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Science Magazine Podcast
Transcript, 5 December 2008 show
http://podcasts.aaas.org/science_podcast/SciencePodcast_081205.mp3
Music
Host – Robert Frederick
Hello and welcome to the Science Podcast for December 5th, 2008. I'm Robert
Frederick. This week: how the fetus tolerates its mother; progress, but still no
consensus, on dark matter; and a potential treatment for the most common form of
muscular dystrophy in boys. All this and more, plus our usual roundup of stories from
our free, online daily news site, ScienceNOW.
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Support for the Science Podcast is provided by AAAS—the Science Society—publishers
of Science magazine. Advancing Science, Engineering, and Innovation throughout the
World for the Benefit of All People: the American Association for the Advancement of
Science, at www.aaas.org.
Music ends
Host – Robert Frederick
During human fetal development, the immune system does something quite different than
previously thought: it generates regulatory T cells that suppress its own immune system.
In a paper in this week's Science, Jeff Mold and colleagues report that generating these
regulatory T cells allows the fetus to become immunologically tolerant of itself and of
any other antigens while in the uterus. In particular, it helps to explain why the fetus is
particularly tolerant of the mother, an immunological tolerance that lasts well into
childhood. The research may lead to insights about how to treat fetal disease and the
pathogenesis of mother-to-child transmission of pathogens such as HIV, in utero. I spoke
with Mold from the Division of Experimental Medicine at the University of California
San Francisco.
Interviewee – Jeff Mold
What we found is that fetal T-cell responses are actually quite a bit different than what
was previously thought. The maternal cells actually enter the fetus during pregnancy,
and that upon exposure to these cells, the fetal immune system responds by generating a
population of T cells whose job is to suppress further immune responses, such that we
can detect this level of regulatory T cells in the fetus, which are actively suppressing fetal
antimaternal immune responses.
Interviewer – Robert Frederick
That makes the fetal immune system quite different than the adult immune system,
doesn’t it?
Interviewee – Jeff Mold
Yeah, it does, actually. So, what had previously been thought is that the immune system,
in a fetus, was quite a bit more naïve, I would say, than the adult immune system or
maybe even some would say dysfunctional, such that people didn’t really consider this
type of challenge to be a possibility. But, what we found is that fetal T cells are actually
quite functional, it’s just the way they respond to alloantigens, at the very least, is quite a
bit different than how the adult responds.
Interviewer – Robert Frederick
Is the human fetal immune system unique in doing this – the generating these regulatory
T cells?
Interviewee – Jeff Mold
So, that’s an interesting question. The human fetus is unique in having an immune
system compared to the mouse. It’s not been very well studied in many species, other
mammals, but it’s likely that primates, and even other higher mammals have longer
gestational periods might have an immune system earlier on. There is evidence that mice
develop regulatory T cells against noninherited maternal alloantigens as a result of fetal
exposure, although, the mechanism is likely to be quite a bit different because the mouse
doesn’t really develop T cells until after birth. So, one of the interesting clues that we
had that something was going that was quite interesting about the human is that the
frequencies of regulatory T cells are very high, early in gestation, at the onset of the
development of the fetal immune system, and they taper off towards birth. And, that’s
quite a bit different than what has been reported in the mouse where they start off at, you
know, 0% at birth and build up to levels that are seen in adulthood.
Interviewer – Robert Frederick
Now, you said the maternal cells are crossing over and are found in the fetal tissues. So,
the immune response of the fetus is suppressed only for the maternal antigens, or is this
suppression sort of general for pretty much anything?
Interviewee – Jeff Mold
I would guess that it, it would be general for pretty much anything. We chose to look at
fetal antimaternal responses – for one reason because it was the easiest thing to look at.
Isolating a single self antigen, for example, would have been very difficult considering
that there’s likely to be thousands of them that an immune response would be generated
against. And, there was some clinical evidence, dating back quite a few years, that
there’s likely to be exposure to noninherited maternal alloantigens in the form of
maternal cells crossing the placenta during pregnancy, and that that exposure might lead
to tolerance. So, we had some reason to suspect that that could be one of the antigens
that the fetal immune system would be exposed to during pregnancy.
Interviewer – Robert Frederick
So, the suppression, then, if it’s in response to pretty much anything, what then would be
sort of the point of having even developed an immune system, at that point?
Interviewee – Jeff Mold
The way I like to think about it is that the fetus itself is a very rapidly kind of changing
environment, like there’s many organ systems that are developing at this stage, and the
stuff that the immune system is going to be exposed to is likely to be fairly dynamic,
early on. So, having an immune system, at this very early stage of development, the
purpose may be to kind of get a feel for what’s out there and to try to become tolerant to
all those things that are present early on. I mean, another unique feature of the fetus,
compared to the adult, is that under normal conditions there’s not likely to be exposure to
the wide array of environmental pathogens and bacteria and so forth – all that happens
after birth. So, in theory, you don’t really need to have an “effector” type of immune
response early on, or an immune response that’s capable of attacking things. At that
stage, you probably want to be kind of surveying and saying, “Okay, this is me.
Everything that’s here I’m going to protect myself from attacking myself against.” And,
stuff that, you know, comes along later will be entering an environment where there’s
already this kind of state of tolerance that’s in check against all things that are part of the
fetal systems. And, if maternal cells get across at this time, they may just become
recognized as part of the fetus.
Interviewer – Robert Frederick
How long does that recognition of a mother’s cells continue to regulate the immune
system after birth? In other words, when does the immune system of a child grow up?
Interviewee – Jeff Mold
That’s, you know, a very good question and has been something that a lot of people have
been studying for quite a long time. And, I, I don’t think we know. You know, we
looked at this window that was fairly early in development, it’s quite a bit harder to look
after the time that we looked at stages between, you know, midgestation and birth.
Certainly, the immune system of a neonate is different than that of an adult, in ways that
are not fully understood. But, in terms of the regulatory T cells that are generated, at the
stage that we’ve looked at, we could find some evidence that they still exist into, you
know, later periods of childhood and even, you know, young adulthood, if you want to
consider the later teenage years that. And, you know, there is some clinical evidence that
suggests that young adults are capable of responding, or of tolerating, noninherited
maternal alloantigens present on sibling organ transplants better than they are at
tolerating noninherited paternal alloantigens or foreign HLA molecules. So, it could be
that the tolerance that’s generated very early on, lasts for quite a long period. As far as
the ability to generate that tolerance – that aspect of the immune system is really not
understood at all. I think that’s what we’re looking at right now.
Interviewer – Robert Frederick
Well, Jeff Mold, thank you very much.
Interviewee – Jeff Mold
Thanks.
Host – Robert Frederick
Jeff Mold is lead author of a paper on the development of fetal regulatory T cells in utero.
Read the paper in this week’s Science.
Music
Host – Robert Frederick
The Bush Administration is moving to put a number of new regulations on the books
before President-elect Barack Obama takes office. Here with more about it is Science
deputy editor Barbara Jasny.
Deputy Editor – Barbara Jasny
Sixty-one rules have gone through in the past month, and more are on the way.
The "midnight regulations," as they are known, pertain to a wide range of issues. Many
benefit industry, such as final or near-final rules that would ease constraints on oil and
shale development, or inhibit Congressional power to halt logging and mining on public
lands. Federal development projects might be able to proceed without undergoing
independent scientific review under the Endangered Species Act.
Other controversial rules involve government regulation of toxic substances in the
workplace, accelerated judicial review for death sentences, and Medicaid cuts that state
officials worry could jeopardize dental care for children and other types of healthcare.
Bush isn't the first president to engage in midnight regulations. Still, dozens of advocacy
groups are taking note and some may try to block implementation of the regulations via
lawsuits or other means. In addition, Democrats in Congress have pledged to work with
incoming President Obama to seek to overturn some of the new rules. However, for
some of these rules, it could be a complicated or time-consuming process.
Host – Robert Frederick
That was deputy editor Barbara Jasny with a policy update from Science and the AAAS
Center for Science, Technology, and Congress.
Music
Host – Robert Frederick
If you can measure distance and speed of stars as they move about, you can determine the
mass of what you see using Doppler shift measurements. But in interpreting those
measurements, scientists have shown that there's a lot more mass in the Universe than we
can see. This is the "dark matter" of the Universe. And in a Perspective in this week's
Science, Gerry Gilmore writes about how two large projects -- the Gaia satellite and
Large Hadron Collider -- will shed new light on this dark matter. I spoke to Gilmore
from a conference in Munich at the European Southern Observatory, where he was giving
a talk about how to measure dark matter on small scales. I began by asking him the most
basic question, "What is dark matter?"
Interviewee – Gerry Gilmore
What is dark matter? Well, there is no consensus, actually, at all, as to what dark matter
is. There is merely a set of observations from astronomy, which essentially show that
every time we try to determine the mass of something, we discover that there is very
substantially more gravitating mass around every object, on scales bigger than the solar
system only, than we can see shining as baryons, just ordinary matter, shining. So, every
time we try to weigh a galaxy, try to weigh a cluster of galaxies, try to weigh the whole
universe – it seems there is very substantially more mass there than the luminous mass.
And, probably the total is about eight times greater than the ordinary matter, the baryons,
that we can identify. We have no idea what this stuff is.
Interviewer – Robert Frederick
So, this is the difference, then, between what is called “baryonic dark matter”, comprised
of neutrons and protons…
Interviewee – Gerry Gilmore
That’s correct, yes.
Interviewer – Robert Frederick
…and, and non-baryonic dark matter.
Interviewee – Gerry Gilmore
Yes, that’s right. Although the number we can determine pretty well, actually, from
weighing the whole universe, is the total amount of mass in the universe. And, we can
determine indirectly, but probably very reliably – from modeling the relative amounts of
hydrogen, helium, and the other light elements from the Big Bang – the total amount of
baryonic matter, and that’s just, baryonic matter is just matter that knows about the strong
interaction, the weak interaction, and the electromagnetic interaction. So, it’s protons and
neutrons and hydrogen atoms, and stuff like that. We can determine those two numbers
pretty accurately; the two numbers are quite different. There’s a, sort of subsidiary issue,
which isn’t really fundamental, that we can’t actually find most of the baryons, either.
But, there are very, very good indirect evidence that that’s just because they are quite hot,
and so, they’re not quite hot enough to be visible as x-rays, but they’re too hot to be
detectable in optical absorption lines, so they’ll be shining at us in the hot ultraviolet
somewhere, and we just don’t have any easy way of determining where they are, but we
can see those same atoms at high redshift. So, we can see them directly at high redshift,
we can indirectly deduce the number of them from Big Bang nucleosynthesis modeling.
So, we’re pretty confident about those – it’s the other stuff we’ve got no idea about.
Interviewer – Robert Frederick
And, there’s a lot more of that, right?
Interviewee – Gerry Gilmore
That’s right, about eight or nine times of it, as I say. So, normal matter, in any definition
of “normal”, whatever the universe is made of, normal matter is not made of the stuff
we’re made of, it’s made of something else. We’re very confident it’s not baryons, the
simplest reason for that being that we can actually see the high redshifts in the universe.
And, if all the stuff was out there, almost ordinary matter of the universe would be
opaque, and it isn’t – it’s highly transparent. So, that very simple robust observation tells
us, that whatever this stuff is, it’s transparent – and so, it doesn’t know about Maxwell's
equations, it’s not made of electrons.
Interviewer – Robert Frederick
So, the next physical steps in understanding dark matter include the LHC, the Large
Hadron Collider experiments, looking for the Higgs boson. Anything else?
Interviewee – Gerry Gilmore
Well, that’s the part that joins in with astrophysics because particles are the first to
anticipate that the Large Hadron Collider, starting maybe a year from now, when its first
results will come out, will discover actually a whole bunch of new different sorts of
particles. The Higgs itself is quite a hard thing to find – that’ll be a few years
downstream, and that will be related directly to mass. But, the assumption is there’ll be
whole families of new types of particles – the sort of big brothers and big cousins and big
partners of the existing families of particles that we know about already. These are called
supersymmetric particles in the trade. People sort of hope they’re there because that’s the
expectation – that their properties will allow us to solve these problems. And so, the
Large Hadron Collider will start to discover these sets of particles. The challenge then is
to say, “Well, okay, we now then have a new set of ingredients in our recipe for how
nature is put together, but what is the recipe that uses this set of ingredients; i.e., what
mix of these particles does nature actually use to create the universe, and how?” And, this
is where the connection with astronomy comes in because the particle physicist will give
us this list of ingredients, and we can then look at nature, look at the universe and say,
“Okay, what recipe did nature actually use, how many of this one, how much of that one,
and so on – to actually create what in inverted commas one might reality. And so, this is
the astroparticle connection. And so, that’s why we also are putting a lot of effort into try
to weigh things rather carefully.
Interviewer – Robert Frederick
How do we weigh things better, then?
Interviewee – Gerry Gilmore
Okay, the key there is to measure the speeds of things very, very accurately, indeed.
And, the distances of things very, very accurately, indeed, and for that we need a new
type of telescope. And, this is under construction at present – it’s called Gaia, will be
launched in three years from now, the end of 2011, on its present schedule. And, the key
to Gaia is that it is an ultra-precision measuring device. The precision to which Gaia
measures positions, the number in nanoradians, which doesn’t mean anything to anybody,
or microarcseconds, ditto, but it’s equivalent to the size of a normal shirt button, as seen
on the moon. What Gaia does uniquely is very accurately measure positions, and then it
measures positions repeatedly, over five years, and during those five years things move.
And, you can use that movement to tell you two things. The first is how far away stuff is;
and Gaia will do this ten thousand times better than we’ve ever done before – and ten
thousand times is a huge advance. I mean ten thousand just doesn’t happen, right, I mean
this is really creating an entire new subject. It will also do it, astonishingly, for objects
ten thousand times fainter than we’d ever done before. So, we’ve got another ten
thousand coming in there – and this is just unbelievable. So, this is millions of times
better than anything we’ve had before, and that’s just a revolution. And so, what Gaia
will do is measure the distances of stuff and how they’re moving in three dimensions
around space to much better precision than we have before, which will allow us to weigh
things on all sorts of scales, down to the smallest scales we can find, down to solar
system type scales, much more accurately than we’ve had before. And, those weight
measurements are the distribution of mass. And so, they will tell us, to exquisite
precision, how the dark matter is distributed in space, which is the recipe we need to
determine its properties, particularly its speed and its temperature.
Interviewer – Robert Frederick
Gerry Gilmore, thank you very much.
Interviewee – Gerry Gilmore
‘Tis a pleasure.
Host – Robert Frederick
Gerry Gilmore is professor of experimental philosophy at the University of Cambridge.
Read his Perspective on dark matter in this week’s Science.
Music
Host – Robert Frederick
The most common form of muscular dystrophy is called Duchenne muscular dystrophy,
affecting 1 in every 3500 boys. It's caused by an absence of the protein dystrophin,
which helps keep muscle cells intact, and survival is rare past age 30. In this week's
Science, news writer Elizabeth Pennisi reports on clinical trials that are under way for a
treatment to stem the paralysis caused by Duchenne muscular dystrophy.
Interviewee – Elizabeth Pennisi
So, this is a story about a potential treatment for Duchenne muscular dystrophy, which is
a progressive muscle wasting disorder that affects boys. What happens is, because of a
genetic defect, the body doesn’t make a protein called dystrophin that’s really important
to make muscle cells function correctly. Without this protein, the muscle cells are leaky,
and once they’re leaky they don’t work properly, and gradually the boys become
paralysed. So, this treatment involves a technique called exon skipping. Exons are the
coding regions of genes – so that’s genes have stretches of sequence that are not coding
and other stretches that specify what amino acids are necessary to make a protein.
Interviewer – Robert Frederick
Wouldn’t exon skipping make a faulty protein?
Interviewee – Elizabeth Pennisi
Yes, it would, but it’s better than no protein at all. So, in exon skipping what happens is
you skip over the bad part of the gene, and therefore you’re able to make a protein that
works almost as well as the regular protein, and that helps the kids with this disease
because in Duchenne’s muscular dystrophy, most of the time no protein is made at all.
Through exon skipping, what you get is a protein that is a little shorter than the regular
protein but still functions. And, we know that a shorter, not-quite-correct protein, works
because there’s another muscular dystrophy syndrome called Becker’s muscular
dystrophy, wherein there’s a genetic defect, but you still get a dystrophin protein, it’s just
not quite a perfect protein. And, in those cases, sometimes there are no symptoms at all.
Interviewer – Robert Frederick
So, this exon skipping, then, would essentially turn a Duchenne muscular dystrophy
patient into potentially a Becker’s muscular dystrophy patient.
Interviewee – Elizabeth Pennisi
That’s correct. And, the outcome for Becker’s patients is much better. There are some
patients that have no paralysis at all, they just have abnormal biochemistry, muscle
biochemistry, and there are others that have various degrees of paralysis, but it’s never as
bad as with Duchenne.
Interviewer – Robert Frederick
Is this a potential treatment for all people with Duchenne muscular dystrophy?
Interviewee – Elizabeth Pennisi
Well, yes and no. In theory it is, but what happens is the exon skipping is very much
tailored to where in the gene the mutation is, and the mutation could be in any number of
places, and different boys have different mutations. So, this would be truly personalized
medicine, in that there would have to be a exon-skipping drug designed for each patient,
depending on where his mutation was.
Interviewer – Robert Frederick
I imagine that’s going to make it pretty hard to do clinical trials to bring this kind of
treatment to market.
Interviewee – Elizabeth Pennisi
Exactly. And, that’s one of the big obstacles, or hurdles, that researchers developing this
technique have to deal with. One approach is to try and get regulatory agencies to
approve sort of the general method, or the general chemistry, because what happens is
you design the drug, and it has a backbone to it, and then you put bases on the drug in the
specific sequence that matches the bad exon. And so, the hope is that once you’ve
designed and tested this backbone with one kind of sequence, then it will be okay to use it
with just a slightly different sequence, on a different patient, without having to do
extensive clinical trials. Now that, of course, has yet to be determined – whether that
approach will work or not.
Interviewer – Robert Frederick
Because that’s not all that’s left, the regulations, there’s still some major scientific
hurdles to overcome?
Interviewee – Elizabeth Pennisi
Well, there’s still a question of how you deliver the drug effectively, how long the drug
will last. This exon-skipping molecule will have to reach every cell in the body, and it’s
hard to get to every muscle cell in the body, especially in the heart. So, researchers are
refining the exon-skipping molecules, modifying them in ways so that they get into cells
better. They also are, need to figure out if you give the drug, for a certain amount of
time, and the body makes the dystrophin, the protein that you need, for how long can you
stop giving the drug, and is it still effective?
Interviewer – Robert Frederick
Well, is anyone looking at possibly introducing it into the stem cells, the precursors that
give rise to the muscle cells?
Interviewee – Elizabeth Pennisi
Yeah, there are other approaches. And, one other approach is to do something just like
that – whereas you design a minigene, and the minigene carries the code for the exonskipping molecule. And so, the minigene is put into a muscle stem cell, the muscle stem
cell is reintroduced into the body, and this is a stem cell that’s taken from the body of the
patient – stem cell is reintroduced in the body, it gets established, and it, as a matter of
course, will make or express this minigene, and so, it makes the exon skipping molecule,
and it corrects itself. That would preclude needing daily, weekly, whatever injections.
Interviewer – Robert Frederick
What kind of timeframe are we looking at before we see this as a potential treatment
option or even clinical trial?
Interviewee – Elizabeth Pennisi
Clinical trials are already underway in Europe. There’s two right now that are going on –
one in the United Kingdom and one in the Netherlands. In the U.S., we’ve not gotten
anything off the ground, clinical trial-wise. I think it’s unclear how long it will take
before you can see a drug, partly because it’s a new kind of drug, and it’s not clear how it
should be regulated, so that even if the clinical trials are successful, there’s a lot of
logistics to overcome as well.
Interviewer – Robert Frederick
Elizabeth Pennisi, thank you very much.
Interviewee – Elizabeth Pennisi
Thank you.
Host – Robert Frederick
Science news writer Elizabeth Pennisi writes about a potential new therapy for Duchenne
muscular dystrophy. Read her article in this week's Science.
Music
Host – Robert Frederick
Finally today, David Grimm, editor of Science's free, online daily news site,
ScienceNOW, joins us to talk about the latest science news. Hi, David.
Interviewee – David Grimm
Hey, Rob.
Interviewer – Robert Frederick
So, what stories do you have for us today?
Interviewee – David Grimm
Well, Rob, we’re going to be talking about finding a genetic basis for the placebo effect;
using lasers to locate meteor craters; and, finally, what Tony Soprano has in common
with amoebas.
Interviewer – Robert Frederick
Well, let’s start with the genetic basis of the placebo effect. This is the effect in which
you don’t actually get a medicine, but you still have a good outcome.
Interviewee – David Grimm
Exactly. You know, think of a clinical trial where one group of patients would get the
actual medication, and another group would get, say, a sugar pill. And, what scientists
have known for a long time is that sometimes even these people that get the sugar pills
get better. And, this is known as the placebo effect.
Interviewer – Robert Frederick
And, there’s some genetic component to this?
Interviewee – David Grimm
Well, the idea is that even though we’ve known about the placebo effect for a long time,
there’s still a lot of mystery about what goes on in our body that makes us respond in this
way to fake medication.
Interviewer – Robert Frederick
So, what’d these researchers do?
Interviewee – David Grimm
Well, these researchers built on previous studies that had shown that the neurotransmitter
dopamine might be somehow responsible for the placebo effect. When we anticipate a
therapy, it’s kind of like anticipating a reward. And, dopamine is tied to the reward
pathway, in our brain, and when our brain releases dopamine it can reduce, say, the
symptoms of chronic pain and depression. But, another group of researchers said, “Well,
what about other conditions – conditions that don’t have anything to do with pain or
depression?” And, they focused on a condition known as social anxiety disorder, or SAD.
It’s an abnormal fear of being judged by others. And, one thing researchers know about
SAD is that it seems to be tied to a neurotransmitter called serotonin. People with SAD
tend to have overactive amygdalas, which is a region of our brain that’s tied to the fear
response, which makes sense if you’re thinking about the symptoms of SAD. But, they
can also have variations in genes that are responsible for regulating the neurotransmitter
serotonin, which has also been shown to be tied to a more active amygdala. And, to see
how the placebo effect might tie into this disorder, the researchers ran a clinical trial
where they took 108 patients who had been diagnosed with SAD, and they gave half of
them a serotonin medication—so, a real drug—and they gave the other half a sugar pill—
so, a placebo. And, during the course of the trial, they had these people prepare and give
speeches in front of a small group of people – so it’s something that would stimulate this
social anxiety. And, what they found is after the trial concluded, after 8 weeks, ten of the
people that got the placebo got better – so they did experience the placebo effect. And,
what was really interesting is that these people had variations in this gene that was tied to
serotonin production. So, this is actually the first evidence that there’s a genetic basis to
the placebo effect – because people that had this particular variation were much more
susceptible to the placebo effect than those that didn’t have that genetic variation.
Interviewer – Robert Frederick
I imagine that’s something that every pharmaceutical company would like to know – is
more about the genetics of the people in the clinical trials?
Interviewee – David Grimm
It does raise some privacy issues.
Interviewer – Robert Frederick
Well, from finding a gene that’s associated with the placebo effect to finding previously
undiscovered meteor craters using a new laser system. What is this new laser system?
Interviewee – David Grimm
Well, this is a technology called LIDAR. And, this has actually been around for a while,
but this is a new application of the technology. But, first let’s back up a bit. Earth is
actually hit with a lot of meteors, in its history, and especially over the past 12,000 years
about every decade or so Earth has been hit with a sizable meteorite, big enough to cause
a crater about forty meters wide. But, we’ve only found about five of these craters so far,
and that’s because once these strike Earth, they tend to erode, before we can find them, or
they’re covered by lakes, or forests, or some other covering that makes them difficult to
locate.
Interviewer – Robert Frederick
Other than curiosity, what’s the point in finding these things in the first place?
Interviewee – David Grimm
Well, these meteors are a treasure trove of information for geologists and astronomers
because they can provide information about our early solar system and how everything
formed in the first place. So, it’s early important to find these craters, but scientists, as
I’ve said, have had a very hard time doing so.
Interviewer – Robert Frederick
We’ve only found five.
Interviewee – David Grimm
We’ve only found five so far. And, so what this team did, getting back to LIDAR, is they
employed this laser technology. And, how it works is you’re up in an airplane, and you
basically shoot laser beams, down at the Earth and they bounce back, and as they bounce
back they give you very detailed topographical information. And, what’s great about
LIDAR, versus something like radar, is that the lasers pierce things like lakes and forests,
so they can give you very detailed information of the ground, even if it’s covered by
something. In employing the technology the researchers were able to find a crater thirtysix meters wide in central Alberta, Canada, that had never been discovered before.
Interviewer – Robert Frederick
So, we’re up to six.
Interviewee – David Grimm
So, we’re up to six now. And, further studies of the site revealed some fragments from
the meteorite and also information about just how the meteor crashed to Earth - what kind
of orbit it was in; what kind of speed it was traveling at. And, this is really important
information, too, because it tells us where the meteorite may have come from; how it
entered Earth; and things of that nature that also help shed light on the origins of the solar
system.
Interviewer – Robert Frederick
So, do you have to fly a plane over every single square kilometer of the Earth to use this
LIDAR to find these craters?
Interviewee – David Grimm
Well, you don’t necessarily have to do that. In fact, researchers often have a general
sense of where a meteorite crashed. In fact, two weeks ago there was a similarly sized
meteorite, that crashed somewhere in Canada, that researchers haven’t found yet, but they
have a general idea of where it may’ve hit. So, using LIDAR they can scan that area and
hopefully pinpoint the crater. But, for older meteorites, where we don’t know where they
would have hit, you would have to conduct a much broader search.
Interviewer – Robert Frederick
Well, from the search for missing meteorites to the search for the connection between
Tony Soprano and an amoeba. First, who’s Tony Soprano?
Interviewee – David Grimm
Well, for those of you out there who didn’t watch “The Sopranos,” Tony Soprano was the
chief mobster in a television show on HBO. And, Tony Soprano, like a lot of mobsters,
was known for valuing family above all else. And, it turns out amoeba also value family
above all else. And, this story has to do with how amoeba find food. And, it deals with a
particular type of social amoeba known as Dictyostelium discoideum, if I’m saying that
correctly. And, this amoeba usually lives alone, it dines on bacteria on the forest floor.
But when food becomes very scarce, it pals up with tens of thousands of its neighboring
amoebae, and they form a blob, which about a third the length of an eyelash. And, it
slithers much farther along the forest floor than any amoeba could. And, when it finds an
area that’s more promising for food it forms what’s called a “fruiting body”. And, what
this is is it looks like a little stalk, about 20% of the amoeba form a stalk, and the rest of
the amoeba form this ball of spores on the top of the stalk. And, as animals pass by, these
spores get stuck on the animal, they get transferred to greener pastures, where they can
land on the ground and start feeding again. Well, the downside of this fruiting body is all
the amoeba that make up this stalk, because they don’t get to get transferred, they
basically sacrifice themself for the good of the rest of the group. And…
Interviewer – Robert Frederick
…for the good of the family…
Interviewee – David Grimm
…for the good of the family, exactly. And, researchers have wondered what’s in it for
them – why would this 20% sacrifice themself for the rest of the group? And, they
figured it, as you said, it might have something to do with family – perhaps if they know
that they’re helping family out, they’re more likely to do it. But, the researchers also
wondered about cheaters. If you’re an amoeba, and you’re forming a fruiting body,
obviously you want to be in the spore, you don’t want to be in the stalk. So, how do the
amoeba protect themselves against cheaters? They are the ones that are going to stay out
of the stalk and only go to the fruiting body, and they’re going to sort of “cheat” their
way into the next generation.
Interviewer – Robert Frederick
Keeping in mind that the amoeba actually don’t “know” anything, they’re just “sensing”
it.
Interviewee – David Grimm
Right. We’re anthropomorphizing here a little bit. What the researchers did was they
took fourteen different strains of amoeba, and they paired them together with a laboratory
strain of the same type of amoeba. Now, these fourteen strains varied widely in how
related they were to each other – some were very closely related, and some weren’t
related at all. And, what they did was they also made the laboratory amoeba glow in the
dark. Then they, one by one, mixed these amoeba together, with the laboratory amoeba,
and they starved them so that they would form these fruiting bodies. And, what they
found was that when the strains that were mixed were very closely related, they all mixed
together in this fruiting body, and they were very well blended so that some of them were
in the stalk, and some of them were in the spore, so that the ones that died, and the ones
that would have passed on were members of both groups. But, when they mixed amoeba
that were distantly related, or not related at all, what they found is they didn’t come
together to form a fruiting body – they formed their own fruiting bodies, they completely
segregated. So, one family, if you will, formed its own fruiting body, and the other
family formed its own fruiting body.
Interviewer – Robert Frederick
So, these earliest organisms are balancing cooperation with self-interest. Have the
researchers figured out how they actually can tell the different families apart?
Interviewee – David Grimm
They don’t know. But, it is interesting that such a simple organism is able to tell friend
from foe. I mean, this is something we usually associate with much more complex
organisms. But, it turns out even the humble amoeba can determine who is family, and
who’s not. And, you can see a really cool video of all the stuff I’ve been talking about,
the fruiting body formation, the spore formation, on the site.
Interviewer – Robert Frederick
Okay. Well, thanks, Dave.
Interviewee – David Grimm
Thanks, Rob.
Interviewer – Robert Frederick
So, what other stories are you covering on ScienceNOW?
Interviewee – David Grimm
Well, Rob, in addition to covering all the science news from around the world, we’ve just
started this brand new blog called ScienceInsider. And, this is a really exciting endeavor
for us. The blog’s been running for a couple of weeks now, and it’s breaking news from
the world of science policy. So, everything from how Obama’s new advisors are going to
affect science to how the governments dealing with bioterrorism threats to even where
the UK government stands on smoking pot.
Interviewer – Robert Frederick
So, there are international issues, too.
Interviewee – David Grimm
International issues – everything in science policy that affects science, that affects
research, that even affects your daily life. This is a very frequently updated blog, and
there’s also a link for feedback and tips, so if anybody out there has a tip, they can submit
it on the site. So, be sure to check out the site frequently for breaking science policy
news.
Host – Robert Frederick
David Grimm is the editor of ScienceNOW, the free, online daily news site of Science.
You can check out the latest science news, plus the ScienceInsider blog, at
sciencenow.sciencemag.org.
Music
Host – Robert Frederick
And that wraps up the December 5th, 2008, Science Podcast. If you have any comments
or suggestions for the show, please write us at [email protected]. The show is a
production of Science Magazine and of AAAS, the Science Society. The content is
provided by the news and editorial staff of Science, and Jeffrey Cook composed the
music. I'm Robert Frederick. On behalf of Science Magazine and its publisher, the
American Association for the Advancement of Science, thanks for joining us.
Music ends