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      <p>
 Every month, California normally sees between 80 and 100 cases of pertussis—more commonly known as whooping cough. That’s changed in just the last two weeks, though. In the first half of June, there have been 800 cases.
</p>
<p>
 California isn’t alone; the CDC reports that pertussis cases are up by 24% across the country. For older children and adults, the illness is debilitating, but manageable and often ultimately recoverable. But infants face a different set of statistics. About half of infants one year old or younger with pertussis are hospitalized, and 1-2% of those die. Two infants have already died this year in California.
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      <p>
 Pertussis works by disabling the respiratory system’s self-cleaning mechanism, the millions of tiny hairs called cilia that normally sweep mucus and other debris out of the airway. The bacteria that causes whooping cough,
 <i>
  Bordetella pertussis
 </i>
 , secretes a toxin that paralyzes those cilia. With the cilia out of commission, mucus and debris build up in the airways. Clogged airways lead to coughing fits, which—because the bacterial toxin also causes inflammation—are followed by a telltale “whoop” as the patient tries to catch her breath.
</p>
<p>
 It’s an exhausting cycle that can go on for weeks and often causes pneumonia or other respiratory problems. But it’s also easily preventable. The Tdap vaccine, which also protects against tetanus and diphtheria,.is highly effective—fully protecting around 80-90% of children who receive it. But pertussis still has some opportunities to sneak in.
</p>
<p>
 Monte Morin, writing for the
 <a href="http://www.latimes.com/local/la-me-whooping-cough-20140614-story.html">
  L.A. Times
 </a>
 :
</p>
  

  
      

<blockquote>
    <p>
 The earliest age an infant can be vaccinated is six weeks. Because of this, health officials say every pregnant woman should get a Tdap vaccination in the third trimester of pregnancy, as the mother’s immunity will transfer to her baby — at least temporarily.
</p>
<p>
 Unlike the measles vaccine, pertussis vaccines do not provide lifelong immunity. It’s partially for this reason that whooping cough is cyclical: It reaches epidemic levels every three to five years.
</p>
</blockquote>

  

  
      <p>
 Those three-to-five-year outbreaks have been getting more and more severe in the last decade. The Tdap vaccine, introduced in 2005, has a lower risk of side effects than the older form of the vaccine but doesn’t seem to last as long. New strains of whooping cough could also be contributing to the increase.
</p>
  

  
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      <p>
 But a third possibility, and one that’s becoming increasingly common, is that lower immunization rates in certain communities are eroding the vaccine’s ability to prevent an outbreak.
</p>
<p>
 Whooping cough is so contagious that more than 90% of a population must be vaccinated to keep it from spreading. Statewide vaccination rates in California approach that level, but there are certain communities—especially in affluent, highly-educated areas—where the majority of school-age children aren’t immunized. In 2010, the year of California’s most recent epidemic, a study published in
 <i>
  Pediatrics
 </i>
 showed that the likelihood of a pertussis outbreak spiked near those communities.
</p>
<p>
 More than 9,000 cases—and ten deaths—were reported in California in 2010. If this year’s epidemic maintains its current pace, it will match those statistics.
</p>
  

  
      <div class="newsletter"></div>
  

  
      <p>
 Photo Credit:
 <a href="https://www.flickr.com/photos/worldbank/14138695785/in/set-72157632183580917 (CC BY-NC-ND)">
  World Bank/flickr
 </a>
</p>
  



Infants less than one year old face the greatest risk from pertussis.

<p>The CDC reports that pertussis cases—more commonly known as whooping cough—are up by 24% across the country.</p>

Whooping Cough Sweeps California, Putting Infants at Risk





  
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      <p>
 When a photon of light hits a plant’s photosystem, it has to make a decision—fast. Which path would be the most efficient way to the molecular machinery that converts light into sugars? Like computer scientists who want to perform superfast calculations, they turn to quantum computing.
</p>
<p>
 When light hits a plant cell, its chromophores—light-sensitive molecules—capture the photons and convert them to energy packets called excitons. The excitons bounce among the cell’s chromophores until they eventually arrive at the reaction center where water and carbon dioxide mingle to produce sugar and oxygen. The excitons could take any number of paths to get there—and indeed they do. Thanks to the quantum phenomenon known as coherence, excitons test out every pathway simultaneously,
 <a href="http://www.pbs.org/wgbh/nova/blogs/physics/2014/03/quantum-life/">
  ultimately taking the most efficient route
 </a>
 .
</p>
<p>
 At least, we suspect those quantum calculations are made in the name of efficiency. Without knowing what happens in a cell when this quantum computing is turned off, it’s impossible to know exactly what function it’s performing.
</p>
  

  
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      <p>
 Paul Curmi, a professor at the University of New South Wales, and his colleagues found a class of algae called the cryptophytes where quantum coherence is used in some but not all species. Cryptophytes are perfect candidates for testing quantum-enhanced photosynthesis because they inhabit dim environments underwater or beneath sheets of ice, where they subsist on meager scraps of light. To survive on this starvation diet, cryptophytes have to make the most of every photon they can get.
</p>
<p>
 Curmi and his colleagues identified a genetic mutation in one group of cryptophytes that, puzzlingly, blocks quantum coherence, Ashley Yeager
 <a href="https://www.sciencenews.org/blog/science-ticker/genetic-mutation-quenches-quantum-quirk-algae">
  explains
 </a>
 for Science News. The mutation slips in an extra amino acid, wrenching the two subunits of the algae’s main light-absorbing protein away from each other. That extra distance seems to be enough to keep the cell’s chromophores too far apart for the excitons to sample all the pathways between them.
</p>
<p>
 Scientists still don’t know why some cryptophytes use coherence while others don’t, but learning how the non-coherence system works—and what advantages it might confer—could shed light on why plants became quantum computers in the first place.
</p>
  

  
      <div class="newsletter"></div>
  

  
      <p>
 Photo credit: CSIRO
</p>
  



<p>A professor and his colleagues found a class of algae called the cryptophytes, which inhabit dim environments underwater or beneath sheets of ice. Quantum coherence is used in some but not all cryptophyte species.  </p>

Plants Use Quantum Computing to Gain Efficiency—So Why Doesn’t This One?





  
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 <p>
  They’re found huddling in the soil near the roots of coca plants and swimming in the industrial waste from pharmaceutical factories. They’re a bacteria called
  <em>
   Stenotrophomonas maltophilia
  </em>
  . And they eat cocaine.
 </p>
 <p>
  Cocaine overdoses send half a million people to emergency rooms in the United States every year—but once they get there, there’s not much doctors can do beyond alleviating the symptoms. Opiate overdoses can be treated with naloxone, which dulls opiate action by competing with the drug for binding sites; addicts can be given safer alternatives like methadone. But there aren’t any approved medications for cocaine toxicity, and addiction treatment is mostly limited to behavioral and psychological approaches.
 </p>
 
            <figure class="richtext-image full-width"><img alt="4923866114_cf260d947e_o" class="richtext-image full-width" height="450" width="800"
            src="https://www.pbs.org/wgbh/nova/media/images/4923866114_cf260d947e_o-e1404233687390.width-800.jpg"/><figcaption>
  Unlike opiate addiction, there aren't any pharmaceutical treatments for cocaine addiction. A bacterial enzyme could change that.
 <div class="credit"></div></figcaption>
            </figure>
            
 <p>
  So Lei Fang, a postdoctoral researcher at the University of Kentucky’s College of Pharmacy, turned to
  <em>
   S. maltophilia
  </em>
  , which produces an enzyme called cocaine esterase that breaks down cocaine into inactive molecules. Split up into its constituent parts, cocaine can’t provide its characteristic high—or the risks associated with it. You can’t just inject the bacterial enzyme into humans, though. Cocaine esterase molecules need to be in pairs to work, and because protein structure is so temperature-sensitive, the natural enzyme can’t stay paired up for longer than about 12 minutes at human body temperature.
 </p>
 <p>
  Bethany Brookshire,
  <a href="https://www.sciencenews.org/blog/scicurious/mutated-bacterial-enzyme-gobbles-cocaine">
   writing
  </a>
  for Science News:
 </p>
 <blockquote>
  <p>
   Fang and colleagues set about trying to make cocaine esterase a more stable dimer at body temperature. They carefully switched out the building blocks of the protein, amino acids, at the site where two enzymes become a matched pair. The scientists have already been able to create a version of cocaine esterase that can withstand human body temperature for six hours. And it’s already in a
   <a href="https://clinicaltrials.gov/ct2/show/NCT01846481">
    phase II clinical trial
   </a>
   to treat cocaine overdose.
  </p>
 </blockquote>
 <p>
  But Fang was hoping to do more than just treat overdoses—he wanted to find a drug that could treat addiction. To do that, you’d need cocaine esterase to function for a lot longer than six hours. So he and his colleagues used computer models to watch exactly what happens when heat unravels the enzyme. That helped them find the enzyme’s weak spots, and with just two more mutations they produced a new form that can stay paired up and active for more than 100 days. Injecting mice with this reinforced enzyme protects them from lethal cocaine overdoses for more than three months—the longest lasting effect that’s ever been demonstrated.
 </p>
 <p>
  The reinforced enzyme is more active, too—it metabolizes cocaine a thousand times faster than the human body does on its own. If cocaine esterase could digest cocaine faster than addicts could get high, it might be able to disrupt the reward circuits that feed addiction. It would be an entirely new tool for helping the country’s more than one million cocaine addicts get clean—all from a little bacterium that lives in dirt and wastewater.
 </p>
 <p>
 </p>
 <p>
 </p>
</section>

  

  
      <p>
 Photo Credit:
 <a href="https://www.flickr.com/photos/spookman01/4923866114">
  Lee Morley / Flickr (CC BY-NC-ND 2.0)
 </a>
</p>
  



Cocaine-Eating Enzyme Could Combat Addiction





  
      <p>
 When it comes to genetic engineering, we’re amateurs. Sure, we’ve known about DNA’s structure for more than 60 years, we first sequenced every A, T, C, and G in our bodies more than a decade ago, and we’re becoming increasingly adept at modifying the genes of a growing number of organisms.
</p>
<p>
 But compared with what’s coming next, all that will seem like child’s play. A new technology just announced today has the potential to wipe out diseases, turn back evolutionary clocks, and reengineer entire ecosystems, for better or worse. Because of how deeply this could affect us all, the scientists behind it want to start a discussion now, before all the pieces come together over the next few months or years. This is a scientific discovery being played out in real time.
</p>
  

  
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      <p>
 Today, researchers aren’t just dropping in new genes, they’re deftly adding, subtracting, and rewriting them using a series of tools that have become ever more versatile and easier to use. In the last few years, our ability to edit genomes has improved at a shockingly rapid clip. So rapid, in fact, that one of the easiest and most popular tools, known as CRISPR-Cas9, is just two years old. Researchers once spent months, even years, attempting to rewrite an organism’s DNA. Now they spend days.
</p>
  

  
      

<div class='pullquote'>
  <p>
 “This is one of the most exciting confluences of different theoretical approaches in science I’ve ever seen.”
</p>
</div>

  

  
      <p>
 Soon, though, scientists will begin combining gene editing with gene drives, so-called selfish genes that appear more frequently in offspring than normal genes, which have about a 50-50 chance of being passed on. With gene drives—so named because they drive a gene through a population—researchers just have to slip a new gene into a drive system and let nature take care of the rest. Subsequent generations of whatever species we choose to modify—frogs, weeds, mosquitoes—will have more and more individuals with that gene until, eventually, it’s everywhere.
</p>
<p>
 Cas9-based gene drives could be one of the most powerful technologies ever discovered by humankind. “This is one of the most exciting confluences of different theoretical approaches in science I’ve ever seen,” says Arthur Caplan, a bioethicist at New York University. “It merges population genetics, genetic engineering, molecular genetics, into an unbelievably powerful tool.”
</p>
<p>
 We’re not there yet, but we’re extraordinarily close. “Essentially, we have done all of the pieces, sometimes in the same relevant species.” says Kevin Esvelt, a postdoc at Harvard University and the wunderkind behind the new technology. “It’s just no one has put it all together.”
</p>
<p>
 It’s only a matter of time, though. The field is progressing rapidly. “We could easily have laboratory tests within the next few months and then field tests not long after that,” says George Church, a professor at Harvard University and Esvelt’s advisor. “That’s if everybody thinks it’s a good idea.”
</p>
<p>
 It’s likely not everyone will think this is a good idea. “There are clearly people who will object,” Caplan says. “I think the technique will be incredibly controversial.” Which is why Esvelt, Church, and their collaborators are publishing papers now, before the different parts of the puzzle have been assembled into a working whole.
</p>
<p>
 “If we’re going to talk about it at all in advance, rather than in the past tense,” Church says, “now is the time.”
</p>
<h2>
 “Deleterious Genes”
</h2>
<p>
 The first organism Esvelt wants to modify is the malaria-carrying mosquito
 <i>
  Anopheles gambiae
 </i>
 . While his approach is novel, the idea of controlling mosquito populations through genetic modification has actually been around since the late 1970s. Then, Edward F. Knipling, an entomologist with the U.S. Department of Agriculture, published a substantial handbook with a chapter titled “Use of Insects for Their Own Destruction.” One technique, he wrote, would be to modify certain individuals to carry “deleterious genes” that could be passed on generation after generation until they pervaded the entire population. It was an idea before its time. Knipling was on the right track, but he and his contemporaries lacked the tools to see it through.
</p>
<p>
 The concept surfaced a few more times before being picked up by Austin Burt, an evolutionary biologist and population geneticist at Imperial College London. It was the late 1990s, and Burt was busy with his yeast cells, studying their so-called homing endonucleases, enzymes that facilitate the copying of genes that code for themselves. Self-perpetuating genes, if you will. “Through those studies, gradually, I became more and more familiar with endonucleases, and I came across the idea that you might be able to change them to recognize new sequences,” Burt recalls.
</p>
<p>
 Other scientists were investigating endonucleases, too, but not in the way Burt was. “The people who were thinking along those lines, molecular biologists, were thinking about using these things for gene therapy,” Burt says. “My background in population biology led me to think about how they could be used to control populations that were particularly harmful.”
</p>
  

  
      

<div class='pullquote'>
  <p>
 “There’s a lot to be done still, but on the scale of years, not months or decades.”
</p>
</div>

  

  
      <p>
 In 2003, Burt penned an influential article that set the course for an entire field: We should be using homing endonucleases, a type of gene drive, to modify malaria-carrying mosquitoes, he said, not ourselves. Burt saw two ways of going about it—one, modify a mosquito’s genome to make it less hospitable to malaria, and two, skew the sex ratio of mosquito populations so there are no females for the males to reproduce with. In the following years, Burt and his collaborators tested both in the lab and with computer models before they settled on sex ratio distortion. (Making mosquitoes less hospitable to malaria would likely be a stopgap measure at best; the
 <i>
  Plasmodium
 </i>
 protozoans could evolve to cope with the genetic changes, just like they have evolved resistance to drugs.)
</p>
<p>
 Burt has spent the last 11 years refining various endonucleases, playing with different scenarios of inheritance, and surveying people in malaria-infested regions. Now, he finally feels like he is closing in on his ultimate goal. “There’s a lot to be done still,” he says. “But on the scale of years, not months or decades.”
</p>
<h2>
 Cheating Natural Selection
</h2>
<p>
 Cas9-based gene drives could compress that timeline even further. One half of the equation—gene drives—are the literal driving force behind proposed population-scale genetic engineering projects. They essentially let us exploit evolution to force a desired gene into every individual of a species. “To anthropomorphize horribly, the goal of a gene is to spread itself as much as possible,” Esvelt says. “And in order to do that, it wants to cheat inheritance as thoroughly as it can.” Gene drives are that cheat.
</p>
<p>
 Without gene drives, traits in genetically-engineered organisms released into the wild are vulnerable to dilution through natural selection. For organisms that have two parents and two sets of chromosomes (which includes humans, many plants, and most animals), traits typically have only a 50-50 chance of being inherited, give or take a few percent. Genes inserted by humans face those odds when it comes time to being passed on. But when it comes to survival in the wild, a genetically modified organism’s odds are often less than 50-50. Engineered traits may be beneficial to humans, but ultimately they tend to be detrimental to the organism without human assistance. Even some of the most painstakingly engineered transgenes will be gradually but inexorably eroded by natural selection.
</p>
<p>
 Some naturally occurring genes, though, have over millions of years learned how to cheat the system, inflating their odds of being inherited. Burt’s “selfish” endonucleases are one example. They take advantage of the cell’s own repair machinery to ensure that they show up on both chromosomes in a pair, giving them better than 50-50 odds when it comes time to reproduce.
</p>

            <figure class="richtext-image full-width"><img alt="gene-drive-family-tree" class="richtext-image full-width" height="449" width="800"
            src="https://www.pbs.org/wgbh/nova/media/images/gene-drive-family-tree.width-800.png"/><figcaption>
  A gene drive (blue) always ends up in all offspring, even if only one parent has it. That means that, given enough generations, it will eventually spread through the entire population.
 <div class="credit"></div></figcaption>
            </figure>
            
<p>
 Here’s how it generally works. The term “gene drive” is fairly generic, describing a number of different systems, but one example involves genes that code for an endonuclease—an enzyme which acts like a pair of molecular scissors—sitting in the middle of a longer sequence of DNA that the endonculease is programmed to recognize. If one chromosome in a pair contains a gene drive but the other doesn’t, the endonuclease cuts the second chromosome’s DNA where the endonuclease code appears in the first.
</p>
<p>
 The broken strands of DNA trigger the cell’s repair mechanisms. In certain species and circumstances, the cell unwittingly uses the first chromosome as a template to repair the second. The repair machinery, seeing the loose ends that bookend the gene drive sequence, thinks the middle part—the code for the endonuclease—is missing and copies it onto the broken chromosome. Now both chromosomes have the complete gene drive. The next time the cell divides, splitting its chromosomes between the two new cells, both new cells will end up with a copy of the gene drive, too. If the entire process works properly, the gene drive’s odds of inheritance aren’t 50%, but 100%.
</p>

            <figure class="richtext-image full-width"><img alt="gene-drive-schematic" class="richtext-image full-width" height="449" width="800"
            src="https://www.pbs.org/wgbh/nova/media/images/gene-drive-schematic.width-800.png"/><figcaption>
  Here, a mosquito with a gene drive (blue) mates with a mosquito without one (grey). In the offspring, one chromosome will have the drive. The endonuclease then slices into the drive-free DNA. When the strand gets repaired, the cell's machinery uses the drive chromosome as a template, unwittingly copying the drive into the break.
 <div class="credit"></div></figcaption>
            </figure>
            
<p>
 Most natural gene drives are picky about where on a strand of DNA they’ll cut, so they need to be modified if they’re to be useful for genetic engineering. For the last few years, geneticists have tried using genome-editing tools to build custom gene drives, but the process was laborious and expensive. With the discovery of CRISPR-Cas9 as a genome editing tool in 2012, though, that barrier evaporated. CRISPR is an ancient bacterial immune system which identifies the DNA of invading viruses and sends in an endonuclease, like Cas9, to chew it up. Researchers quickly realized that Cas9 could easily be reprogrammed to recognize nearly any sequence of DNA. All that’s needed is the right RNA sequence—easily ordered and shipped overnight—which Cas9 uses to search a strand of DNA for where to cut. This flexibility, Esvelt says, “lets us target, and therefore edit, pretty much anything we want.” And quickly.
</p>
<p>
 Gene drives and Cas9 are each powerful on their own, but together they could significantly change biology. CRISRP-Cas9 allows researchers to edit genomes with unprecedented speed, and gene drives allow engineered genes to cheat the system, even if the altered gene weakens the organism. Simply by being coupled to a gene drive, an engineered gene can race throughout a population before it is weeded out. “Eventually, natural selection will win,” Esvelt says, but “gene drives just let us get ahead of the game.”
</p>
<h2>
 Beyond Mosquitoes
</h2>
<p>
 If there’s anywhere we could use a jump start, it’s in the fight against malaria. Each year, the disease kills over 200,000 people and sickens over 200 million more, most of whom are in Africa. The best new drugs we have to fight it are losing ground; the
 <i>
  Plasmodium
 </i>
 parasite is evolving resistance too quickly. And we’re nowhere close to releasing an effective vaccine. The direct costs of treating the disease are estimated at $12 billion, and the economies of affected countries grew 1.3% less per year, a substantial amount.
</p>
<p>
 Which is why Esvelt and Burt are both so intently focused on the disease. “If we target the mosquito, we don’t have to face resistance on the parasite itself. The idea is, we can just take out the vector and stop all transmission. It might even lead to eradication,” Esvelt says.
</p>
<p>
 Esvelt initially mulled over the idea of building Cas9-based gene drives in mosquitoes to do just that. He took the idea to to Flaminia Catteruccia, a professor who studies malaria at the Harvard School of Public Health, and the two grew increasingly certain that such a system would not only work, but work well. As their discussions progressed, though, Esvelt realized they were “missing the forest for the trees.” Controlling malaria-carrying mosquitoes was just the start. Cas9-based gene drives were the real breakthrough. “If it let’s us do this for mosquitos, what is to stop us from potentially doing it for almost anything that is sexually reproducing?” he realized.
</p>
  

  
      

<div class='pullquote'>
  <p>
 “What is to stop us from potentially doing it for almost anything that is sexually reproducing?”
</p>
</div>

  

  
      <p>
 In theory, nothing. But in reality, the system works best on fast-reproducing species, Esvelt says. Short generation times allow the trait to spread throughout a population more quickly. Mosquitoes are a perfect test case. If everything were to work perfectly, deleterious traits could sweep through populations of malaria-carrying mosquitoes in as few as five years, wiping them off the map.
</p>
<p>
 Other noxious species could be candidates, too. Certain invasive species, like mosquitoes in Hawaii or Asian carp in the Great Lakes, could be targeted with Cas9-based gene drives to either reduce their numbers or eliminate them completely. Agricultural weeds like horseweed that have evolved resistance to glyphosate, a herbicide that is broken down quickly in the soil, could have their susceptibility to the compound reintroduced, enabling more farmers to adopt no-till practices, which help conserve topsoil. And in the more distant future, Esvelt says, weeds could even be engineered to introduce vulnerabilities to completely benign substances, eliminating the need for toxic pesticides. The possibilities seem endless.
</p>
<h2>
 The Decision
</h2>
<p>
 Before any of that can happen, though, Esvelt and Church are adamant that the public help decide whether the research should move forward. “What we have here is potentially a general tool for altering wild populations,” Esvelt says. “We really want to make sure that we proceed down this path—if we decide to proceed down this path—as safely and responsibly as possible.”
</p>
<p>
 To kickstart the conversation, they partnered with the MIT political scientist Kenneth Oye and others to convene a series of workshops on the technology. “I thought it might be useful to get into the room people with slightly different material interests,” Oye says, so they invited regulators, nonprofits, companies, and environmental groups. The idea, he says, was to get people to meet several times, to gain trust and before “decisions harden.” Despite the diverse viewpoints, Oye says there was surprising agreement among participants about what the important outstanding questions were.
</p>
<p>
 As the discussion enters the public sphere, tensions are certain to intensify. “I don’t care if it’s a weed or a blight, people still are going to say this is way too massive a genetic engineering project,” Caplan says. “Secondly, it’s altering things that are inherited, and that’s always been a bright line for genetic engineering.” Safety, too, will undoubtedly be a concern. As the power of a tool increases, so does its potential for catastrophe, and Cas9-based gene drives could be extraordinarily powerful.
</p>
<p>
 There’s also little in the way of precedent that we can use as a guide. Our experience with genetically modified foods would seem to be a good place to start, but they are relatively niche organisms that are heavily dependent on water and fertilizer. It’s pretty easy to keep them contained to a field. Not so with wild organisms; their potential to spread isn’t as limited.
</p>
  

  
      

<div class='pullquote'>
  <p>
 There’s little in the way of precedent that we can use as a guide.
</p>
</div>

  

  
      <p>
 Aware of this, Esvelt and his colleagues are proposing a number of safeguards, including reversal drives that can undo earlier engineered genes. “We need to really make sure those work if we’re proposing to build a drive that is intended to modify a wild population,” Esvelt says.
</p>
  

  
      <div class="newsletter"></div>
  

  
      <p>
 There are still other possible hurdles to surmount—lab-grown mosquitoes may not interbreed with wild ones, for example—but given how close this technology is to prime time, Caplan suggests researchers hew to a few initial ethical guidelines. One, use species that are detrimental to human health and don’t appear to fill a unique niche in the wild. (Malaria-carrying mosquitoes seem fit that description.) Two, do as much work as possible using computer models. And three, researchers should continue to be transparent about their progress, as they have been. “I think the whole thing is hugely exciting,” Caplan says. “But the time to really get cracking on the legal/ethical infrastructure for this technology is right now.”
</p>
<p>
 Church agrees, though he’s also optimistic about the potential for Cas9-based gene drives. “I think we need to be cautious with all new technologies, especially all new technologies that are messing with nature in some way or another. But there’s also a risk of doing nothing,” Church says. “We have a population of 7 billion people. You have to deal with the environmental consequences of that.”
</p>
  

  
      <p>
 Image credits: Tom Ellenberger, Washington University School of Medicine/NIH, Esvelt et al 2014
</p>
<p>
 Sources:
</p>
<p>
 Burt, Austin. 2003. "Site-specific selfish genes as tools for the control and genetic engineering of natural populations."
 <i>
  Proceedings of the Royal Society of London B
 </i>
 270: 921-928. DOI:
 <a href="http://dx.doi.org/10.1098/rspb.2002.2319">
  10.1098/rspb.2002.2319
 </a>
</p>
<p>
 Esvelt, Kevin M., Andrea L. Smidler, Flaminia Catteruccia, and George M. Church. 2014. "Concerning RNA-Guided Gene Drives for the Alteration of Wild Populations."
 <i>
  eLife
 </i>
 . DOI:
 <a href="http://dx.doi.org/10.7554/eLife.03401">
  10.7554/eLife.03401
 </a>
</p>
<p>
 Oye, Kenneth A., Kevin Esvelt, Evan Appleton, Flaminia Catteruccia, George Church, Todd Kuiken, Shlomiya Bar-Yam Lightfoot, Julie McNamara, Andrea Smidler, and James P. Collins. 2014. "Regulating gene drives."
 <i>
  Science
 </i>
 DOI:
 <a href="http://dx.doi.org/10.1126/science.1254287">
  10.1126/science.1254287
 </a>
</p>
  



Scientists have figured out how to use a cell's DNA repair mechanisms to spread traits throughout a population.

<p>Scientists are proposing a technology that could change nearly any sexually reproducing species anywhere.</p>

Genetically Engineering Almost Anything





  
      <p>
</p>
<p>
 Every action creates an equal and opposite reaction. It’s perhaps the best known law of physics, and Guido Fetta thinks he’s found a way around it.
</p>
<p>
 According to classical physics, in order for something—like a spaceship—to move, conservation of momentum requires that it has to exert a force on something else. A person in roller skates, for example, pushes off against a wall; a rocket accelerates upward by propelling high-velocity combusted fuel downward. In practice, this means that space vessels like satellites and space stations have to carry up to half their weight in propellant just to stay in orbit. That bulks up their cost and reduces their useful lifetime.
</p>
  

  
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      <p>
 With that in mind, Fetta designed what he called the “Cannae Drive,” which he claims creates momentum without pushing against seemingly anything at all. He recently convinced a team at NASA to test it, who presented the results at a conference yesterday.
</p>
<p>
 The NASA team, using a torsion pendulum, or a device that can measure minute forces, found that Fetta’s drive created 30-50 micronewtons’ worth of thrust. That’s not a lot of force—even one whole Newton is less than the weight you feel in your hand when you hold an iPhone—but according to the laws of classical physics, Fetta’s device shouldn’t have produced any at all.
</p>
<p>
 Fetta, an independent inventor with a background in chemical engineering,
 <a href="http://vimeo.com/29840866">
  explains
 </a>
 that the drive is a “superconducting resonating cavity.” According to him, the cavity is designed with little wells along the bottom edge to trap electrons, so that when electromagnetic waves bounce around inside the cavity, more electrons push up on the top surface of the cavity than push down on the bottom. This imbalance, Fetta says, creates upward thrust.
</p>
  

  
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      <p>
 In the paper, NASA seemed reluctant to dive into the drive’s mysterious physics. They wrote nothing to suggest how, exactly, the force was produced. In fact, the mysterious drive actually worked even when they modified it in such a way it shouldn’t have produced any thrust, suggesting the mechanics of the system are hazily understood. The one exception was a reference, in the paper’s abstract, to a possible interaction with the “quantum vacuum virtual plasma.”
</p>
<p>
 David Hambling, writing for Wired.co.uk, explains what that might mean:
</p>
  

  
      

<blockquote>
    <p>
 This […] implies that the drive may work by pushing against the ghostly cloud of particles and anti-particles that are constantly popping into being and disappearing again in empty space.
</p>
</blockquote>

  

  
      <p>
 A similar “microwave thruster” drive, proposed by British engineer Roger Shawyer, was tested last year by a Chinese team. Those results were largely dismissed. NASA’s results, though, seem to lend some credence to the idea that supposedly impossible “unbalanced forces” can actually result in momentum.
</p>
<p>
 The NASA team stresses that the drive needs to be tested more thoroughly—but if it really works, it could be a major breakthrough for deep-space exploration. Because a drive like this could be powered solely by solar energy, satellites and space stations could stay on course and in orbit without having to lug around so much propellant.
</p>
<p>
 Hambling:
</p>
  

  
      

<blockquote>
    <p>
 A working microwave thruster would radically cut the cost of satellites and space stations and extend their working life, drive deep-space missions, and take astronauts to Mars in weeks rather than months.
</p>
</blockquote>

  

  
      <p>
 We still don’t know if Fetta’s propellant-less drive works the way he claims it does—and we need more evidence before we can be sure that it even works at all. But if it does—watch out, space. We’re coming for you.
</p>
  

  
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      <p>
 Photo credit: Cannae Drive
</p>
  



A schematic of the lower half of the Cannae Drive cavity Photo credit: Cannae Drive

Improbable Thruster Seems to Work by Violating Known Laws of Physics





  
      <p>
 Triclosan is an indiscriminate killer, wiping out bacteria even in places where microbial communities are hard at work keeping us healthy, like sewage treatment plants.
</p>
<p>
 Sewage treatment plants often incorporate anaerobic digesters to reduce the volume of waste they have to deal with. Bacteria adapted to an oxygen-free environment break down organic waste, including sewage, to produce small molecules like ammonia, carbon dioxide, and methane (which can be burned as a fuel). The amount of indigestible material that’s left is much more manageable.
</p>
  

  
      <div class="ad"></div>
  

  
      <p>
 It’s a win-win system, but it won’t work without bacteria—which makes the ubiquity of antibacterial products troubling. Triclosan is one of the most common antibacterial agents, popping up both where you might expect it—in hand sanitizer and anti-acne face wash—and where some you might not—lip gloss, toothpaste, dish soap, gym clothes, even pencils. A lot of that triclosan ends up down the drain and eventually makes its way to a sewage treatment plant.
</p>
<p>
 There, it can really mess with the plant’s bacterial tenants, according new data published in
 <i>
  Environmental Science and Technology
 </i>
 . Beth Mole,
 <a href="https://www.sciencenews.org/article/triclosan-may-spoil-wastewater-treatment">
  writing
 </a>
 for Science News, explains “in wastewater treatment plants, the omnipresent antimicrobial can sabotage some sludge-processing microbes and promote drug resistance in others.” The solids that are left over are often spread on fields as fertilizer—antibiotic-resistant bacteria and all.
</p>
  

  
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      <p>
 The research team, led by Paige Novak at the University of Minnesota, also found that at concentrations like those in the most triclosan-contaminated plants, methane production starts to swing erratically, suggesting that the bacterial community is close to collapsing.
</p>
<p>
 This problem has an easy solution, though: stop using triclosan. Trading in antibacterial soap for the regular kind isn’t likely to cause an uptick in communicable diseases: hand washing alone helps prevent the spread of illness, and studies haven’t found that antibacterial soaps make it more effective. In light of that data and others that implicate triclosan in endocrine disruption and the development of antibiotic-resistant bacteria, the FDA issued a statement in 2013 statement asking companies to justify including triclosan in their products.
</p>
<p>
 Triclosan isn’t the only drug that’s ending up in our waste water. Plenty of pharmaceuticals make their way down our drains, and scientists are unsure whether that poses a problem. But just like with triclosan,
 <a href="http://www.pbs.org/wgbh/nova/next/body/pharmaceuticals-in-the-water/">
  there are some easy solutions
 </a>
 .
</p>
  

  
      <div class="newsletter"></div>
  

  
      <p>
 Photo credit: Lars Klintwall Malmqvist/Wikimedia Commons
</p>
  



Washing your hands with antibacterial soap isn't any more effective at preventing disease.

<p>A lot of triclosan ends up down the drain and eventually makes its way to a sewage treatment plant.</p>

Antibacterial Soap is Fouling Up Sewage Treatment Systems





  
      <p>
</p>
<p>
 In the Sandhills of North Carolina, scrubby pine and oak forests now cover what used to be sand dunes twenty million years ago, when the sea came 150 miles further inland. Coral snakes used to hide in the tall grasses here, their red and black bands inspiring rhymes that warn hikers to avoid the United States’ most toxic snake. No one has seen a coral snake in the Sandhills since 1960.
</p>
<p>
 But in a way, the coral snake is still present here. An impostor, the relatively harmless scarlet kingsnake, flashes its own red and black rings from its hiding places among pine needles and rotting logs. The kingsnakes’ borrowed disguise is an evolutionary memory, a reminder of the venomous coral snake that used to live in the Sandhills. Most memories wander from their originals and eventually fade—but the scarlet kingsnakes’ mimicry has been getting stronger and more faithful in the decades since the original disappeared.
</p>
<p>
 It’s an evolutionary enigma that David Pfennig is struggling to decipher. “Mimicry has always fascinated me; it’s one of the classic problems of evolution,” says Pfennig, a biologist at the University of North Carolina. It’s one that’s been studied over and over, but never under circumstances quite like this. Something is driving the kingsnake to look more—not less—like the vanished coral snake it impersonates. And Pfennig thinks that something is lurking as a ghostly imprint in the genes of the raccoons and birds and bears that hunt the Sandhills’ snakes.
</p>
<p>
</p>
  

  
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      <h2>
 A Long History
</h2>
<p>
 The study mimicry in evolution dates back to the field’s earliest days, when Charles Darwin was home in England writing up the notes that became
 <i>
  On the Origin of Species
 </i>
 , and naturalist Henry Walter Bates was trekking through the Amazon. Bates was financing his travels by collecting some of the rainforest’s many species of exotic butterflies to sell to collectors. Knee-deep in butterflies, Bates noticed that a group of brightly-colored, smelly (and, he reasoned, presumably poisonous) butterflies never seemed to get eaten by birds—and that a non-smelly butterfly in a totally different family looked very similar. A few hundred miles up the river, when the smelly butterflies looked different, the tasty ones did, too. Bates started to wonder if the resemblance wasn’t accidental.
</p>

            <figure class="richtext-image full-width"><img alt="bates-butterflies" class="richtext-image full-width" height="449" width="800"
            src="https://www.pbs.org/wgbh/nova/media/images/bates-butterflies.width-800.jpg"/><figcaption>
  Bates's butterflies
 <div class="credit"></div></figcaption>
            </figure>
            
<p>
 Darwin published
 <i>
  On the Origin of Species
 </i>
 in 1859. Two years later, Alfred Russell Wallace, who had arrived at many of the same conclusions about natural selection as Darwin, wrote Darwin with a puzzle: he kept running across groups of unrelated butterflies that looked uncannily similar. “And he said he just couldn’t understand that, it couldn’t come under sexual selection, it couldn’t come under any adaptive story that he could think up,” says Harvard biologist Jim Mallet, who spent his childhood collecting butterflies and other insects and today supplements his studies of butterfly mimicry with an extensive knowledge of the history of evolution. “The person who solved it was Bates.”
</p>
  

  
      

<div class='pullquote'>
  <p>
 “Batesian mimicry was probably the first good example of natural selection.”
</p>
</div>

  

  
      <p>
 Bates also wrote Darwin, explaining that the non-toxic butterflies were mimicking the poisonous butterflies to trick predators into avoiding them. Darwin was thrilled. “Believe it or not,” Mallet explains, “Darwin didn’t have any good examples which proved natural selection.” A nontoxic species imitating a toxic one, and changing its appearance when its model did, provided a perfect case study of a population evolving in response to the environment. This phenomenon, which came to be called “Batesian mimicry,” was, Mallet says, “probably the first good example of natural selection.”
</p>
  

  
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      <h2>
 Eye of the Beholder
</h2>
<p>
 The evolutionary strategy Bates discovered in butterflies is played out in nature again and again. Hoverflies sport wasp-like yellow and black stripes, and they sometimes even go so far as pretending to sting. Certain caterpillars’ backsides are decorated with eyespots designed to make them look like snakes. The mimic octopus, a particularly virtuosic practitioner, as its name implies, impersonates at least fifteen 15 other animals, including venomous lionfish and sea snakes. Coral snakes, whose mimics Wallace first noticed during his own travels in South America, inspire imitation more often than any other animal: more than 200 other snakes try to outwit hungry predators by flashing coral snakes’ colors.
</p>
<p>
 These flashy mimics, and their toxic models, are the characters who catch our attention. But, Pfennig says, “in a way, they’re passive actors in this play. It’s really the predators that are driving it.” Whether a mimic’s flamboyant ruse will work hinges on a cost-benefit analysis by a hungry predator: are the consequences of a bad guess outweighed by the nutritional value of the meal? Johanna Mappes, a professor at the University of Jyvälskylä in Finland, points out that “All prey, even if they are really toxic, are also a piece of meat.”
</p>

            <figure class="richtext-image full-width"><img alt="mimic-octopus" class="richtext-image full-width" height="450" width="800"
            src="https://www.pbs.org/wgbh/nova/media/images/mimic-octopus.width-800.jpg"/><figcaption>
  The mimic octopus can imitate a number of different organisms. Here, one impersonates a flatfish.
 <div class="credit"></div></figcaption>
            </figure>
            
<p>
 Figuring out which variables influence that calculation gets tricky, though, and scientists hoping to probe the evolution of mimicry have had to find some creative ways to observe predators in a controlled environment. Mappes, for example, created an aviary filled with simple black-and-white symbols, allowing her to test how quickly birds learned to interpret warning signals without interference from biases that exist with natural prey. Other groups run computer simulations with digital organisms, which can develop, learn, and reproduce far faster than their flesh-and-blood counterparts.
</p>
<p>
 These studies tell us that poison figures heavily in a predator’s risk analysis. Really noxious animals tend to accumulate mimics, Pfennig explains, because predators are strongly motivated to learn to avoid toxic meals. The more toxic the model is, the more quickly mimicry will evolve, and the more protection the mimics will enjoy. This helps us understand why mimicry is so common among snakes. “There are venomous mammals, right, there are a few venomous birds, but not like in snakes. I mean, there are really venomous snakes,” Pfennig says.
</p>
  

  
      

<div class='pullquote'>
  <p>
 Once mimicry evolves, mimics will be more accurate if their model is rare.
</p>
</div>

  

  
      <p>
 But predators always have to weigh nutritional value against any potential toxicity, and an animal’s size also helps determine whether mimicry will be a good strategy. For really tiny animals, the best bet is just to blend in, while for larger animals—which can be particularly rewarding as meals—some kind of physical defense, like horns or claws, may be more useful in deterring a predator. In that sweet spot in the middle—where large insects and small reptiles live—mimicking something toxic can convince a predator you’re not worth it. (Wallace, writing in his
 <i>
  Contributions to the Theory of Natural Selection
 </i>
 , also proposed that snakes are similar enough to each other to make mimicry easy, and that insects’ hard exoskeletons make it possible to change their external appearance without affecting their internal organs. On the other hand, he wrote, “We can hardly see the possibility of a mimicry by which the elk could escape from the wolf, or the buffalo from the tiger.”)
</p>
  

  
      <div class="newsletter"></div>
  

  
      <p>
 A predator’s calculations apparently consider the abundance of toxic and nontoxic prey, too: Mimicry is more likely to evolve if the model is common. In Florida, for example, where coral snakes are abundant, “there’s really strong selection on predators to just avoid anything that looks like a coral snake,” Pfennig explains, even the mediocre impersonators. But once mimicry evolves, mimics will be more accurate if their model is rare. In the Sandhills, where coral snakes were always scarce, a predator is more likely to take a chance on something with only a passing resemblance—statistically, it’s probably not a coral snake. Only very accurate mimics will convince a bird or a bear to stay away.
</p>

            <figure class="richtext-image full-width"><img alt="oleander hawk moth caterpillar" class="richtext-image full-width" height="449" width="800"
            src="https://www.pbs.org/wgbh/nova/media/images/oleander-hawk-moth-caterpillar.width-800.jpg"/><figcaption>
  Many caterpillars, like this Oleander Hawk moth, have eyespots on their tail end, mimicking snakes to ward off birds.
 <div class="credit"></div></figcaption>
            </figure>
            
<p>
 But even when all the conditions are right—a toxic, medium-sized model abundant enough that predators know to avoid it—it’s still not obvious how mimicry would evolve. “It is fascinating; it’s a simple idea on the surface, and textbooks are full of just the simple explanations,” says Tom Sherratt, a professor of biology at Carleton University in Canada. “But when you dig a little bit deeper there’s all sorts of interesting questions there that still have to be resolved.”
</p>
<p>
 Imagine a deadly species, with bright colors warning predators away (itself an counterintuitive development, since conspicuousness is usually a direct route to a predator’s stomach). It seems natural that other, tastier species would adopt those protective patterns, but getting there isn’t straightforward. For one thing, most prey species, which rely on camouflage to escape predators, start out looking nothing like brightly-colored toxic species: different color, different pattern, even different behavior. “How on Earth,” Sherratt asks, “would you gain all of these features in a relatively short period of time?” To go from zero to mimic without going extinct in an awkward in-between phase—where you’re different enough to be conspicuous but not enough like the model to scare predators—seems like a pretty tough evolutionary needle to thread.
</p>
<p>
 The key to this conundrum is realizing that mimicry, as Sherratt points out, “is all about deception,” which means that all that matters is a predator’s perception. A mimic doesn’t need to deceive a taxonomist—although many eventually do—it just needs to deceive a predator. And it turns out that even a minor costume change may be enough. A recent study in Finland showed that birds pick up on color much more quickly than shape or pattern. (Humans do, too, Sherratt says.) “It suggests that when mimicry evolves, all you really need, to begin with at least, is the color,” Sherratt explains. “Those other details only matter when predators start to pick up on potential differences and start to learn that not every yellow is bad to eat, and so on.” Like a novice art critic who starts off not being able to tell the difference between a Degas and a Monet, the predator can be initially fooled by a sloppy mimic, but slowly becomes more and more discriminating, gradually driving the evolution of more accurate mimicry by learning to avoid the really toxic critters and eat the forgeries.
</p>
<h2>
 Innate Avoidance
</h2>
<p>
 In the world of mimicry, though, the coral snake is stands apart, and it presents an additional mystery. “The coral snake, it’s not like in other mimicry complexes, like in certain butterflies where the consequences of a predator making a mistake might just be that it gets a tummy ache,” Pfennig says. “Here there’s a really high risk of death to a predator that makes a mistake.” In a sense, coral snakes are too toxic: A predator that chows down on a coral snake won’t learn to avoid one for its next meal—it won’t have a next meal. That throws a wrench into understanding mimicry in terms of predator learning.
</p>
<p>
 So how did avoidance of coral snakes develop so strongly that hundreds of other snakes can hide under its umbrella? In the 1970s, Susan Smith, a biology professor at Mount Holyoke, ran a series of experiments with birds that had been raised in captivity and had never seen a coral snake in their lives. When these birds were presented with a wooden stick painted with red and yellow rings, they fled to the other side of their cage. Coral snakes, apparently, have cultivated an innate, genetically-programmed avoidance in their would-be predators.
</p>
<p>
 It looks like the same thing is happening in the Sandhills: predators who were born long after the last coral snake died are still avoiding the lookalikes. “Selection hasn’t broken down yet, even though there’s been no coral snakes that any herpetologist has collected since 1960,” Pfennig says.
</p>
  

  
      

<div class='pullquote'>
  <p>
 “Selection hasn’t broken down yet, even though there’s been no coral snakes that any herpetologist has collected since 1960.”
</p>
</div>

  

  
      <p>
 Smith’s experiments weren’t perfect. Some birds simply avoid attacking anything unfamiliar, so it’s not clear that the coral-snake pattern, in particular, was what spooked them. The study could stand to be repeated, and while Pfennig says he would love to do it himself, regulations for experiments involving vertebrates have grown stiffer since the ’70s, and the red tape is daunting. Instead, researchers now leave painted clay models in the wild and tally up bite and beak marks over subsequent days and weeks. Without being able to monitor the interaction between predator and prey, we can’t fully understand the mix of perception and psychology that helps a predator decide whether to pounce or turn away. “Maybe predators in these areas, they have increased sensitivity to these ringed patterns, or maybe to the really bright colors or a combination of those two, or it could be, you know, decision rules in their brain,” Pfennig speculates. “It’s a fascinating question.”
</p>
<p>
 But we are starting to accumulate a few clues: Recent evidence suggests that red might be such a common warning color because, to the eye of a bird, it provides a high contrast to the (often green) background and looks the same, even when the light varies. If birds’ visual systems are primed to see red, and toxic animals take advantage of that sensitivity, birds that are especially jumpy around red prey would be more likely to survive and reproduce. But we still don’t know. “I think the psychology of the predators is a real black box to us, and I think that’s actually where the answers lie,” admits Butch Brodie, a professor at the University of Virginia. “Is there just something nasty about a red belly, an animal that curls up and shows you its red belly, that tweaks some part of the nervous system that says ‘don’t eat me’?”
</p>
<h2>
 Evolutionary Momentum
</h2>
<p>
 Whatever it is, the Sandhills’ kingsnakes are still exploiting it. And what’s more, Pfennig says, is that they’ve gotten even better at it. In the decades since coral snakes left the Sandhills, the kingsnakes’ appearance has gotten even more coral-snake-like. (But in Florida, where there are still plenty of coral snakes, kingsnake appearance has stayed the same).
</p>
<p>
 “It was definitely not what I expected,” Pfennig admits, although he says that the fact that mimicry tends to get better as the model gets more rare could have led them to predict it. The ingrained avoidance of coral snakes is apparently so strong that it created what Pfennig calls “evolutionary momentum:” a trait that persists after the environmental conditions that molded it—in this case, the presence of coral snakes in the Sandhills— have changed.
</p>
<p>
 But of course, the real trigger for coral snake mimicry isn’t the coral snakes at all—it’s the way the predators respond to them. The predators will determine how long that momentum lasts. If food gets scarce in the Sandhills, even genetically-programmed wariness can be overridden by hunger. “No defense,” Mappes, the Finnish professor, reminds us, “is perfect.”
</p>
  

  
      <p>
 Photo credits:
 <a href="https://www.flickr.com/photos/myfwcmedia/9295709294/">
  Florida Fish and Wildlife/Flickr (CC BY-ND)
 </a>
 ,
 <a href="http://commons.wikimedia.org/wiki/File:Batesplate_ArM.jpg">
  Henry Walter Bates/Public domain
 </a>
 ,
 <a href="http://www.flickr.com/photos/pacificklaus/6209075735/">
  Klaus Stiefel/Flickr (CC BY-NC)
 </a>
 ,
 <a href="https://www.flickr.com/photos/jacobs_ian/11077936136">
  Ian Jacobs/Flickr (CC BY-NC)
 </a>
</p>
  



Decades after the coral snake disappeared from North Carolina's Sandhills, its mimic, the scarlet kingsnake, has been evolving to look more like it.

<p>In North Carolina, a group of snakes survives by impersonating a toxic species that disappeared decades ago.</p>

Eleanor Nelson

Articles