This week’s World Wide Wednesday* features 3 stories about invasive species, which are non-native plants, animals, or other organisms that have been introduced to a particular ecosystem usually through human activity. Invasive species generally cause ecological and economic damage to their new habitat by competing for resources or preying on native species. This week we’ll explore examples of harmful invasive species as well as an invasive species that’s playing nice with its new neighbors.
Beware soft fruits, the Drosophila suzukii are coming!
Most Drosophila species, including the popular lab strain D. melanogaster, are attracted to rotting fruit in which to lay their eggs, but not Drosophila suzukii. Otherwise known as the spotted-wing drosophila, D. suzukii prefer to inject their eggs directly into the flesh of fresh fruit. Once hatched, D. suzukii larvae will eat the fruit from the inside and is therefore an economic threat to fruit crops such as cherries, blueberries, raspberries, blackberries, peaches, nectarines, apricots and grapes:
Unlike other Drosophila species, female D. suzukii have a rather diabolical (to fruit at least), saw-like adaptation of their ovipositor, the external organ that deposits eggs, which allows it to pierce the skin of soft fruits:
Originally identified in Japan and Asia in the early 20th century, D. suzukiifirst appeared in California in 2008 and quickly spread across the Pacific Northwest. It has since found its way to Southeastern US states, Michigan, Wisconsin, and even Maine. More recently, the spotted-wing drosophila has been spotted in European countries as well. The spread of D. suzukii is most likely due to the export and import of affected fruits.
A smug nutria asks, “When is an invasive species no longer invasive?”
Last week, the New York Times posted this Op-Doc animated short by filmmaker Drew Christie that explores the existential question facing all invasive species, “How long does it take to become a native?” The short video provides a brief history of how nutria were originally brought to America to start fur farms and rightfully lays the blame on human activity for the introduction of the over-sized rodents to the Pacific Northwest. As nutria fur demand declined, many farmers simply released nutria into the wild. Drawing comparisons to other invasive species to the Pacific Northwest such as the American bullfrog, grey squirrels, house sparrows, and oh yeah humans, the nutria asks, “why do I get all the grief?”
Photo credit: Petar Milošević
The answer of course lies outside of the video. Nutria are capable of destroying vast areas of wetland through their destructive feeding and burrowing habits. In sensitive ecosystems, such as the Louisiana wetlands, the havoc that nutria wreak can exacerbate existing degradation thereby increasing the threat and potential damage of flooding due to hurricanes and sea level rise. Various population control methods have been implemented with varying success. The Louisiana Dept. of Wildlife and Fisheries runs a nutria hunting and trapping incentive program. Nutria has also been marketed for human consumption (although that has not gained much traction) as well as“guilt-free” fur.
Not all invasive species from Asia are bad…
Asian Shore Crab (Hemigrapsus sanguineus)
You might remember from the end of last year the story of Samantha Garvey, the recently (at the time of the story) homeless 18-year-old Brentwood High School senior whose research project made her an Intel Science Talent Search semifinalist. The subject of her research? How the presence of the Asian shore crab, an invasive predator, affected the thickness of the shells of its prey, the ribbed mussels native to Long Island Sound. Although at first glance this might make the Asian shore crab seem like another bad invasive species story, research from Brown University scientists suggest otherwise. Appearing on US shores over 20 years ago, most likely by piggybacking on commercial ships originating from Asia, the Asian shore crab has populated almost the entire eastern seaboard without disrupting native ecosystems. In fact, the Brown University researchers found that the success of the Asian shore crab did not come at the expense of indigenous inhabitants since the study found a positive correlation between the number of invasive crab and a greater number of native species.
Asian shore crabs also make great bait fortautog, one of my favorite fish to catch in RI:
This is my first installment of Around the Web Wednesdays. Every week I will gather interesting stories from around the worldwideweb to share with you all (drum roll please)…This week we will explore what Kareem Abdul-Jabbar, FASEB, and climate change scientists have in common.
Athlete as Academic Advocate
Uncontent with being just a 6x NBA champion, 6x NBA MVP, and the NBA’s all-time leading scorer, Kareem Abdul-Jabbar, he of Game of Death and Airplane! fame, has taken on a new mantle: advocate for STEM education. Earlier this month, Kareem Abdul-Jabbar visitedDr. Martin Luther King Preparatory High School on Chicago’s South Side stressing that there “are only about 450 jobs in the NBA and some of them are taken, but there are thousands of jobs in science and engineering.” The relative invisibility of black/African-American academic role models when compared to black entertainment and sports celebrities was not lost on Kareem Abdul-Jabbar, who has authored a children’s book titled, What Color is My World: The Lost History of African American Inventors.
Abdul-Jabbar remarked, “If you go to Harlem and talk to the young people there, I would say that over 90 percent of them would either want to be LeBron James or Jay-Z. And they don’t have any idea of what their potential is beyond those two areas (of sports and entertainment). And they see that as the only things available to them.” Being a green-bleeding Celtics fan, I don’t normally heap this much praise on a Laker, but in Kareem’s case he deserves it for both accomplishments on and off the court. Here’s a heartfelt thank you to Kareem Abdul-Jabbar.
How to be a science advocate
Earlier this month, as many of you know, I attended the annual Drosophila Research Conference in Chicago. In addition to learning about current research in the field, the conference offers a host of workshops that focus on career development and advocacy. Unfortunately, due to timing I missed the Advocacy Lunch hosted by FASEB‘s Director of Legislative Relations, Jennifer Zeitzer. Luckily for me, Eva Amsen covered the lunch on her blog at the Node. The take home message? Any one, regardless of where they are in the science careers, can become an advocate. Points to keep in mind: Be vocal,Have a clear message, Contact politicians and build relationships, & Generate public awareness.
Science advocacy: How far are you willing to go?
Last month, documents surfaced discrediting the Heartland Institute and its anti-global warming stance. Turns out that Peter Gleick, hydrologist and president of the Pacific Institute for Studies in Development, Environment and Security in Oakland, Calif., had assumed a fake identity to get his hands on said documents. In light of this recent revelation, Juliet Eilperin explores the inherent risks associated with the lengths to which scientists will go in the name of advocacy. This quote from Peter Frumhoff, director of science and policy at the Union of Concerned Scientists just about sums it up, “Integrity is the source of every power and influence we have as scientists. We don’t have the power to make laws, or run the economy.”
Would you eat it? Chances are, you already have. Pink slime, or lean finely textured beef (LFTB) trimmings, is made from the leftover meat after all of the marketable cuts of beef have been harvested. These are undesirable because they are fattier, contain connective tissues, and are more highly susceptible to E. coli and salmonella contamination. This is where Beef Products Inc. (BPI) steps in and processes these trimmings by centrifuging at high speed to separate the meat from the fat and then sterilizes the separated product with gaseous ammonium hydroxide (ammonia plus water). This step increases the pH of the meat creating an intolerable environment for the bacteria. The USDA allows up to 15% of ground beef content to be LFTB and does not require any labeling to indicate that ammonium hydroxide-treated LFTB has been used as filler.
The recent uproar over LFTB was triggered last week when The Daily broke the news that the federal government was set to purchase ~7 million pounds of LFTB for the national school lunch program. This sparked concerned “mother of two Bettina Siegel to start an online petition on Change.org asking Secretary of Agriculure Tom Vilsack to please put an immediate end to the use of ‘pink slime’ in our children’s school food.” (1) Another petition is pushing for stricter labeling requirements for products that contain pink slime. This, however, is not the first time that LFTB has garnered negative attention. In December 2009, The New York Times examined how effective the ammonium hydroxide treatment eliminated E. coli and salmonella, while last season’s premiere of Jamie Oliver’s Food Revolutionfeatured a segment in which he recreated how he imagined LFTB was made. While I stand with the public’s concern over the safety of LFTB as well as the demand for stricter labeling requirements so that consumers can make informed decisions, I do have a bone to pick with Jamie Oliver and food blogs covering this issue. If their agenda is to educate the public about LFTB then I think it is their duty to do it fairly and accurately.
Let’s start with Jamie Oliver
Here is the segment from last’s seasons premiere where he essentially admits he doesn’t know what he’s talking about (also, look for the woman in the shades who looks like she’s about to vomit and cry at the same time. I bet you she’d have that reaction if she saw how animals are butchered. period.):
So, let’s see at 2:12 he says, “This is how I imagine the process to be.” Imagine is not good enough. Then at 3:15, after dousing the meat with household cleaning ammonia (complete with skull and crossbones on the bottle) and some water, he admits, “I don’t know how much and the water. There’s a specific ratio but basically they wash this meat and that kills the E. coli and the salmonella and kind of pathogens.” Sure, dramatically bathing any food in ammonia that came from a bottle marked with a skull and crossbones is going to get your point across. Unfortunately for Jamie Oliver, ammonium hydroxide as a food additive is generally regarded as safe (GRAS) by the FDA and is found in a variety of food products. Furthermore, while his theatrical demonstration suggests that too much ammonia is used, the real issue, as the December 2009 New York Times articles reports, might be that not enough ammonia is used, since E. coli and salmonella was still found in some of BPI’s LFTB (2). According to BPI’s website, “By adding a tiny amount of ammonia (gas) to the beef, we raise the pH in the beef to help kill any harmful bacteria that could possibly be present.” He then later goes quasi-conspiracy theorist on us and criticizes the USDA. You can almost taste the contempt he has for his audience.
And now a word about food blogs…
I’ve seen a number of inaccuracies and misinformation being spread through blogs, in particular food blogs. The following excerpt from Eat Like No One Else struck me since it was biological in nature:
Let’s go back to why they use ammonia in the first place – to kill any E. coli bacteria. This is one of those fixing the problem we caused situations. E. coli is as natural as ammonia. We have it in our bodies right now. It became a problem when people started feeding corn to cows. This caused a mutation to occur with the E. coli bacteria in the cow, which lead to a strain that is harmful to us. Biologists from the USDA and Cornell University have known about this since 1998.
The harmful strain to which the blogger is referring is E. coli O157:H7. There is no evidence that the switch to feeding corn to cows caused a mutation that led to this harmful strain of E. coli. The O157:H7 strain is harmful because along its evolutionary path it picked up the ability to produce Shiga-like toxins, thus named because of its similarity to the Shiga toxin produced by another bacteria, Shigella dysenteriae. Shiga-like toxins bind to components on the outside of blood vessels, in particular those of the GI tract, kidneys, and lungs. The toxin is then pulled into the cells of the blood vessels where it shuts down the cellular factories (insert Bain Capital joke) that make proteins and results in cell death. Ultimately, this breaks down the lining and leads to bloody diarrhea typical of O157:H7 infection.
How did O157:H7 come to produce Shiga-like toxins? Through horizontal gene transfer. While we typically think of passing on genetic material as happening vertically from parent to child, or mother cell to daughter cell, there are exceptions. In bacteria, genetic material can be transferred “horizontally,” independent of reproduction. This can happen in several ways, a) transformation, where the bacteria takes up DNA from its environment, b) transduction, the integration of genetic material mediated by bacteriophages or phages (viruses that infect bacteria) or c) conjugation, direct transfer of genetic material from one bacteria to another through cellular contact. It’s through the second process that O157:H7 obtained the ability to produce Shiga-like toxins.
Some viruses, when they infect cells, can undergo either a lytic cycle or a a lysogenic cycle. Lytic cycles are characterized by the production of more viruses by hijacking the infected cell’s machinery. The infected cell will eventually burst and release more viruses into the environment. When viruses adopt a lysogenic program, they insert their genetic material into the genome of the infected cell thereby piggybacking on the cell’s DNA replication cycle in order to perpetuate. Under certain stressful conditions, these dormant viruses (prophages) can be coaxed into entering the lytic cycle to produce more viruses and abandon the infected cell that is under stress. With their penchant for popping in and out of genomes, you can think of viruses as nature’s recombinant DNA engineers.
Biologists have known that the E. coli O157:H7 E. strain became toxic through infection by Shiga-like toxin- converting phages for several reasons. First, the production of these viruses could be induced by subjecting the O157:H7 to irradiation (3). Furthermore, these viruses could in turn be harvested and infect a different E. coli strain and consequently confer the ability to produce Shiga-like toxins. Then in 2001, biologists sequenced the genome of O157:H7 and confirmed the presence of DNA sequences from Shiga-like toxin-converting phages (4).
Back to the biologists from Cornell. What they were studying was how cattle diet affected the acid resistance of E. coli. Normally, the acidity of our stomachs is inhospitable to many microorganisms. However, E. coli can survive extreme acidity if it is first habituated under mildy acidic conditions. When exposed to an acidic environment, E. coli responds by initiating an innate acid resistance program (5). This is no more a mutation than how our own body responds with a fever to infections. The researchers at Cornell observed that the pH in the colons of cattle fed corn was lower (more acidic) than that of cattle fed hay (6). This is because, in contrast to hay, the difficult-to-digest starch in corn passes through the cattle’s GI tract and ends up in the colon where it ferments and acidifies the environment. Therefore, the researchers hypothesized that any E. coli that ends up in the colon could become acid-resistant thereby increasing the likelihood of contaminating meat during slaughter as well as increasing the ability of the bacteria to survive the acid shock of our stomachs. What they found was that colonic E. coli from cattle fed corn were in fact acid-resistant. However, since the cattle they used in the study tested negative or the O157:H7 strain, they confirmed the ability of O157:H7 to become acid resistant in the lab. In contrast, E. coli from cattle fed grass or hay were less acid resistant and could not survive an “acid shock” comparable to the environment of the human stomach. This prompted the scientists to suggest that switching from corn to hay feed days before slaughter might reduce the load of acid- resistant E. coli. Unfortunately, many follow-up studies have yielded results that directly contrast the oft-cited study from Cornell and call into question the importance of acid-resistance in O157:H7 virulence (7,8).
Now, this is by no means a tacit defense of the meat industry, whose practices leave much to be desired. While much focus has been on the O157:H7 strain, there are other pathogenic strains of bacteria that are associated with the beef industry. To BPI’s credit, they have voluntarily started testing for 6 other strains of virulent E. coli following the 2011 outbreak in Germany. However, I do echo the demands made by the public (as well as Mr. Oliver and aforementioned food blogs) that the labeling requirements for products containing LFTB be of a higher standard so that consumers can make informed choices. That being said, how we inform the public must also be held to a high standard or we run the risk of undercutting and discrediting the importance of the message.
3. O’Brien, A., Newland, J., Miller, S., Holmes, R., Smith, H., & Formal, S. (1984). Shiga-like toxin-converting phages from Escherichia coli strains that cause hemorrhagic colitis or infantile diarrhea Science, 226 (4675), 694-696 DOI: 10.1126/science.6387911
4. Perna, N., Plunkett, G., Burland, V., Mau, B., Glasner, J., Rose, D., Mayhew, G., Evans, P., Gregor, J., Kirkpatrick, H., Pósfai, G., Hackett, J., Klink, S., Boutin, A., Shao, Y., Miller, L., Grotbeck, E., Davis, N., Lim, A., Dimalanta, E., Potamousis, K., Apodaca, J., Anantharaman, T., Lin, J., Yen, G., Schwartz, D., Welch, R., & Blattner, F. (2001). Genome sequence of enterohaemorrhagic Escherichia coli O157:H7 Nature, 409 (6819), 529-533 DOI: 10.1038/35054089
5. Foster, J. W. Escherichia coli acid resistance: tales of an amateur acidophile. Nature Reviews Microbiology2, 898–907 (2004).
6. Diez-Gonzalez F, Callaway TR, Kizoulis MG, & Russell JB (1998). Grain feeding and the dissemination of acid-resistant Escherichia coli from cattle. Science (New York, N.Y.), 281 (5383), 1666-8 PMID: 9733511
7. Hancock, D. & Besser, T. E. coli O157: H7 in hay-or grain-fed cattle. College of Veterinary Medicine (2006).
Last night’s “Future Advances in Drosophila Research” session of the Drosophila Research Conference concluded with Ross Cagan‘s eloquent defense of using Drosophila for better drug design and better disease models. He argues that Drosophila has significant advantages, including genetics, generation time, and tools, over other organisms (sorry mice) to model complexity (and complex diseases) He started with the premise that single genes that drive diseases such as cancer are not always the best therapeutic targets. Why? Because often times targeting their activity is highly toxic to the cell. He then went on to describe a Drosophila model for medullary thyroid carcinoma (MTC). About 95% of all MTC cases are due to genetic mutations that activate the RET kinase. Despite the fact that Drosophila do not have thyroids, Dr. Cagan was able to model MTC in the fly by directing expression of RET kinase mutants responsible for MTC in the eye which led to tumor growth:
Furthermore, when he directed the expression more globally, the flies died before reaching adulthood. He then went on to describe a drug that was highly effective at rescuing these phenotypes known as AD1. Surprisingly, AD1 was not a very effective inhibitor of RET kinase activity or in his words the “world’s worst kinase inhibitor.” It wasn’t very specific and it wasn’t very effective. But this broad spectrum behaviour of AD1 was precisely why it was effective at rescuing the defects in the fly. RET kinase is a protein that regulates the activity of other kinases such as RAS, Src, PI3K (all of which are involved in cancer). Guess what? AD1 was targeting all of them. When the activity of other structurally similar compounds, AD2 and AD3, were compared to AD1 they were less efficacious because they were unable to target all of those other kinases. More importantly, since AD1 was “the world’s worst kinase inhibitor” it displayed little toxicity to the animal as a whole indicating that tumors might have lower tolerance thresholds for drugs than the entire animal. All of which to say is that a focused approach on a single target over a multitarget approach is not always the best course given that cancer is a complex disease.
This multitarget approach segued nicely into the second part of his talk where he focused on building better models for disease in Drosophila. He highlighted the work done by a post doc in his lab, Erdem Bangi (a former graduate student the Wharton lab where I work in now), who is designing a better model for colorectal cancer. Treatment for colorectal cancer is an unmet need in the healthcare. Building on the idea of multiple targets and the fact that tumors often exhibit mutations in multiple closely associated genes rather than just one gene, Dr. Bangi is creating mutant flies with different combinations of mutations in different genes. We’re talking double, triple and quadruple mutants. In these multiple mutant flies, Dr. Bangi found that drugs that were previously effective in models where only one particular gene was mutated were effectively useless. This harkens back to the original premise that targeting the single gene driving disease is not always the best approach. Dr. Bangi is now using these multiple mutant flies to design and discover more effective drugs.
The work highlighted by Dr. Cagan last night is important in that it represents a shift in how we discover drugs and how we should think about treating diseases. Rather than just taking a chemical and testing to see if it can rescue a particular phenotype, this research underscores the importance of knowing the role of multiple gene targets in disease progression. His talk highlighted not only the value of basic research in drug discovery and design but also the intrinsic advantages of Drosophila as a model organism. Can we do it better in Drosophila? Come on everybody altogether: Yes we can! (and my pandering to Chicago continues…)
Every year, hundreds maybe even thousands of biologists converge on a lucky US city like fruit flies swarming on yeast. The reason? The Drosophila Research Conference, or as people in the know call it…The Fly Meeting. This year, the annual meeting rolls into Chicago. The Windy City. Chi-Town*. The City of Big Shoulders. Home of such notables as Subrahmanyan Chandrasekhar, winner of the Nobel Prize in Physics, Vladimir Drinfeld, mathematician, winner of the Fields Medal, President Barack Obama, and of course Kanye West:
In terms of conferences I’ve been to, the Fly Meeting is like the Pitchfork Festival of scientific conferences. (I was going to go with Bonnaroo or Coachella at first, but I went with pandering instead.) Over the next 5 days, Drosophila researchers are going to get down and dirty, immersing themselves in the latest research and scientific techniques, catching up with old colleagues, establishing new collabo’s, attending concurrent research talks and poster sessions. Oh the poster sessions! Imagine an auditorium filled with rows upon rows of posters and hundreds of scientists buzzing from one poster to the next and the atmosphere is thick and dank. The uninitiated might mistake the odor for lack of hygiene, but us pros know…it’s the sweet smell of science.
A couple of weeks ago I was reproached on Facebook for overenthuiastic tweeting and my apparent affinity for hashtagging. Here’s a sampling of their criticisms:
“what’s with all these GD pound signs?”
In their defense, I hadn’t quite figured out how to selective tweet and so was probably spamming their feed, which coincidentally looks a lot like a Twitter feed. Regardless, I felt rebuked by my peers and I have to admit, it stung a little bit.
Full disclosure: I hated the very thought of “tweeting” at first. I was under the impression that tweets were basically glorified “Away Messages”–remember those?– or a medium for people to spit out attention-grabbing, sometimes clever, sometimes funny one-liners. And in reality, a lot of Twitter IS just that. However, coinciding with the launch of my blog, I decided to join Twitter under the strong advice of a very capable, scientific blogger (@Katie_PhD) as a means to advertise and network. I don’t regret following her input and here are the reasons why I think Twitter can help science:
Twitter has been my stock ticker of science news, constantly updating with stories and commentary. I haven’t felt this up-to-date on popular science, policy and outreach in years…maybe ever. I’d go as far to say that in many ways Twitter (and also blogging) has rekindled this disenchanted, graduate student’s interest in all things science, which had long gone dormant. And yes, the news cycle is fast, but I don’t fear missing anything since most of the days science stories is retweeted.
My Wishlist: what’s trending amongst my followers/followees rather than globally.
Information is disseminated and can be accessed quickly, which can be used to promote your research or exploited as a tool to mobilize people into action–think the Arab Spring, in which both Twitter and Facebook were instrumental. Of more relevance to this blog, it was used to rally opposition against the Research Works Act (#RWA). Furthermore, rapid movement of knowledge is inline with a trend toward more “open science.”
Unlike other social media, Twitter is decidedly public in nature. You have access to people outside of your normal circles or networks since strangers can follow your tweets. Think about it, when was the last time you friended a stranger on Facebook. Never. It doesn’t happen because it’s weird. Twitter allows you to interact with strangers without it feeling, for the most part, creepy. I am, therefore, able to get my blog out to a larger audience faster. And for those concerned about privacy, the simple interface means that profiles are very limited. The only thing that’s public, really, is what you tweet.
For many comedians, the Twitter format is a godsend. It allows their personalities to shine through in 140 characters or less (read: one-liners). And it’s an art, which I think @michaelianblack absolutely kills. Now, I know this is hard to believe, but lo and behold, there are funny scientists. And witty ones. And interesting ones. And some of them are on Twitter. What’s great about Twitter is that it lends itself to the re-branding and re-headlining of science news (and all news really) through wit, sarcasm, insight and commentary. This is all value-added, and can make the difference between whether someone reads an article or not. Random example from my feed:
Ultimately, Twitter can help make science more accessible to the public. One of my goals in starting this blog was to increase science accessibility to the public and bridge the divide between the public and science. I think an effective way of doing this is through humor and personality. And in a larger context, the issue of personality is important because where before scientists have been pigeonholed into the role of the dull and charmless nerd, there is now pushback. For evidence, check out these projects:This is What a Scientist Looks Like andI am Science.