and over. After pupation, when organs and muscles
melt (this one lasted 5 weeks) a moth emerged and Dr. Weiss presented them with
same odor. As you probably already guessed, they hated it! (Radiolab Podcast 2014, 12:4) Despite the
cataclysmic changes that occur during metamorphosis, the memory makes it through the goo.
The mysteries of metamorphosis continue to perplex scientists in a variety of fields. Understanding the mechanisms behind this major transformational stage had major implications for neuron generation in the early part of last century and is now helping inform fields such as to hormone signaling. So if you can take the time to visit Pismo beach you may be dazzled by more than just pretty pictures of butterflies from your youth.
EXTRA!!!! Stay tuned for the yet-to-be released BBC documentary on metamorphosis that will feature footage created with micro-CT scans, or x-rays that capture cross-sections of an object that can be combined into three-dimensional virtual models. (www.fastcoexist.com)
REFERENCES
Abumrad, J. and R. Krulwich. 2014Black Box. Radiolab Podcast. NPR.com. 12:4 from http://www.radiolab.org/story/black-box/
Bauer, V. 1904. Zur innern metamorphose des
zentrinervensystems der insecten. Zool. Jb.,
Abt. Anat. u. Ontog. 20:123-152
Brower, L. 2000. Inside the Chrysalis. Journey North from http://www.learner.org/jnorth/tm/monarch/ChrysalisDevelopmentLPB.html
Nordlander, R.H. and J.S. Edwards. 1969. Postembryonic brain
development in the Monarch Butterfly Danaus
plexippus plexippus, L. Wilhelm Roux’ Archives 162:197-217.
Oberhauser, K.S. and M.J. Solensky. 2004. Monarch butterfly biology & conservation. Ithaca, NY: Cornell University Press.
Suzuki Y., T. Koyama, K. Hiruma, L.M. Riddiford, and J.W.
Truman. 2013. A molt timer is involved in the metamorphic molt in Manduca sexta larvae. Proceedings of
Natational Academy of Science. Inaugural Articles:1-8
Tiegs, O.W. 1922. Researches on the insect metamorphosis. Royal Society South Australia. 46:222-224.
