Saltwater Crocs: Showing How Dinosaurs Are Evolutionary Pansies Since 200,000,000 BCE

Title

In the waning years of the World War II Pacific campaign, British Marines and the 36th Indian Infantry Brigade landed on the shores of Ramree Island, Burma, after hours of aggressive naval bombardment. A swampy mud-soaked coastal island housing a wide variety of deadly wildlife and diseases, Ramree was key to gaining an Allied foothold on mainland Burma and reversing the spread of Japanese aggression in the region. The few thousand Japanese forces entrenched on Ramree repelled the Allied invasion during the initial weeks of heavy fighting.

January 26th, 1945, the battle turned when a force of about 1,000 Japanese defenders was routed by Allied forces. Surrounded on three sides by enemy units and hoping to rejoin the larger Japanese battalion on the other side of the island, the retreating Japanese opted for the most direct path; a beeline through the thick mud of a dense mangrove swamp. Their retreat was marred not only by the pursuing Allies but also by starvation, dehydration, mosquitos, scorpions, snakes, and one of the most infamously prolific people-murderers outside of the human species: saltwater crocodiles.

This is the last thing I’d want to run into at night in a warzone after being shot at for the past few weeks. Image source: unknown

It doesn’t take a vivid imagination to figure out that saltwater crocodiles are nothing short of gifted killers. At up to 22 feet long and more than two tons, they’re the largest reptile alive today. Saltwater crocs inhabit salty, brackish, and some fresh waters from the Indian peninsula through northern Australia and Southeast Asia, historically spanning northward to Japan. These waters are some of the most densely-populated human areas on earth, meaning the rate at which crocs and people meet face-to-face is higher than more fear-inspiring predators like sharks, hippos, bears, lions, tigers, wolves, cheetahs, dragons, mermaids, and unicorns.

Saltwater crocs, or salties, are primarily ambush predators, meaning they lay elaborate traps (jaws) in high-traffic areas (any volume of murky water larger than 5 liters) and wait for unsuspecting prey (anyone that will be dearly missed) to wander closely by (within 6-10 miles). Saltwater crocs in particular have the widest diet variety of any living crocodile. Crocs are typically apex predators in their communities, meaning they have the ability to catch, consume, and digest pretty much any other animal species from lower levels of the food web. Their prey includes smaller animals such as fish, crustaceans, and birds, but they’ve also been documented feeding upon larger mammals like deer, antelope, domesticated livestock, and humans. Given their size and musculature, it’s a wonder that saltwater crocs are surprisingly not voracious eaters and can go for weeks between meals. Let that thought give you comfort as you’re devoured alive.

Not only do salties eat nearly anything that moves, they also strike with deadly aggression.

Their bite force is the highest ever recorded; a large Australian saltwater croc broke the record with a bite force of 36,000 newtons. By contrast, this is about 40 times the force a human exerts and almost 8 times that of lions, tigers, and  hyenas. This number even rivals that of another famous predator, breaking into the lower estimates for that of T. rex. Scientists studying the evolution of crocodiles noted that the skull took on its characteristic shape, musculature, and bite before the emergence of other croc-like traits like body size, shape, joint structure, and limb placement, indicating that the bite force of crocs was a primary driver of crocodilian evolution.

On the other hand, saltwater crocs have very poor opening strength, and according to the Wikipedia article on their bite musculature, a few layers of duct tape can hold a saltie’s jaws shut. I’m not trying that anytime soon.

Once saltwater crocs get a hold of their prey, it may perform a famous behavior called the death roll. Keeping their strong hold on their prey, the croc will spin until the animal becomes separated or until the croc no longer detects movement. Most theorize that the death roll is largely an attempt to drown terrestrial prey, making them easier to consume. Others speculate that the purpose of the behavior is to rend torso from limb and produce manageable portions for easier digestion. Either way, the death roll is something with which the retreating Japanese on Ramree Island became all too familiar.

British scouts documented the horror the Japanese experienced in their retreat across Ramree. Screaming and desperate splashing were common sounds heard by the Allies in the night, sometimes punctuated by the characteristic sound of Japanese gunfire. Many speculated what horrors befell the dehydrated, starving, mosquito-plagued Japanese. Few outsiders witnessed and documented the event. Among the British forces scouting the Japanese retreat from outside the swamp was naturalist Bruce Stanley Wright. In his 1962 book Wildlife Sketches Near and Far, Wright elaborates on the event:

“The crocodiles, alerted by the din of warfare and the smell of blood, gathered among the mangroves, lying with their eyes above water, watchfully alert for their next meal. With the ebb of the tide, the crocodiles moved in on the dead, wounded, and uninjured men who had become mired in the mud.

The scattered rifle shots in the pitch black swamp punctured by the screams of wounded men crushed in the jaws of huge reptiles, and the blurred worrying sound of spinning crocodiles made a cacophony of hell that has rarely been duplicated on earth. At dawn the vultures arrived to clean up what the crocodiles had left…Of about 1,000 Japanese soldiers that entered the swamps of Ramree, only about 20 were found alive.”

Though many admittedly doubt the accuracy of Wright’s reported number of casualties, the statistic has earned the Guinness World Record for “most fatalities in a crocodile attack”. If Wright’s numbers are accurate, Ramree would be the deadliest attack by any animal on human beings in recorded history.

Few doubt the capability for saltwater crocs to bring that degree of torture upon humans. Many attacks like these occur in remote regions among populations of humans that fail to reliably collect attack data. Much of what we know about croc attack numbers comes from Australia where news reports and eyewitness accounts are more accurately described and distributed to the public. In Australia’s Northern Territory alone, 18 lethal croc attacks have taken place since 1987. Across all of Australia, the rate of deadly attack has skyrocketed from one every two years in 1971 to seven times that number in 2013, totaling 99. Of those, 27% were fatal, a low statistic compared to the country’s neighbors. In nearby Sumatra, 107 people have been attacked since 2007, almost 50% of which were fatal.

Image source: Outbackcooking.blogspot.com

One such attack was made famous by Hugh Edwards in his book Crocodile Attacks in Australia and made even more so by Bill Bryson in his entertaining travel novel In a Sunburned Country. In 1986, many moviegoers were entranced by the release of Crocodile Dundee, inspiring droves to visit the Australian wilderness. One such traveler was 24-year-old American model Ginger Meadows. Aboard the luxury yacht Lady G, Meadows and her newly-earned Australian friend stopped for a swim near the waterfalls at the beautiful King Cascades. The two women were quickly pinned in the water between a croc and a steep cliff. The girls began shouting, throwing their shoes, and tried to wait out the croc, but nothing could deter it. Meadows, a strong swimmer, attempted to make a break for the nearby embankment but vanished in a cloud of splashing in seconds. Caught in a death roll, Meadows looked to her friends desperately, but no one could do anything to help before she vanished. Her body was found floating and armless two days later.

The King Cascade falls, the site of the vicious crocodile attack on American model Ginger meadows in 1987. The attack occurred in the alcove left of the falls. Image source: Tripadvisor.com

Cases like these are hardly solitary. In 2003, a group of three adult friends were repairing an ATV in the Northern Territory when a crocodile fatally attacked one of them and chased the other two into a tree for 22 hours. In 2009, a 5-year-old Queensland boy was eaten in his own backyard trying to protect his new boxer puppy. In 2013, a New Zealand man was trapped alone on an island for two weeks when a crocodile attacked him each time he neared his boat. Last year, a 61-year-old man was snatched from his fishing boat while his family had their backs turned.

It must be said that a majority of attacks are non-fatal. It’s a common occurrence, especially in the Northern Territory, for locals to boast about close encounters with crocs. Sometimes, bait or cleaning buckets attract crocs to wayward limbs. Campsites, public spaces, or private residences located adjacent to croc habitat also can contribute to croc encounters. Excessive alcohol has also been tied to many attacks. Other times, the crocs attack objects like boat hulls, motors, fishing gear, and other inedible objects completely without warning or agitation.

Damage to an outboard motor done by an unprovoked saltwater croc in Australia’s Northern Territory. Source: ntnews.com.au

Though it’s hard to find any heart-warming aspects of the saltwater croc’s story, such things do exist. For one, a collection of Australian laws were passed in the 1970s that outlawed the unregulated trade of saltwater croc skins, a large contributor to critically low crocodile numbers. In the first ten years, the population exploded from 4,000 to nearly 30,000 animals, and today the number may be as high as 150,000 in the Northern Territory alone. To date, the recovery of croc populations from near extinction is the most successful predator conservation program in history.

Though saltwater crocs are among the most aggressive, deadly, and fearsome species in the animal world, they have also fascinated millions. From Steve Irwin to Mick Dundee, the raw power of saltwater crocodiles appeals to man’s primal urges of dominance and aggression. Crocs remind us of a by-gone era where reptiles the size of automobiles waged war on planet Earth. Perhaps that’s why we’re so entranced by them. Perhaps that’s also why we fear them so.

Further reading:

http://shadowreports.com/2011/04/13/eaten-alive-five-killer-croc-attacks-part-one-22-hours-in-hell/

http://www.couriermail.com.au/news/queensland/crocodile-tragedy-boys-family-leaves-daintree-river-home/story-e6freoof-1225812013828

http://mysteriousuniverse.org/2014/08/the-horrific-crocodile-massacre-of-ramree-island/

Cone Snails: The reason why I won’t be sleeping tonight

TitleSometimes, when I’m camping, I dream about angry bears ripping through my tent and attacking me for that forgotten bit of food I left in my pack. A perfectly logical nightmare, all things considered, but far from my worst. In that one, I was SCUBA diving with my cat when she encountered a 6-inch long cone snail. In a sudden flash of activity, one of my best buds was murdered in a rush of sadness and a chorus of bubbly muffled screaming.

I must have been about 12 years old at the time I had the nightmare, and it keep recurring. These nightmares started the same night that I first learned about cone snails and their cat-murderingly lethal toxins from a Disvocery Channel documentary. Not once have I had a nightmare about a Badass Biology topic, let alone one that still rips at the psychological wounds 13 years later.

What about cone snails makes them so horrible? So memorable? Get comfortable, I have a lot to write.

The 6 reasons why cone snails deserve to invade my nightmares:

1) I’m convinced cone snails are heralds to the war of the end times.

Cone snails look pretty innocent. In fact, many of them, like the textile cone pictured below, have intricate colors and gorgeous patterns that would make them desirable for any unsuspecting shell-lover to snatch in an instant. Just look at this little guy here:

Textile cone. I’d would seriously be inclide to play with this shell if I saw it, then I’d remember this article and swim away in a panic. I’d likely also wet myself in fear. Image source: Wikimedia

How cute, right? I think so. I’d hold him. However, what I wouldn’t expect is for that fleeting joy to be one of the last thoughts my brain could process before I’d rapidly be dead.

Unlike the garden variety of snail, cone snails are carnivorous marine snails. They’re common in Indo-Pacific waters, though they also inhabit the temperate waters around California, the Mediterranean, and South Africa among other habitats. The smaller varieties eat benthic invertebrates, though the larger ones must be quick and deadly to capture the small fish they feed upon. This selection pressure created one of the most badass weapons in the natural world.

To catch their quick prey, cone snails possess a small harpoon-shaped structure within the snail’s radula, a feeding structure that other snails use to scrape food from surfaces. In cone snails, the harpoon carries a toxic cocktail of sometimes hundreds of lethal compounds, all stored in a venom sac that supplies the harpoon with enough venom to apply to their next murder victim. This harpoon is used blindingly quickly, leaving little chance for their prey to escape. Then, after that, the cone snails engulf them whole with a mouth so horrifying that I cannot find the guts to post a picture here, thereby I suggest you just Google it.

HarpoonPic

Pictured above is the anatomy of the venom sac and a microscopic view of the toxin-tipped harpoon. Image source: theconesnail.com

2) Take a moment today to call your mother and let you know you love her.

Cone snails produce more toxins than any genus of organisms discovered by science. In fact, there are so many that an entire database has been developed to catalogue and characterize conotoxins, the potent toxic compounds present in cone snail venom. This database, called ConoServer, presently has 8482 chemical entries from no more than 215 species within the cone snail genus, a staggering number for a single organismal group.

But what are these toxic chemical compounds? Most are peptides, short strings of amino acids chained together with a special carbon-nitrogen bond. If these chains were considerably longer, portions of the string would begin interacting with other parts and fold itself into a protein, a type of molecule I’m sure you’ve heard of. Peptides, though shorter, are still useful molecules to manufacture, forming the surfactants that keep mammalian lung tissue from sticking to itself, adding nutritional value to milk, and in the case of our nightmarish cone snails, killing stuff really really quickly.

Conotoxin peptides are mostly used defensively. Most human stings are caused by a wayward foot delivered to a cone snail hiding in the sediment. However, roughly 10% or so of classified cone snail toxins have been found to be used in foraging and hunting, paralyzing their prey.

3) I am now hoarding Morton’s salt under my pillow in case one tries to break into my home.

All of the 600-700 species of cone snails are capable to stinging and injecting their toxins into humans. Not only are there a multitude of lethal toxins in a cone snail’s sting, but their lethality is nearly unparalleled. A useful way to measure how lethal a toxin can be is to measure what’s called a LD50, or the dosage expressed in mass/kg of body weight at which 50% of a population of test animals (usually rats) are killed. Arsenic, a well-known toxic substance, has an LD50 of around 15mg/kg, meaning it would take about half a teaspoon of crystallized arsenic compounds to kill a male human weighing 83.6kg, or around 181 lbs. The LD50 for some conotoxins can be as low as 0.005mg/kg, meaning you could very well be killed by conotoxin at a volume little larger than 10 medium grains of sand.

How do these toxins kill at such small dosages? If you’re an avid reader of mine, you may remember textrodotoxin, a neurotoxin in blowfish that kills by interfering with ion channels in neurons. Ion channels allow neurons to fire, and conotoxins bind to these channels with startling specificity, prohibiting their ability to function. Conotoxins kill humans in much the same way, and like tetrodotoxin, most human deaths from conotoxins are related to the asphyxia caused by the diaphragm being unable to contract. There is no anti-venom, and in some species like the geography cone, a sting is 70% fatal.

4) I strongly suggest we flee for the mountaintops.

Diabetic or not, you’ve heard of insulin. Insulin too is a peptide, and in humans it acts a hormone to help mediate the amount of glucose present in the bloodstream. Cone snails have now added another use for insulin in the natural world.

In January of this year, researchers published a study characterizing two species of cone snails that possess the first and only recorded case of weaponized insulin in the history of the planet.

That’s right. Weaponized insulin. Used as a predatory tactic, cone snails release insulin into the surrounding water when prey are nearby. It then passes through the gills of prey fish, enters the bloodstream, and drops the blood sugar enough to prevent the fish from having enough energy to flee the encounter,  all in a matter of seconds.

5) Oh dear God, there’s more?!

Conotoxins are so potent that there are serious efforts dedicated to determine whether they can be weaponized and used on mass numbers of victims by terrorists groups. In a paper published in the Journal of Bioterrorism and Biodefense, scientists outline the probability of a terrorist attack in the form of aerosolized conotoxins or contamination of food or water. Their verdict is surprisingly reassuring, citing the difficulty to extract most conotoxins from living animals and the difficulties synthesizing conotoxins in a usable and deliverable form. However, not all varieties of conotoxins face these same issues, and the risk of three broad biochemical classifications of conotoxins are candidates for bioterrorism should those few key technical hurdles be overcome.

THIS IS WHY I KEEP HAVING THESE NIGHTMARES. GAAAAAHHH, DON’T SWALLOW MY CAT!!! Source: AquariumAdvice.com and my darkest nightmares

6) Oh hey, a fact that’s not actually all that terrible.

Remember when I mentioned ConoServer, the online database that combines efforts of dozens of biochemists seeking to catalogue the vast variety of Conotoxins? Why spend the time to catalogue them if terrorists could simply learn to replicate these peptides in vitro?

Many of today’s most common and effective pain-killers carry powerful negative consequences. For example, the narcotic pain medications like the opioids hydrocodone (Vicodin), morphine, oxycodone (Percoset), and codeine are highly addictive and can leave patients with withdrawal symptoms after their course is complete. The hunt is on for a powerful non-habit forming pain killers with few side effects that can be cheap, easy to deliver, and easy to scale up.

Conotoxins may provide the solution. Much like snake venom, most research efforts on conotoxins are geared toward repurposing the toxins to serve as pain killers. Perhaps a single toxin or a cocktail of a few or several toxins could serve as potent yet non-costly painkillers, and collaborative research efforts like ConoServer could rapidly speed progress towards a revolution in patient care and pain management.

One promising conotoxin pain drug is ziconitide, a synthetic drug identical to a toxin produced by the cone snail Conus magus. Ziconitide has been FDA-approved for treating intractable pain and has shown some promise in its effectiveness. However, the drug degrades rapidly and cannot be delivered orally. Instead, ziconitide must be injected directly to the spinal cord via a surgically-implanted pump. Not terribly convenient if you ask me, but it seems to be a good start nonetheless.

Progress is being made to develop oral conotoxins-derived pain medications. In 2014, Dr. David Craik from the University of Queensland presented new evidence at the 2014 meeting of the American Chemical Society. Craik and colleagues looped peptide chains, amplifying their stability over the long-term while preserving their potency as analgesics. The prototype drug was given orally to test animals and showed nearly a 100-fold increase in effectiveness in comparison to the common painkillers morphine and gabapentin.

Overall, I find it pretty badass that such an effective killer lurks in the oceans. It delivers death in seconds to its prey and in minutes to a fully-grown human, and with no anti-venom, its effects are second to none. Hell, these guys even weaponized insulin. On top of that, they may gift humanity with a revolution in pain management. That’s pretty badass.

Want to suggest a future topic? Write it down in the comments below. Do it. Do it do it do it doitdoitdoitdotidoit.

For further reading:

http://www.conoserver.org/?page=about_conotoxins&bpage=keyrefs (list of current review papers on conotoxins as pain killers and the difficulties faced with their use)

http://www.theconesnail.com/ (lab website of the Olivera lab group at the University of Utah)

Don Cowlione: How Cowbirds Run A Songbird Mafia

Title

If I were to imprint on you one main point stringing together every article I’ve ever written for Badass Biology, I hope it would be this: nature has produced no shortage of jerks. I say “jerk” like it’s a bad thing, but take the time to think about the word and you’ll realize “jerk” becomes a bit endearing when we’re talking about nature.

First, let’s review what it means to be called a “jerk” species. First, a jerk has to be abundant enough to merit some sort of attention or recognition, but not more abundant than non-jerks, otherwise the jerk strategy would be much less effective. This population size balance is very delicate, but jerks seem to manage it well.  Second, being a jerk means going against some established natural norm. Usually, jerks exploit some mutually beneficial arrangement between individuals, leaving another party to carry their weight for them. It’s a pretty clever strategy if I say so myself. Third, present a jerk with an opportunity and it’s likely to get snagged. Another admirable trait in favor of biological jerks

Back to the point, Planet Earth has lots of jerks. Consider the bluestreak cleaner wrasse. On Southeast Asian reefs, cleaner wrasse set up cleaning stations where they pick off the tiny parasites that live in the skin of larger fish. This arrangement seems to work for everyone (except the parasites, unfortunately); the wrasse get dinner while the larger fish get a good skin treatment. Some jerk wrasses, let’s call them “wrasseholes”, like to instead bite big chunks out of the mucus membranes on these fish instead, turning this mutualistic interaction into a parasitic one.

To be honest, it’s not that I find this interaction all that neat. The main reason I bring this up is to mention that it DID spawn an article in Discover Magazine with a really clever name: Cheater Cheater Mucus Eater.

Sure, jerks are great and all. My favorite? This little guy:

Awwwwww. SO PRETTYYYYYYY.

Adorable, right? What about now?

The Birdfather

Why yes, I AM proud of this joke.

Make no mistake. This stone cold killa is ruthless, even enough so that I’d put the word “killa” in an article that I’m reasonably sure a future employer will read.

So what about this little bird makes it so much of a wrassehole? To start, an introduction. This is the brown-headed cowbird, a member of the family Icteridae, which consequently means nothing at all to me but sounds pretty badass all the same. What distinguishes cowbirds is that they are notorious brood parasites. They find nests belonging to other aviary families, mostly songbirds but varying from hummingbirds to birds of prey, lay their eggs next to theirs, and let those other poor bird parents feed, raise, protect, bathe, clothe, and attend PTA meetings of cowbird babies. As of 1999, approximately 140 species of birds have been documented raising cowbird young.

Here’s what’s odd about this. I’m sure you’ve guessed that cowbirds are able to get away with this sneaky business because their eggs and young look an awful lot like the birds they’re parasitizing. They don’t. More often than not, cowbird eggs are either much larger than the eggs of their host AND a different color and pattern. Moreover, cowbird chicks are gigantic when they hatch, making little songbird chicks look tiny by comparison.

One of these eggs is a parasitic cowbird’s. Can you guess which one? Did you guess the one on the bottom left? You did!? Very good!

You may be asking yourself, “why do these other birds raise babies that aren’t their own?” Right now, I’m asking myself, “have I smelled like this all day?”, but that’s really of no consequence to anyone (except my wife, I guess).

Oddly, one theory explaining why the hosts hadn’t murdered these little guys is, and I’m serious, that the host birds don’t have the cognitive ability to recognize that these chicks are different from the others. It seems odd to me that the same birds can relocate their nests among thousands of other similar-looking forest objects with near-identical colors and patterns would not be able to recognize that one of their babies is a freakish monster.

Meanwhile, I only learned today that I live 5 minutes from a major interstate highway, but I’m confident that there’s no gigantic monster baby living in my house. One of our cats is pretty large, sure, but I’m not convinced I’m her father or anything.

No, the real reason host don’t viciously murder cowbird young is pretty sinister. In 2007, two researchers from the University of Florida set up a field experiment where they manipulated cowbird presence in predator-free nests of host birds. In “ejector” nests, the researchers removed cowbird eggs from host nests, mimicking a host that rejected a cowbird egg,  whereas “acceptor” nests saw through the raising of a strange foreign cowbird hatchling. In all, 56% of ejector nests saw some the destruction of host bird eggs, but only 6% of acceptor nests were ruined. What happened?

Cowbirds happened. Females, actually. These jerks monitored the nests of their hosts, checking in on the progress of their young from time to time. If cowbirds found that their babies weren’t receiving the star treatment (or weren’t in the nest at all), the cowbirds would lay ruin to the eggs of the host bird. Essentially, these birds were exhibiting mafia behavior, laying down some pretty severe consequences if the host rejects the parasite.

What’s equally sinister is the explanation for destruction in the 6% of acceptor nests. Why kill the young of a nest that’s satisfactorily caring for your own young? Simple: murder creates room in the nest for more cowbirds.

In summation, I quite admire cowbirds. In a group of organisms whose ability to distinguish which egg is their own is questionable, these ladies are clever. It’s pretty rare to see such a sophisticated racket exist in animals with brains the size of beans. Think about the cognitive power cowbirds need to keep track of which nests are parasitized, then decide on whether to murder or not murder depending on what they see. I gotta say I’m impressed.

So, like a Don collecting tribute from his corner of Little Italy, cowbirds command respect. They’re clever, manipulative, aggressive, greedy, and all of it is so sinisterly bundled in a package that I’d rather enjoy petting.  Plus, it’s nice to know that some species out there gives others an offer they can’t refuse.

The 6 rules every grad student needs to know well

(EDIT: Contains minimal biology. Deal with it.)

The past 7 months have been the busiest and most stressful of my life. I decided to abandon my plan to become an academic to move back home and pursue an industry job, where, from an academic’s perspective, the ranks are filled with fat cats that do shady business via coordinated rubbing together of the hands  and menacing ear-to-ear grinning, and where even the low-level employee cubicles are lined with millions of ill-acquired dollars taken from the penniless hands of the National Science Foundation, National Institutes of Health, and [insert your favorite noble scientific organization here].

Before I could graduate and thrust my resume into the tens of thousands of already overflowing piles of identical resumes seeking to get the same entry-level industry jobs as I sought to acquire, I first had to do all of the following within 7 months: 1) design and complete the largest and most ambitious experiment of my research career, 2) author and defend a Masters thesis from scratch, 3) teach an undergraduate lecture course by myself, 4) help my busy fiancée plan and execute a wedding and honeymoon, and 5) coordinate a cross-country move, using only a 4-door Honda Accord to fit everything I own.

So, if you had any question what I was doing with my time over the past few article-less months, please read the above paragraph. Please try not to wince as hard after reading it the second time through.

How did I get all of these things done? Here are a few simple laws that helped me see through all of these goals at once:

1) The 80-20 rule:
Developed by 1906 by the Italian economist Vilfredo Pareto and recently popularized by Timothy Ferris in his stimulating bestseller “The Four-Hour Work Week”, the 80-20 rule describes that, in many situations, 80% of the effects come from 20% of the causes. In business, this might mean that 80% of your income comes from 20% of your clients, or that 80% of your losses come from 20% of your setbacks, and so on. In my case, 20% of my urgent tasks were causing 80% of my stress. This dynamic rule forced me to identify what tasks needed my attention the most and foresee what positive effects I might expect as a result, allowing me to prioritize where my efforts needed to be expended.

2) Don’t drop the same ball twice in a row:
Early in my grad school career, my PI sent an email to the entire lab with advice that read something like the following: “If you have to balance many important tasks in one day, such as work, family, research, and school, you may not have time or energy to adequately address all of them. It’s OK to let one of them go unnoticed. However, it’s whenever we fail to address the same thing several times in a row that the problems begin.” My alteration to the rule: don’t let the same task go unaddressed for two consecutive days. No task got rusty or completely left my mind if I devoted at least a little bit of time to it every other day.

3) Identify and minimize wasted time:
Like all of us, I get distracted by things that are more fun than work. How do you identify what’s the MOST distracting? Simple: RescueTime. RescueTime is a free application that creepily monitors your activity on your computer, categorizes your time by category, and highlights which applications are the most productive or distracting. For example, RescueTime knows whether I’m playing video games or surfing Reddit, and runs a clock to monitor how much time I’ve wasted on each activity. At the end of the day, it alerts me with a report on how much time was productive and builds a profile of my daily and weekly productivity. Your goal should be to beat your previous day’s (or week, etc) productivity score.

If the internet is your big time waster, try StayFocusd. This simple browser add-on allows you to input which websites (Reddit, YouTube, Facebook) rob you of the most time. You can then set a time to share between all sites on your list, and a counter will appear displaying your remaining time on those sites. For example, I allowed myself only 30 minutes per day of combined Reddit and Facebook time. After the 30 minutes, StayFocusd would block access to those sites on my computer, leaving me no way to access them once the clock has run out (unless I disabled the add-on, but that’s cheating).

4) Drink heavily and cry Prioritize sleep over poor-quality work:
Know and understand how sleep can enhance the quality of your workday without increasing the time you spend working. Each person has their own limits and needs; for the lucky few that are alert all day after 6 hours or fewer of sleep, I envy you. I need about 8 plus a 20-minute power nap around 4:30. Others need 10 or more. Experiment on your own, graphing your RescueTime productivity score (y-axis) as a result of the hours you slept the night before (x-axis). After a week or two, clear patterns should start to emerge, and you’ll find your sleepy sweet spot. Once you do, make that amount of sleep your priority, otherwise the quality of your work may decrease with increasing stress.

5) Break large tasks into small ones, each chunk with a firm deadline and a small reward:
Following this rule allowed me to write my graduate thesis draft almost without issue. First, I’d set aside an entire day per week for thesis writing, not worrying about research or teaching or any other day-to-day activities (but not for two consecutive days, see item 2) above). Before I began, I’d spend 5-10 minutes devising my goals for the day: take a section, break it into unambiguous chunks, assign a short deadline for each chunk (see below), and list the reward for finishing on time. Your rewards must be small, like a 10-minute cookie break or a brief play session with the dog. My favorite reward: use the remaining time until your deadline to do whatever time-killing you want to do. If you fail your deadline, you get no reward. Alter your deadlines if you miss them frequently, but it’s important to keep them short.

6) Assign absurdly short personal deadlines:
Another Ferris-popularized idea is a rather clever one; when you assign deadlines, make them shorter than you originally anticipated, within reason. Large tasks often take until the very end of the deadline to complete, so by shortening the deadline, you’re forced to work more diligently and more precisely without truly rushing. Say you’ve got a paper that’s due in 3 months. It will take you from now until the 3 month deadline to think, outline, write, edit, and review the paper, turning it in only at the very end (or at least near it). Instead, shorten that deadline to a single weekend, and you’ve now freed up so much time to devote to tasks that may be more important or urgent. I used this rule for my thesis; during a meeting, my PI asked for the first draft in 8 weeks. Instead, I suggested to make it 4 weeks, forcing me to live up to my goal while still having enough time to get good work done.

This is by no means a comprehensive list of constructive suggestions. These are just 6 things that I found were helpful towards preventing me from feeling overwhelmed.

Now that I have completed all of these really difficult tasks and am looking for full-time employment, I have more time to spend sharing science again. It’s a comforting yet horrifying thing, unemployment. On one hand, I have so much more time to devote to science communication, one of my truest and most rewarding passions. On the other, OH MY GOD IM UNEMPLOYED WHY DO I HAVE SO MUCH FREE TIME YET SO LITTLE MONEY.

In the end, I’m glad I made it through the past 7 months. I now have a Masters’ degree, a loving wife, and work experience that should make hiring managers scramble to send me their official job offers. I don’t mean to brag too much about my accomplishments. I’m just proud that I’ve seen my goals through and have made it to the other side. I wish you luck on doing the same.

Check back soon for more Badass Biology articles, and as always, comment if you have a badass science topic you’d like me to cover!

How settlers and cows changed the face of south Texas prairies.

What you are about to read is udderly amazing. This being an article about the great state of Texas, currently my home, the steaks are high to make this one funny and I butter deliver. If you have any bull with what I have to say, go hoof it or I’ll get cheesed. At least give me the chance to milk this topic before you give me beef. Regardless, much of this article isn’t black and white, and I hope too that in some way you will find this article amoosing. Anyway, let’s herd this along, I’m getting hungry. Agriculture.

Cow Title

How settlers and cows changed the face of south Texas prairies.

Texas: the home of wide open skies, twenty acres, barbecues, and pecan pies. American culture paints an idyllic and rugged picture of Texas. Cowboys herd cattle through vast expanses of fence-less plains. Prairies full of lush grasses as far as the eye can see. The picture in your head probably isn’t too far off from this:

Photo credit: Pondero (http://pawndero.wordpress.com/)

Had you visited central or south Texas 120 years ago, this would’ve been largely accurate. However, over a span of a few decades, an alarmingly large portion of Texas has transformed from a landscape of endless grass to something much much uglier:

What you see nowadays is mesquite, prickly pear cactus, and some small brushy shrubs displacing the miles and miles of grasslands that historically covered much of Texas. How did it get this way? And, more importantly, can we blame something else for it besides ourselves?

Even if you’ve never seen the Lion King, you’re likely still aware of cyclical nature of life. Among these cycles is succession. A habitable area becomes damaged by some event, like an eruption or a bulldozer clearing land for farming. The vacuum of space and resources left behind gets colonized first by r-selected species. These species are really good at dispersing over wide distances and taking root in new places unaided by other species. The unfortunate cost to being an r-selected species is that it’s generally very hard to compete, especially with k-selected species that take longer to colonize a disturbed area but competitively dominate more easily once they’ve done so. So, over time, a community of plants or animals can shift from being primarily r-selected to k-selected, completing the cycle of succession until the next disturbance event.

A typical course of succession on a plot of cleared land. R-selected strategists invade first, but are gradually out-competed by hardier but slower-growing k-selected species like hardwoods. Heh. Hardwoods.

Prior to about the 1880s, the most common form of disturbance in south Texas was fire. Prairie grasses would naturally form dense expanses of flammable material, and the slightest spark could create wildfires that spread for miles. The constant and intense winds blowing from the Gulf would aid in spreading fires over vast distances, removing all the built-up grasses and allowing new ones to take root. Another consequence of these natural fires is that shrubs, cacti, and trees, all more k-selected than the weedy grasses, could not colonize the prairie successfully because the odds of surviving these fires was so low. And because it took such a long time for these plants to move into a space, even one cleared by fire, they never really became dominant in these regions because fires were so common.

The catalyst that sparked change in Texas prairies was the large influx of cattle ranchers in the late 19th century. Early Texas ranchers understood the importance of fires and would perform yearly burns of ranchlands, and it was clear that the annual new growth of grasses improved the health and size of their cattle making for tastier Ribeyes and jucier Sirloins. However, once the density of cattle began to explode, grazing on these grasses intensified, leaving empty patches clear of the combustible material necessary for fires to destroy old growth. Fires became less and less effective and spread to a fraction of the area and intensity that they were mere decades before.

Here’s where the opportunistic k-selected species began to invade. With reduced damage by fires, seedlings of mesquite, oak, and various shrubs had a better chance of setting up a home on the range. Once they did, the shade they created further drove down the density of flammable grasses and added more space between plants, inhibiting fires even further. The end result facilitated the invasion of other plant types including a host of cacti and small shrubs.

Why does any of this matter? Put simply, economic growth in the region took a heavy blow. In a surprisingly well maintained old-ass report published by the U.S. Dept. of Agriculture in 1908, the consequences of bushes on ranching and farming became clear: “South Texas is being rushed under the plow to escape the invasion of bushes. Large tracts which could have been bought a few years ago for a dollar or less per acre…now cost $5 or $10 an acre to clear of woody growth…many thousands of acres are already lost, at least to the present generation, for the bushes are so well intrenched that the cost of clearing would greatly exceed the value of the land”.

Despite these difficulties, the face of south Texas is likely to continue to change. The currently dominant plant species in the area are only transitory, and often they give way to larger trees that can outcompete the smaller brush. Many experts think reforestation is a likely consequence in the coming decades, though a gradual one. Swampify isn’t a word, but it should be.

I want to make clear that despite the usage of the term “south Texas”, the area impacted by mesquite invasion is friggin massive. The amount of land encompassed between Houston, the Rio Grande valley to the south, and the border town of Del Rio to the west is roughly the size of the state of South Carolina; some 32,000 square miles. And these boundaries only generally reflect the affected areas because these are among the only Texas towns I can name off the top of my head. Regardless, the difficulty of this invasion has undoubtedly shaped Texas history and the outcomes of economic competition with other Southern states.

The overall point of cases like these is that human beings have a profound and measurable impact on the land from which we obtain our livelihoods. The issue of responsible land management is arguably one of the greatest problems facing our generation. Properly managing sensitive natural areas is crucial for the future of economic growth and development.  Unfortunately for us, it’s almost never clear what the best approach is to battling habitat degradation. What would have worked in south Texas? Limiting the density of cattle? Denying settlers the opportunity to buy arable land? Freezing growth in a developing Texas? Eating more cows? I am seriously hungry.

Since I’ve moved to Texas, I’ve gotten the chance to do a lot of characteristically “Texas-y” things. I’ve saved a friend’s beer while floating the rapids on the San Marcos. I’ve hiked Guadalupe Peak. I’ve stopped on the highway to take pictures of the springtime explosion of Texas Blue Bonnets. I’ve seen the millions of bats at Devil’s Sinkhole and seen Kemp’s Ridley turtle hatchlings make a run for it on Padre Island. Hell, I’ve even yelled at cows from a moving vehicle. Enjoy these things while they last, because those cows may just eat all your land to death. The end.

How palindromes allowed males to exist

Title

If I were asked to give my two most valuable pieces of advice, they would be these: First, appreciate the near impossibility that you are alive. The atoms that make you have been through some shit; they’ve swirled as stardust, formed a hot molten planet (or crashed into one from elsewhere), boiled, compressed, and decayed to a point where they were incorporated into who-knows-what part of a who-knows-what number of a who-knows-what kind of strange prehistoric organism before they now make you, sitting comfortably at your computer marveling at my repeated usage of “who-knows-what”s. The other piece of advice? Never try to drink a beer without using your hands.

Without getting abundantly philosophical, you by all means shouldn’t exist. I ask that you, at least once daily, come to terms with this fact. Appreciate also that you can come to terms with anything at all, you big-brained multi-talented sculpture of evolution. Appreciate that other humans exist that can love you and carry out services to make you more comfortable. Appreciate pizza, because how did the universe create something so perfect?

Oh, and if you’re male, go ahead and appreciate that you exist. You theoretically should not.

In evolutionary terms, males are dispensable. The adaptive value of males is that they can mix up genes to create new combinations of traits on the off-chance that some of them can help prevent an untimely death, aid in making little ones, or allow one to be more comfortable overall. Males are gene donors. That’s basically it. Yeah, some males aid in parental care or perform tasks to aid group survival, but male uselessness is a common evolutionary motif. Male anglerfish are prime examples.

Gender in humans (along with a lot of other species) is determined by the identities of a pair of sex chromosomes contained in every cell. Both males and females possess one X chromosome, a large and gene-packed chromosome chock full of genetic goodies. Females have a pair of X chromosomes, one from the mother and one from the father. Males, however, have only one X chromosome, donated by the mother, and a shrimpy and scrawny Y chromosome donated from the father. X chromosomes contain some 2000 known genes, Y contains only 78. Bummer.

There’s a good reason why the Y chromosome is so scrawny: DNA damage is pretty common. Being so long and fragile, DNA can become knotted, coiled, unwrapped, kinked, looped, mutated, irradiated, copied wrong, fixed wrong, proofread wrong, chopped, sliced, chunked, choked, broken, inverted, doubled, misread, and misunderstood. Each of your cells possesses a SWAT team of enzymes that try to prevent these things from happening, but they’re not without error. Mistakes happen. So, because our cells possess 2 copies of each chromosome, when one becomes overly mangled, these enzymes can use the other as a template of instructions to repair the damage.

X chromosomes do this beautifully. These, in short, scan each X chromosome and check for inconsistencies, using one or the other to clear up any mismatches in DNA code. Two similar chromosomal regions can also “cross over”, exchanging segments of DNA that encode for roughly the same type of protein. Most of the time, crossing over is beneficial because it throws some genetic variety into the mix.

Crossing over is like holding hands, only after you’re done, your hands trade bodies. Good old nightmare fuel.

X and Y were once paired just as healthily as two X chromosomes are today: both were large, bountiful chromosomes that crossed over frequently and used each other as repair templates. About 300 million years ago, as reptiles and mammals diverged, a mutation caused the Y chromosome to take on more “manly” attributes, including the development of testes, sperm, different hormone production, etc. X and Y were now very different chromosomes. Crossing over ceased between them. Cellular machinery stopped using one to proofread the other. They became distinct and wary of the other. The X chromosome still had a healthy pair in females and could easily use one to keep the other functional, preserving the integrity of the chromosome.

Unfortunately, Y became a genetic desert island, left all by its lonesome with nothing to use as a spell checker in case things went very wrong with its code.

By this logic, many scientists think the Y chromosome should have been obliterated. With more and more DNA mutations accumulating, more and more of the chromosome was snipped away and discarded. To make matters worse, portions of the chromosome inverted themselves. Areas swapped information, mixing things up further. The Y chromosome was rapidly becoming giant mess. Eventually, removing all these errors caused Y to become tiny, almost biting the dust altogether and doing away with males entirely! But it’s still kicking even after 300 million years. With no partner to help proofread its DNA, how did the Y chromosome survive?

DNA and language share many things in common. Almost too many. One of them is that segments of information, called palindromes, can be read from left to right or right to left and read the same way: God, a red nugget, a fat egg under a dog! DNA contains palindromes too, and they can be long, sometimes hundreds of bases in length. The problem with DNA palindromes is that they are a liability; because bases like to chemically pair up with their counterparts, segments of independent DNA can stick together to form looped hairpins, derailing the important cellular machinery necessary for replicating, proofreading, and transcribing DNA into proteins.

Palindromes on two strands of DNA can join to form hairpin regions. These are bad. Imagine a train barreling down track shaped this way and you get the picture.

The Y chromosome in particular is full of palindromes. Normally, high palindrome density is a chromosomal death sentence. However, in the case of the Y chromosome, palindromes were a blessing. Because the Y chromosome had so much repeat information and no paired chromosome to proofread it, Y could use different segments of ITSELF to validate that the information on another segment was correct. Y chromosome palindromes kink together and use one strand to proofread the other, turning large segments of the chromosome into genetic hairpins. Because both are palindromes, one segment should read exactly the same as its folded-over counterpart. So, in a sense, the Y chromosome uses what’s normally a huge flaw as its primary means of keeping information correct.

As an added bonus, this method of palindrome proofreading can create new varieties in the DNA code akin to crossing over in X chromosomes. When one strand is damaged, the enzymes responsible for repairing it can’t distinguish the damaged strand from the undamaged one. All it can do is discriminate one from the other. Therefore, it has to guess which of the two sides needs fixing. Often, this can cause the undamaged segments of DNA to take on the information of the damaged counterpart, creating new combinations of DNA code to form. While this could possibly ruin the genetic meaning of the original, it also presents an opportunity for new traits to become expressed on the ever-changing Y chromosome.

Self-repairing Y chromosome palindromes at work. This is something I’ll surely bring up at the table come Thanksgiving.

I cannot over-emphasize how important palindromes are to the sustainability of the Y chromosome. Without this ingenious little method, human history would have played out very differently. So, while palindromes can be a fun way to parody a Bob Dylan tune, be thankful that they also keep you healthy and keep your identity in check. Add that to your list of things to appreciate.

A special thanks to Sam Kean, whose book “The Violinist’s Thumb” encouraged me to write this article. It’s a fantastic read, I highly suggest it.

For more information:
http://phylogenous.wordpress.com/2010/10/01/y-chromosome-vii-why-palindromes/

http://www.hindawi.com/journals/ijeb/2012/207958/

 

The enzyme that tells aging to go f**k itself

Screw getting old. I’m at a time where I’m on the cusp of some rather grown-up life events. I get married in 6 months. Mere weeks after that, I leave graduate school and enter the job market. In protest of maturity, I thought I’d dedicate an article to some biochemical wizardry that slows down all the harmful shit you do to yourself as you age.

Just to remind you, DNA is a rather pretty-looking double-helical molecule contained in each of your body’s cells that encodes all the information they need to carry out their jobs. The two strands are made of little compounds, called bases, which act as a set of instructions for the assembly of proteins. Turning sequences of these bases into proteins is damn complicated, but know that a number of mistakes can happen in the process that alter the conversion of gene to protein, screwing with the function and health of the cell.

DNA protects itself in a few important ways. First, our cells have methods of preventing errors in DNA code, or mutations, get turned into proteins. There’s a complex set of enzymes, molecules that expedites chemical interactions, that act as a DNA proofreading system, clipping out mismatches between strands or errors encoded within one of them.

Second, DNA doesn’t sit unwrapped and unprotected in your cells; proteins called histones coil DNA and attach to other histones like a giant kaleidoscope of hugs. I could use a good hug. Aggregates of DNA hugs form singular bodies, called chromosomes, which act to preserve its contents and selectively turn on or off different segments of the strand.

DNA is wrapped around proteins called histones which are then condensed into chromosomes. Of course, you’d know this already if you’ve been reading. I’m not sure why I bother to make captions.

Lastly, DNA recruits enzymes called border patrol enzymes that check each gene’s passport and search for contraband. Mistakes still happen, but it’s the illusion of safety and security that counts.

Border enzymes

When each of your cells divides, it has to copy your entire genome, repackage it all into chromosomes, and split up the chromosomes in the right amounts to each daughter cell. You may remember the name of this from middle school biology class. You know, it’s only a little process called photosynthesis. Jeez, get with it, people.

What sucks is that this process isn’t perfect; each time a cell divides, a little bit of DNA on each end can’t be replicated and is disregarded. Because cells divide a lot, you can imagine that this gradual genetic snipping will eventually start screwing around with some damn important genes. Some of these genes may encode proteins that allow your cells to grow, reproduce, or function, and their loss would be devastating.

Our DNA knows what the hell is up though. At the tips of each chromosome are regions called telomeres, long strings of basically non-sense genetic code that is completely dispensable. These telomeres get clipped into nothingness over enough replications, and our important genetic material begins to become lost.

So yeah, here’s a chromosome with some admittedly wimpy-ass telomeres. Come on, guys, three replications and you call it quits?!

At that point, some shit starts to go down. The cells stop growing, can’t divide, or kill themselves. It is at this point that the human body begins to age; skin loses elasticity, muscles atrophy, cognitive function lessens, bones become brittle, and golf starts to sound like fun. Cells may also divide uncontrollably, a condition you may have heard of. People are doing fun runs for it all the time. You may have even had a loved one affected by it. You know, it’s a little disease that goes by the name of viral or bacterial meningitis. Come on, guys.

In 2009, Drs. Elizabeth Blackburn, Carol Greider, and Jack Szostak shared the Nobel Prize in Physiology or Medicine. According to the official Nobel announcement, “They  solved  a  long-standing  fundamental problem  in  biology;  how  can  the  ends  of  chromosomes  be  maintained  and  spared  from erosion  or  rearrangement  during  repeated  cellular  divisions?”

Not only did this trio advance what we know about the protective role of telomeres, but they also discovered a friggin awesome enzyme known as telomerase. As telomeres shorten over time, telomerase can become activated to elongate the shortening ends. Every cell in our bodies has the machinery to manufacture telomerase, though it’s usually inactive even as telomeres are damaged or shortened.

Look at telomerase getting all cozy with that primer. Just delightful.

In my opinion, determining how to activate telomerase and impede the effects of aging is currently among our most important scientific problems. Some researchers and companies are searching for answers. In fact, products are already on the market that claim to assist in the activation of telomerase. A lot of questions still remain:

1) Is it possible to not just inhibit but reverse the effects of aging by activating telomerase?
2) Could we develop a method of recovering lost genetic material?
3) What effects would extended human age have on quality of life, natural resources, and ecosystem health?
4) Does this mean Bill Cosby will never die?
5) I can’t think of any more questions.

Want to see a particular topic discussed on Badass Biology? Post it in the comments below.

For further understanding:

http://www.nobelprize.org/nobel_prizes/medicine/laureates/2009/