Skip to content

We Beasties has moved!

November 1, 2010

We’ve moved to ScienceBlogs! Come check us out at our new digs 🙂

population genetics, evolution, and ocean ecosystems

October 19, 2010

I was trained as an Environmental Scientist long before I was at all interested in Microbes. So, I get excited when I come across microbial studies that are environmentally relevant. I get particularly nerd-cited when these studies take place in the ocean. A paper published in PNAS last week describes identifies what may be the key environmental factor distinguishing the evolution of microbial populations in the North Atlantic and North Pacific sub-tropical gyres.
The finding that populations of the abundant, widespread, and relatively well studied marine microbes Prochlorococcus and Pelagibacter (both) in an Atlantic study site had much higher frequencies of genes related to phosphorus (P) acquisition and metabolism than similar organisms in a Pacific study site was no surprise to the researchers. What was shocking was that virtually all of the genes with significantly different frequencies in the two sites were related to P use or uptake. This implies that reduced P concentrations in the Atlantic (relative to the Pacific) is the primary, and possibly sole, environmental factor driving the evolution of the P limited population. Environmental complexity generally prevents such complete correlations in studies comparing distant environments.

The methods in this study involved sampling water at three different depths at the two sites, isolating and culturing microbes of the two types and they sequencing the genomic DNA each population. Then they analyzed the variety in the sequences, and compared them to previously sequenced lab strains of each type, looking for genes that were present in some, but not all of microbes in the population. Most of these differences were due to random variation and neutral (not evolutionarily advantageous) evolutionary processes (genes are often passed around through horizontal gene transfer, but they not always advantageous). The genes of interest were those that were more abundant (statistically speaking) in one site or the other, because that indicates that that gene is conferring some evolutionary advantage in that environment, but not in the other. In Prochlorococcus, there were 29 such genes, and nearly all of them were more abundant in the Atlantic site, and were phosphorus-related. This pattern was confirmed with Pelagibacter.  The conclusion is strengthened by the fact that these two types organisms are very different.  Prochlorococcus is a photosynthetic cyanobacteria, where as Pelagibacter is a heterotroph

Microbial ecology is a relatively young science, and very little ecological theory has been tested with microbial populations. Studies like this one allow scientists to make predictions (that future work can support or contradict) about how evolution is working in microbial populations in natural environments. These types of studies on marine microbes are especially important because we know so little about these communities, and many of them are beginning to deal with changing environmental conditions. The paper concludes with the following statement.

In this way, population genomics of ocean microbes not only is a powerful tool for diagnosing environmental change, but also can illuminate the fundamental evolutionary processes underlying biological organization.

Coleman ML, & Chisholm SW (2010). Ecosystem-specific selection pressures revealed through comparative population genomics. Proceedings of the National Academy of Sciences of the United States of America PMID: 20937887

Everything’s contaminated (redux)

October 18, 2010

Have you noticed the recent spate of people coming down with terrifying bacterial infections contracted at Apple stores? Yeah, me neither. Still:

A leading Australian expert in infectious diseases says people who use display iPads and iPhones at Apple stores are risking serious infections and the company should do more to maintain hygiene[…]

“You wouldn’t have hundreds of people using the same glass or cup, but theoretically if hundreds of people share the same keyboard or touch pad, then effectively that’s what you’re doing,” Collignon said in a phone interview.

This, following an “investigation” in June by the New York Daily News that showed high levels of various germs on various gadgets in Apple stores. “Ew,” goes one quote from a random person coming out of the store. So should we all start wearing surgical gloves and gas masks when going to the Apple store?

As I’ve said before – the more shocking result would be if they HADN’T found any bacteria. Everything’s contaminated, period. Maybe since the Apple store seems so pristine and sterile, it’s rife for this kind of criticism. But seriously, it’s retarded. Swab any door handle, kitchen countertop, or human forearm and you’d likely be able to write the same sort of scare story. But you don’t generally see people walking around on perpetual regimins of broad-spectrum antibiotics.

A separate test of a sample of 30 mobile phones, conducted by a hygiene expert at Britain’s Which? magazine, found that the average handset carries 18 times more potentially harmful germs than a flush handle in a men’s toilet.

Well, no shit (pun only partially intended). Any half-way decent bathroom is cleaned at least once a day with some serious de-sterilizing cleansers. Unless some guy crapped on his hand and then flushed the toilet just before this test was taken – I would imagine the flush handle to be one of the cleanest locations you could survey.

So relax, play with the pretty gadgets, and if you’re really scared, just make sure you use a Dyson hand dryer after you wash your hands.

The Antibiotics of Color

October 18, 2010

Bacterial infections are problematic for any creature, even the high-flying ones. A new paper in Biology Letters shows that the colorful pigments of parrots may play a role in bacterial resistance:

We exposed a variety of colourful parrot feathers to feather-degrading Bacillus licheniformis and found that feathers with red psittacofulvins degraded at about the same rate as those with melanin and more slowly than white feathers, which lack pigments. Blue feathers, in which colour is based on the microstructural arrangement of keratin, air and melanin granules, and green feathers, which combine structural blue with yellow psittacofulvins, degraded at a rate similar to that of red and black feathers.

The paper is pretty straightforward – it’s all right there in the abstract – but the claims they make about importance aren’t really backed up by any data.

Bacterial growth over timeHere, they’re plotting the concentration of certain bacterial bi-products over time when an initial inoculation of Bacillus licheniformis is allowed to grow on different colored feathers (the different shapes correspond to different pigments present). On the one hand, it seems pretty clear that white feathers (the top line – upside-down triangles) are very permissive to bacterial growth, but black, red and blue feathers (the bottom 4 lines) are restrictive.

On the other hand, the claim that these pigments evolved for the purpose of blocking bacterial growth is unsubstantiated. It seems totally plausible, don’t get me wrong, but all birds have feather-degrading bacteria, and many have evolved bright pigments that don’t necessarily have this anti-microbial activity. It might be interesting to follow this up with an epidemiological study to see if these parrots in the wild are less prone to bacterial infection in order to make a more direct causal link.

Burtt EH Jr, Schroeder MR, Smith LA, Sroka JE, & McGraw KJ (2010). Colourful parrot feathers resist bacterial degradation. Biology letters PMID: 20926430

Ig Nobel awards go microbial

October 17, 2010

This post was team co-written by Dipti and Heather

Dipti and Heather dressed like microbes, handing out plush giant microbe at this year's Ig Nobel Awards

The well-renowned Nobel Prize speaks for its own worth. Scientists, activists, economists, politicians and others who have made an exceptional mark in their respective fields are bestowed this great and rare honor.
What happens to the quirkier researchers though? What honor can one hope to receive in recognition for making bras that can act as emergency gas masks, proving that a digital rectal massage can cure long term hiccups, studying the intricacies of bat fellatio or showing how magnets can be used to levitate frogs?. They win the equally quirky Ig Nobel Prize – the lesser known, far more entertaining cousin. This prize is awarded for “achievements that first make people laugh, and then make them think”.

Each year the Ig Nobel awards are given out in Harvard’s Sanders Theater honoring the most outstanding “Improbable Research” of the year in various categories. For example this year’s Ig Nobel Peace Prize this year was given to Richard Stephens, John Atkins, and Andrew Kingston of Keele University, UK, for confirming the widely held belief that swearing actually relieves pain, while the engineering prize was awarded to Karina Acevedo-Whitehouse and Agnes Rocha-Gosselin of the Zoological Society of London, UK, and Diane Gendron of Instituto Politecnico Nacional, Baja California Sur, Mexico, for perfecting a method to collect whale snot, using a remote-control helicopter.

Actual Nobel Laureates hand out these awards and quite a show is put on about the whole thing. There is music, drama, absurd costumes, audience participation, science demonstrations, and it all makes for a very entertaining show.
Each year a theme is chosen that comes up repeatedly throughout the night. Evelyn Evelyn – a band starring conjoint twins, of which one is Amanda Palmer – kickstarted the award ceremony with an aptly titled song called Bacteria Bacteria to announce this microbial years theme – bacteria! Two of the contributors to this blog were in attendance and even got to march in at the beginning dressed as bacteria representing Harvard’s Microbial Sciences Initiative (see photo above). Bacteria did get a bit of a bad rap during the show… there was much attention paid to the pathogenic bacteria, but given how much a tooth can ache, we suppose that is justified.

The microbial highlight of the evening was, in fact, a 3 act opera that took place on the surface of a woman’s tooth.
If nothing else, these awards are definitive proof that many (We might even say most) top-notch scientists have a sense of humor, albeit a quirky one. Please note that quirky, improbably science can be serious and noteworthy simultaneously. One Ig Nobel award winner (from 2000) won a Nobel prize in Physics this year and another the Macarthur genius grant last year. The Ig Nobel is our favorite science prize precisely because it recognizes quirky but GOOD science, doesn’t take itself seriously, and has a soft spot for bacteria.

More on protein folding and video games

October 15, 2010

A while ago, I wrote about an awesome paper in Nature that had people play a video game to learn about protein folding. Well, I was just catching up on a back-log of podcasts, and in a Meet the Scientist podcast last month, Carl Zimmer interviews David Baker, the lead author of that study.

Carl Zimmer is easily my favorite science journalist, and if you don’t read his stuff, you should. The podcast isn’t half-bad either.


Implications of the Immune response

October 14, 2010

I started writing this post before I read ERV dissecting some “the immune system is perfect” BS. Go read hers, then come back if you want more.

Now that I’ve gone through the basics of a typical immune response, I think it’s necessary to point out some of its many flaws. In many of the immunology courses I’ve taken, the mammalian immune system is presented almost as the pinnacle of evolution, but it is far from perfect. In fact, in many ways, we might be better off if it had never evolved at all.

First up – Autoimmunity. T-cells and B-cells generate random receptors that can in principal see any molecular shape, and that includes shapes that our own body produces. Intrinsically, T and B cells (collectively called lymphocytes) have no way of knowing if their receptor sees some virulent strain of E. coli or they myelin sheath of your own neurons. To counteract this problem, we have evolved elaborate mechanisms to promote immune tolerance of our own tissues. Developing lymphocytes are programed to self-destruct if their receptor binds something early on (before they are likely to have seen a real pathogen), and they get turned off if they bind something in the absence of a danger signal (usually provided by a pattern recognition receptor). There are also regulatory cells flying around the blood stream, tamping down runaway signals and trying to keep them quiescent.

But these mechanisms often break down, and we have diseases like multiple sclerosis, type-1 diabetes, rheumatoid arthritis, Crohn’s disease, Lupus, etc. In addition, there are so-called hyper-inflammatory disorders in which the immune system over-reacts to harmless molecules, yielding the wonderful trifecta of allergies, asthma, and IBD.

“But surely,” you say, “those are rare side-effects of a system that, on balance, is protective.” I’m not so sure. The second obvious flaw with our immune system is that it doesn’t actually protect us from the virulence of pathogens. This statement seems deeply counterintuitive (especially coming from an immunologist), but hear me out. How many of you readers have never gotten sick? I feel pretty confident saying that no one raised their hand. “But without an immune system, that pathogen would have killed me,” you say, and this is sort of true. Certainly, people with compromised immune systems are at a much higher risk for death from fairly routine infections, but the real question is, if no one had an immune system, what would be the outcome?

To understand this point, I think it helps to look at this from the pathogens’ perspective. What is the goal of a rhinovirus (that might cause a cold), or Plasmodium falciparum (which causes malaria), or Bacillus anthracis (better known as anthrax)? The goal is not (necessarily) to kill you. The goal is to maximize replication and transmission. And depending on the mode of transmission, there are different levels of virulence (ability to make you sick) that are more beneficial.

Transmission of a cold virus occurs by person-to-person contact. You’ll infect far more people if you’re just sick enough to still go to work or go to buy groceries. If that rhinovirus made you as sick as malaria, you’d never infect anyone. Plasmodium falciparum, on the other hand, has mosquito vectors that carry it around, and you’re actually less of a threat to the mosquitos if you’re incapacitated. It doesn’t want to kill you, because then the parasite will die as well. People do die from malaria, but that’s an unintended side effect, and in any case those people have probably already fed many mosquitos and passed the disease on. B. anthracis doesn’t care if you die, but that’s because its method of transmission doesn’t depend on its host living. It just wants to replicate as much and as quickly as possible, devouring whatever nutrients it can get its hands on. If and when the host dies, Bacillus can form spores, which are extraordinarily hearty. They can withstand all kinds of extremes (even autoclaves – the industrial sterilizers used in labs and hospitals won’t kill Bacillus spores), and can lay dormant for decades or even centuries, just waiting for a new hapless host to wander along.

This whole idea is called virulence theory, and if you think about it, the best way to guess how virulent a pathogen will be is to look at its method of transmission. Of course, there are exceptions, but the exceptions aren’t particularly successful pathogens. Several hemoragic fever viruses (think Ebola) spring up now and again and wipe out whole villages, but then they die off because they incapacitated and then killed their entire host supply too rapidly to make it to a neighboring village. But what does all this have to do with the immune system?

Pathogens have evolved to expect an immune system, and they’ve gauged their virulence accordingly. That’s why an AIDS patient can die from a normally harmless bacterial infection – those bacteria expect push-back from an immune system that isn’t there. But if we had never evolved immune systems, the pathogens wouldn’t have evolved all of those ways around it, and we would all expend far less energy and arrive at the same outcome. This is a classic example of an Red Queen evolution – an arms race between competitors. And you can see it everywhere in life, from cheetahs and antelopes to hundred-foot tall redwood trees. And my larger point is not really that the immune system is useless – clearly it was beneficial enough to our ancestors to be worth the price of energy expenditure and potential autoimmunity. The larger point is that when I write (as I often do) about the ways that pathogens get around our high and mighty immune system, remember that these evasion strategies are the rule, not the exception.