John Williams, the beekeeper at Down House in England, talks about Darwin's bees. And May Berenbaum, entomologist at the University of Illinois at Urbana–Champaign, talks about the latest publication related to colony collapse disorder and ribosome damage in the Proceedings of the National Academy of Sciences. Web sites related to this episode include www.bee-craft.com
Steve: Welcome to Science Talk, the weekly podcast of Scientific American, posted, on August 25th 2009. I'm Steve Mirsky. This is the special third part of our two-part bee podcast. It was going to consist solely of an interview I had done in July with John Williams, the beekeeper at Down House, Darwin's home in England, but on August 24th, May Berenbaum from the first two parts of this series, her student, Reed Johnson and their colleagues, published a major paper on colony collapse disorder in the Proceedings of the National Academy of Sciences. So, I called May Berenbaum the morning of August 25th, and we'll hear that conversation, after which John Williams will talk about Darwin's bees. So one more time, here's May Berenbaum speaking from her office at the University of Illinois in Urbana–Champaign.
Steve: Dr. Berenbaum, in part 1 of the podcast, which was recorded actually in February, you talked about the fact that your student, Reed Johnson was doing the genomic analysis of the honeybees and that might yield some really interesting clues as to what's really going on with colony collapse and just fortuitously for our scheduling, on August 24th, your paper was published in the Proceedings of the National Academy of Sciences. Can you just talk about what new information you've gotten so far?
Berenbaum: Well, back in February, the results of [the] microarray analysis, we knew that we were seeing these potentially broken ribosomes in the bees afflicted with colony collapse disorder.
Steve: Broken ribosomes!
Berenbaum: You know, ribosomes are the protein factor[ies]s in the cell. Every cell has a nucleus, which is kind of the headquarters that provides instructions and beyond the headquarters building, the nucleus, there is the surrounding cytoplasm, that's where all the instructions to the nucleus are carried out. The ribosome is a cell structure where proteins are made, based on the instructions from the nucleus. So, every cell needs ribosomes to make proteins, so the sight of these broken ribosomes suggests that something was profoundly wrong with the bees afflicted with colony collapse disorder. So we knew what the damage was, at least we had a fairly reliable indicator of the damage associated with CCD. What we didn't really have a plausible explanation for is what was busting up the ribosomes. And since February, what we also noted on the microarray, in addition to honeybee genes, the microarray included genetic material from some of the most widespread pathogens or disease-causing organisms.
Steve: So, when you're doing your searching you're able to look at both what genes are active in the honeybees and what genes are active in the parasites that could attack the honeybees.
Berenbaum: Basically, yes. Because we included these pathogens in the microarray because it's kind of a twofer; you can extract the genetic material that comes out of the bees and look at the genetic material that belongs to the bees and the genetic material that doesn't belong there in the first place, that is from the pathogens. And one thing we noticed is that the bees with colony collapse disorder had multiple infections with a particular type of pathogen called the "picornalike" virus. Now, picornalike: pico means little, RNA means the genetic instructions that are based on DNA, so— "little RNA" viruses. And this was quite eye-opening because, as it turns out the picornalike viruses all attacked the ribosome. And in the past, there had been previous studies that linked colony collapse disorder to [a] particular picornalike virus. In September of 2007, Diana Cox-Foster and her collaborators identified a new virus called the Israeli acute paralysis virus, which is one of these picornalike viruses, and associated it with CCD. But it didn't appear to cause it, it wasn't there every time. Well, our finding was, it wasn't one particular virus, but multiple viruses that all seemed to attack the ribosome, and ultimately the ribosome can't send them off, what happens is these viruses take over the ribosome and instead of making bee proteins, the ribosomes start making viral proteins. So the bee apparently has the capacity to deal with one or two of these, but multiple viral infections, basically the whole system breaks down.
Steve: So, is this the smoking gun?
Berenbaum: Well, the analogy I've used with respect to this particular study, [it's] not the smoking gun, it's the bullet hole.
Steve: It's the bullet hole!!! Okay, which we didn't have until now.
Berenbaum: Right. What exactly the cause of the, I mean, still a correlative study, but we now have an explanation for what went wrong: Bees can't survive without functional ribosomes. The ribosomes make the proteins that allow bees to respond to pesticides, to respond to diseases, to respond to poor nutrition. So, the ribosomal fragments that we were finding explain a lot of things. It explains among other things the observation that CCD seems to be caused by everything. In fact, it very well might be that once the ribosomes cease functioning properly, then anything can cause bees to go under.
Steve: Right, in that way you could think of it maybe as being similar to an HIV infection in humans.
Berenbaum: With the caveat [that] it's not the immune system that's affected.
Steve: Right. Yeah, exactly. All I mean is that that might not be the immediate cause of, you know, the death of the individual, it's just that now they're susceptible to anything that ordinarily they could have dealt with.
Berenbaum: Exactly. So an opportunistic stress. It just can't be handled.
Steve: So now, what's the next step in the overarching research project to try to find the cause of CCD and deal with it.
Berenbaum: Well, one thing we really like to do, we are proposing that these, an overabundance of these ribosome fragments can be used as a genetic marker for CCD; that's something that we've been lacking up till this point. Colony collapse disorder is diagnosed subjectively, based on the number of frames in a hive that appear to be affected; the relative ratio of forgers to bee workers that go out in the field versus bee workers that stay inside; the ratio of adult to immature bees. And these are very changeable parameters— they change geographically, they change throughout the season. So with an objective molecular diagnostic tool, we can actually see if in fact colony collapse disorder is one phenomenon or whether bees all over the world are disappearing for multiple reasons.
Steve: Very interesting. I don't know if you can hear the cicadas by the way. I forgot to close the window where I'm recording, and we're really teaming with cicadas over here, and so it's kind of a nice background sound for our whole insect chat. Well, this is all really fascinating stuff, and I guess, you know, once you've dealt with the media talking to you over the next couple of days, it's going to be right back to the lab to go back to work on this problem.
Berenbaum: I sure hope so, although I have to say it's a real challenge explaining in simple terms what our findings represent, because it's not simple. It's not, you know, a whodunit, it's not the butler who did it.
Steve: Right, it's not a game of Clue, it's not that easy, it's not the butler, I forget who the Clue characters are but in the kitchen with the …
Berenbaum: Colonel Mustard in the Library with the candlestick!.
Steve: There you go, yes. It's three people in four different rooms with six different implements.
Berenbaum: Yeah and kind of requires sort of a basic lesson in cell biology, in the central dogma of contemporary biology.
Steve: Right, because that ribosome is this little machine in the cell that makes the proteins, and if that goes awry than everything starts to collapse.
Berenbaum: That's at least our operative hypothesis now.
Steve: Great, thank you very much.
Berenbaum: Thank you.
Steve: Don't forget to check out May Berenbaum's new book The Earwig's Tail. In early July, I was in London for a conference, I took an afternoon and went up to Darwin's house in Down where I ran into beekeeper John Williams.
Steve: Tell me about what you do and what you do specifically here at Down House.
Williams: Well, I am a beekeeper, and I became involved with English Heritage a few years ago when they really wanted to put on a display of what Charles Darwin did with honeybees. It is quite a lot in the Origin of Species which Darwin wrote about the building of cells, the hexagonal shape of cells, and so that's how I got involved with the project, and I found it very interesting too.
Steve: So, you live nearby and you're an avid beekeeper.
Williams: Yes, I am an very enthusiastic beekeeper, and I live nearby and that was the main reason why I was asked to help them.
Steve: And the actual exhibit we have here is a working, living hive inside Darwin's old laboratory.
Williams: Yes, it is an observation hive; you can't compare it really with a production hive. It's purely for observing bees and of course that's one of the things that Darwin did. He had an observation hive here in Down. We don't know exactly where it was because the laboratory hadn't been built at that time he had the observation hive, which was in 1858, when he had a few types of hives here trying to solve the question of how will bees build the hexagonal cells? Many people thought it was the mathematical skills they were given especially by God to build the cells, but Darwin was able to explain how the building of the cells was achieved in evolutionary terms.
Steve: And in a nutshell or a hive cell how do you explain [it] in evolutionary terms?
Williams: The best explanation is that he studied the cells built by bumblebees and also by a Mexican stingless bee, which showed that any cells that intersected or nearly intersected, the bees built a straight wall in between the points of intersection. And of course if you have a bundle of cylinders to get close together there would be six cylinders around one cell; and inevitably if you then aim to save wax and that's the other instinct of the honeybee, is to build cylinders and to save wax. To save wax you'll inevitably end with six-sided hexagonal cells.
Steve: So minimum expenditure of the bee's resources.
Williams: Absolutely. It's very similar in a way to why the Giant's Causeway, for example, in Northern Ireland, are also hexagonal and there are in nature other examples of hexagonal forms, because it is the most economical form for containing larva, pupae, and, of course, for the storage of honey.
Steve: And anybody who is fortunate enough to come and visit Down House will be able to see this observation hive which is also connected to the outside world.
Williams: Well, we are trying to do that now, trying to get that connected through the BeeCraft Web site, that's a magazine for beekeepers as you could have guessed, and that, I think, will also be on the English Heritage Web site in due course.
Steve: So there will be a camera set up here, so anybody anywhere in the world should be able to take a look at this.
Williams: It is a frightening thought isn't it?
Steve: It is, so behave yourself when you're here. But there also is a plastic tube that's connecting the observation hive to another room or to the outside …
Williams: To the outside world.
Steve: So free living bees can come in and join the hive.
Williams: Of course the bees need to fly out. Because it's permanently sited here throughout the season but not through the winter; it's too cold for them in winter to keep the colony warm in such a small hive.
Steve: And you have not personally witnessed the kind of decrease in bee populations though we've been seeing in the States.
Williams: No, personally I haven't suffered the losses, but we are very concerned about some of the new diseases that are coming along. I think we are learning a lot about how to manage the population of the Varroa mite, which appears to cause a lot of trouble, the interaction between the mite and various viruses. And some of our scientists, I believe, are learning a lot about that, and we are able to keep the mite under control in terms of population and I think that's saved us a lot of losses. We have suffered losses through poor summers and that is usually, we suffer the losses during the following winter.
Steve: And the poor summers begin the cascade downward because?
Williams: Well, because in the mating of the queen, the new queens for next year's honey crop, the mating takes place in flight and the ideal conditions are lovely, warm days— like we have today— with minimal breezes, so that the drones, the male bees, will form into congregation areas which is what we now know they do, and the queens fly into those areas to be mated. And. of course, poor summers means it's opportunity for queen mating more limited, and that usually manifests itself during the winter when she runs [out of] male sperm and is producing only drone bees — male bees— instead of the worker female bees that we need for the spring.
Steve: Anybody who is listening to this and would be interested in accessing your columns in your publication, can do so how?
Williams: Well, the magazine BeeCraft, they have a Web site and I think if you Google "beecraft" you undoubtedly will be able to get that.
Steve: BeeCraft and John Williams.
Williams: Well, yes and there are many other beekeepers right across. It's a very interesting monthly magazine especially for, of course aimed at beekeepers.
Steve: Great talking to you. Thank you very much for your time.
Williams: It has been a pleasure.
Steve: If you don't feel like googling, the Web site for beecraft magazine is www.bee-craft.com.
Steve: Well, that's it for this episode of Science Talk. Check out www.ScientificAmerican.com for the latest science news including an article on a new bone cement for fractures— no it is not Felix Unger's barnacle glue. And the story on the new state-of-the-art research into high-temperature ice cream. You thought I was going to say superconductivity, didn't you? No, I am talking about something really important here. And we will be back later in the week with our regularly scheduled podcast featuring a discussion related to the special September Origins issue of Scientific American magazine. For Science Talk, the weekly podcast of the aforementioned Scientific American, I'm Steve Mirsky. Thanks for clicking on us.