While I wish to be posting more frequently, trying to finish a few papers and work on grant proposals is taking up most of my work and free time. I am not a fan of posting random links on my blog, but a little music now and then can be refreshing.
Gerry Niewood (saxophonist, playing flute in the video) and Coleman Mellett (guitarist), two band members with Chuck Mangione, died in the flight 3407 crash outside Buffalo Feb. 13, 2009.
A Panel Discussion and a bonus comparison of science fairs
Well after having a pretty damn good time at the Minnesota Atheists panel discussion on evolution, creationism, and the classroom, I decided to stop into the creationist (attempt at-)science fair. BTW I am that freaking stupid.
First, the panel was outstanding, although the moderation could have been improved somewhat in my opinion. I learned a few things I wish I hadn't. Randy Moore told us that 25% of all Minnesota public school students have been taught creationism, this includes students taking AP biology in case you wanted to use that as a hopeful crutch (I did when I first heard the statistic). Think about that everyone, 1/4 of all students are being subjected to illegal instruction.
(BTW, to any of the hard working public school teachers for my son, if you teach creationism in a science class in anything other than a historical context I will be your worst fucking nightmare. Also, to any hard working public school science teachers in the area, if you need some help or a guest speaker for some reason, Im happy to help.)
Secondly, I was disheartened to hear questions from the audience that showed a profound misunderstanding of evolution. Along the lines of "as the most complex organisms on the planet...." "since western civilization is so evolutionarily advanced" type of questions. I appreciated Dr. Phillips response to a "destroy the planet" type question, we can kill ourselves and a great many other higher eukaryotes, but the planet will be just fine without us and life will go on pretty much as it always had.
Third, kudos to Dr. Cotner and her response to the question "Can't we just tell students to say what we want on the tests, get their passing grade, and move on?" Her response, paraphrasing, BULLSHIT! You explain the data, the facts, the real world that everyone can see and study, but nope this tool is going to go on believing some mythological bullshit that is really no different than the mythological bullshit the ancient Egyptians were believing, and we're supposed to be happy with that?
Personally, I dont need a student to rehash shit I already know to stroke my mental ego, my ego is just fine. I want them to understand (not simply memorize and regurgitate) the world around them. Also, I find that question tantamount to saying, ok students if you disagree with me, go ahead and lie to get your grade. As an active practicing scientist, nothing could more define anathema than advocated lying.
Fourth, and finally "free will." The question that basically derailed the discussion, mostly because time was up but also because the questioner was trying to set up yet another false dichotomy. I realize some people will never be happy unless someone tells them that they are better than something. So for all you self-esteem emo-kid wannabes, you are better than something out there for some as yet undefined reason. Feel better?
Alright, I left this talk, which despite my criticisms above was a lot of fun. I got to see some colleagues I havent seen in too long and also got to meet Randy Moore and Mike Haubrich (of Minnesota blogging fame).
I decided to stop into the Creationist Fair on the way home and I dont have much to say. In fact, I really only want to contrast it with the K-8 science fair I was a judge at early in the week. A more complete assessment can be found at Pharyngula. However, one of the commenters (Kimberly #34) noted that the age appropriate breakdown should go something like: K-1st: Collections with labeling to explain relationships; 2nd Demonstration with explanations of what is happening; 3rd use a model and explain the advantages and disadvantages of the model; 4th Experiment/demostration; 5th Experiment or invention.
I would say that of the K-8 public school exhibits most were in the demonstration/model-explanation vein. Whereas the creationist fair was mostly in the experiment/demonstration vein. Of course I dont have numbers to say how many of each grade level I am comparing so this is just my overall feel. However, the presentations actually being judged at the K-8 fair were outstanding! The students did a great job addressing a scientific question (not all questions are scientific, which is something the creationist fair organizers could have learned.) In fact the presentations were so good of three judges, all of us had different orders for 1, 2, 3 and all of our 1, 2, 3, scores were tightly grouped. Anyway my take home point was that the creationist fair was nowhere near as blatantly non-scientific as last year and was more like any other science fair. However, the failing came with what was considered an acceptable question. The remedy for this requires some parental/organizer involvement Of course, since any parent can teach their children anything there tends to be little to no expertise (unlike public school teachers that require licensures). Thus, I can see why failure to adequately teach scientific methodology would be more lacking in the homeschool environment than the public school environment.
First, the panel was outstanding, although the moderation could have been improved somewhat in my opinion. I learned a few things I wish I hadn't. Randy Moore told us that 25% of all Minnesota public school students have been taught creationism, this includes students taking AP biology in case you wanted to use that as a hopeful crutch (I did when I first heard the statistic). Think about that everyone, 1/4 of all students are being subjected to illegal instruction.
(BTW, to any of the hard working public school teachers for my son, if you teach creationism in a science class in anything other than a historical context I will be your worst fucking nightmare. Also, to any hard working public school science teachers in the area, if you need some help or a guest speaker for some reason, Im happy to help.)
Secondly, I was disheartened to hear questions from the audience that showed a profound misunderstanding of evolution. Along the lines of "as the most complex organisms on the planet...." "since western civilization is so evolutionarily advanced" type of questions. I appreciated Dr. Phillips response to a "destroy the planet" type question, we can kill ourselves and a great many other higher eukaryotes, but the planet will be just fine without us and life will go on pretty much as it always had.
Third, kudos to Dr. Cotner and her response to the question "Can't we just tell students to say what we want on the tests, get their passing grade, and move on?" Her response, paraphrasing, BULLSHIT! You explain the data, the facts, the real world that everyone can see and study, but nope this tool is going to go on believing some mythological bullshit that is really no different than the mythological bullshit the ancient Egyptians were believing, and we're supposed to be happy with that?
Personally, I dont need a student to rehash shit I already know to stroke my mental ego, my ego is just fine. I want them to understand (not simply memorize and regurgitate) the world around them. Also, I find that question tantamount to saying, ok students if you disagree with me, go ahead and lie to get your grade. As an active practicing scientist, nothing could more define anathema than advocated lying.
Fourth, and finally "free will." The question that basically derailed the discussion, mostly because time was up but also because the questioner was trying to set up yet another false dichotomy. I realize some people will never be happy unless someone tells them that they are better than something. So for all you self-esteem emo-kid wannabes, you are better than something out there for some as yet undefined reason. Feel better?
Alright, I left this talk, which despite my criticisms above was a lot of fun. I got to see some colleagues I havent seen in too long and also got to meet Randy Moore and Mike Haubrich (of Minnesota blogging fame).
I decided to stop into the Creationist Fair on the way home and I dont have much to say. In fact, I really only want to contrast it with the K-8 science fair I was a judge at early in the week. A more complete assessment can be found at Pharyngula. However, one of the commenters (Kimberly #34) noted that the age appropriate breakdown should go something like: K-1st: Collections with labeling to explain relationships; 2nd Demonstration with explanations of what is happening; 3rd use a model and explain the advantages and disadvantages of the model; 4th Experiment/demostration; 5th Experiment or invention.
I would say that of the K-8 public school exhibits most were in the demonstration/model-explanation vein. Whereas the creationist fair was mostly in the experiment/demonstration vein. Of course I dont have numbers to say how many of each grade level I am comparing so this is just my overall feel. However, the presentations actually being judged at the K-8 fair were outstanding! The students did a great job addressing a scientific question (not all questions are scientific, which is something the creationist fair organizers could have learned.) In fact the presentations were so good of three judges, all of us had different orders for 1, 2, 3 and all of our 1, 2, 3, scores were tightly grouped. Anyway my take home point was that the creationist fair was nowhere near as blatantly non-scientific as last year and was more like any other science fair. However, the failing came with what was considered an acceptable question. The remedy for this requires some parental/organizer involvement Of course, since any parent can teach their children anything there tends to be little to no expertise (unlike public school teachers that require licensures). Thus, I can see why failure to adequately teach scientific methodology would be more lacking in the homeschool environment than the public school environment.
My Darwin Day Contribution or On a Mechanism of Speciation
How do new species originate? This is a question I am not going to ultimately answer here, but I am interested in this issue and have had some thoughts about it. Now the first issue that needs to be dealt with is "what is a species?" Since many people have been fighting with that question for centuries without coming up with a clear precise definition that applies to all organisms, I am not about to answer it here. So, I will limit our concept of species to sexually reproducing organisms. This allows us to define a species as a group of organisms that can interbreed and give rise to fertile offspring. This allows us to separate horses and donkeys into separate species, since mules are viable but not fertile.
OK, so we have defined a species. Now what? Well in general terms there are four ways speciation can occur: allopatric, parapatric, peripatric, and sympatric speciation. The first three of these modes of speciation involve the spatial separation of two populations of a species in various ways. Once separate, the two populations then evolve independently ultimately becoming distinct species. Its the last mode of speciation, sympatric, I am interested in here.
First it is helpful to think about the ultimate output of the genetic material (aka genes), which is proteins. In many, if not most, cases, proteins do not act as individual molecules, doing their job, and moving on. In fact, most proteins act in complexes with other proteins. What this means is that the proteins must physically interact with each other, and if they don't, the process they are involved in fails. Second, there is a lot of variation out there in the world. Most of this variation is neutral, neither good nor bad, it just is. (Bad variation generally disappears quickly; good variation generally is fixed quickly.) These are our assumptions both of which are well documented, read some textbooks/journal articles for support of my first assumption (proteins act in complexes); go to the mall and people watch for support of my second assumption (variation is out there).
OK, lets take a hypothetical example. In the species of blue-butted gnus, two proteins (A and B) interact to make the blue pigment in said gnus butts. In the first couple of blue-butted gnus we studied, we saw that the gnus had alleles A1 and B1 of these proteins and of course their butts were blue. However, we looked at several other gnus and identified alleles A2 and B2 of these proteins. Upon closer examination, we find lots of A1B1 gnus and a few A1B2 and A2B1 gnus, but no A2B2 gnus. That seems odd, so as junior scientist-heroes, we grab an A1B2 animal and mate it to an A2B1 animal and find out that low and behold we can get an A2B2 animal!!!11!1 But HOLY SHIT, it has a green butt! Did we just make a new species of green-butted gnus? Sadly, we find that gnus, regardless of butt color only want to mate with blue-butted gnus with blue butts. So, no gnus will mate with a green-butted gnu, which as you know is not good news for the green-butted gnu. Now the A2 and B2 alleles do not matter at all, except when combined together, so this has the effect that gnus with the A2 or B2 alleles tend to become isolated, the A2 gnus tend to be at the left hand side of the field over by the swamp, whereas the B2 gnus are found more often at the other side of the field near the woods. What we've done is begun to genetically isolate populations. So although all blue-butted gnus can mate, green-butted gnus are immediately removed from the population. Of course random drift can lead to the complete loss of either A2 or B2, which would end this discussion. However, additional random mutations can and will occur and genetic drift now has a mechanism that can further genetically isolate these gnus into distinct, but spatially overlapping populations. Give me another 40,000 years and a glass of wine and Ill give you two species of gnus: the swampland blue-butted gnu and the woodland blue-butted gnu.
That was hypothetical example (my wife says "lame" is a better word than hypothetical), the paper is a real life example. Saccharomyces cerevisiae (beer/bakers yeast) has been isolated from many sources over the last hundred years and studied in detail. S. cerevisiae is great because it is stable as a haploid or diploid and comes in two mating types and you can mate them in the lab no problem (which is why S. cerevisiae is THE eukaryotic genetic system. One thing that was noted early in studies with S. cerevisiae is that some strains do not mate to give rise to viable progeny. So, strains A and B do not mate well. However, strain C can mate with either A or B just fine. So what gives? Well, the read the paper, but the short story is that there are alleles of genes encoding proteins in an essential complex. When these alleles are in the right combinations the proteins are incompatible and make a defective complex, which equals death, or at least a lack of life.
I think that this model, genetic isolation, may be a common mechanism of separating populations, which can lead to speciation. So why are the other three mechanisms so widely taught (particularly allopatric speciation)? Well its simple to observe and study: find an island and see how the species are similar/different from the mainland. Its also conceptually a little easier, a big giant mountain range comes up splitting a species into two distinct populations, they can and will vary independently. But just because something is easier to observe, doesnt mean its the most important just the most studied (take natural selection vs genetic drift).
OK, so we have defined a species. Now what? Well in general terms there are four ways speciation can occur: allopatric, parapatric, peripatric, and sympatric speciation. The first three of these modes of speciation involve the spatial separation of two populations of a species in various ways. Once separate, the two populations then evolve independently ultimately becoming distinct species. Its the last mode of speciation, sympatric, I am interested in here.
In sympatric speciation the two populations are not separate but occupy the same niche. There are several models describing how sympatric speciation can occur, including sexual selection models and polyploidization. However, I want to discuss a third model which is based on an initial genetic isolation. The paper that really got me thinking about it was one we discussed in my course from PLoS Genetics. Well this paper and the fact that I have never been happy with the primacy of allopatric speciation (a post for another time).
First it is helpful to think about the ultimate output of the genetic material (aka genes), which is proteins. In many, if not most, cases, proteins do not act as individual molecules, doing their job, and moving on. In fact, most proteins act in complexes with other proteins. What this means is that the proteins must physically interact with each other, and if they don't, the process they are involved in fails. Second, there is a lot of variation out there in the world. Most of this variation is neutral, neither good nor bad, it just is. (Bad variation generally disappears quickly; good variation generally is fixed quickly.) These are our assumptions both of which are well documented, read some textbooks/journal articles for support of my first assumption (proteins act in complexes); go to the mall and people watch for support of my second assumption (variation is out there).
OK, lets take a hypothetical example. In the species of blue-butted gnus, two proteins (A and B) interact to make the blue pigment in said gnus butts. In the first couple of blue-butted gnus we studied, we saw that the gnus had alleles A1 and B1 of these proteins and of course their butts were blue. However, we looked at several other gnus and identified alleles A2 and B2 of these proteins. Upon closer examination, we find lots of A1B1 gnus and a few A1B2 and A2B1 gnus, but no A2B2 gnus. That seems odd, so as junior scientist-heroes, we grab an A1B2 animal and mate it to an A2B1 animal and find out that low and behold we can get an A2B2 animal!!!11!1 But HOLY SHIT, it has a green butt! Did we just make a new species of green-butted gnus? Sadly, we find that gnus, regardless of butt color only want to mate with blue-butted gnus with blue butts. So, no gnus will mate with a green-butted gnu, which as you know is not good news for the green-butted gnu. Now the A2 and B2 alleles do not matter at all, except when combined together, so this has the effect that gnus with the A2 or B2 alleles tend to become isolated, the A2 gnus tend to be at the left hand side of the field over by the swamp, whereas the B2 gnus are found more often at the other side of the field near the woods. What we've done is begun to genetically isolate populations. So although all blue-butted gnus can mate, green-butted gnus are immediately removed from the population. Of course random drift can lead to the complete loss of either A2 or B2, which would end this discussion. However, additional random mutations can and will occur and genetic drift now has a mechanism that can further genetically isolate these gnus into distinct, but spatially overlapping populations. Give me another 40,000 years and a glass of wine and Ill give you two species of gnus: the swampland blue-butted gnu and the woodland blue-butted gnu.That was hypothetical example (my wife says "lame" is a better word than hypothetical), the paper is a real life example. Saccharomyces cerevisiae (beer/bakers yeast) has been isolated from many sources over the last hundred years and studied in detail. S. cerevisiae is great because it is stable as a haploid or diploid and comes in two mating types and you can mate them in the lab no problem (which is why S. cerevisiae is THE eukaryotic genetic system. One thing that was noted early in studies with S. cerevisiae is that some strains do not mate to give rise to viable progeny. So, strains A and B do not mate well. However, strain C can mate with either A or B just fine. So what gives? Well, the read the paper, but the short story is that there are alleles of genes encoding proteins in an essential complex. When these alleles are in the right combinations the proteins are incompatible and make a defective complex, which equals death, or at least a lack of life.
I think that this model, genetic isolation, may be a common mechanism of separating populations, which can lead to speciation. So why are the other three mechanisms so widely taught (particularly allopatric speciation)? Well its simple to observe and study: find an island and see how the species are similar/different from the mainland. Its also conceptually a little easier, a big giant mountain range comes up splitting a species into two distinct populations, they can and will vary independently. But just because something is easier to observe, doesnt mean its the most important just the most studied (take natural selection vs genetic drift).
Happy Darwin Day everyone!!!
(Incompatibilities involving yeast mismatch repair genes: a role for genetic modifiers and implications for disease penetrance and variation in genomic mutation rates. Demogines A, Wong A, Aquadro C, Alani E. PLoS Genet. 2008 Jun 20;4(6):e1000103.)
Come celebrate Darwin's Birthday
LIFE: A Journey Through TimeNorth American Premiere /Darwin Day Opening Event
Thursday, February 12, 2009, 7 to 9 p.m.
Bell Museum Auditorium
$10/ free to museum members and University students
Celebrate the 200th anniversary of Charles Darwin's birthday with a special preview of LIFE: A Journey Through Time. The event will feature top University biologists using Lanting's photographs as a springboard to deliver a rapid-fire presentations relating their research on evolution to the images. From the big bang to the human genome, hear the newest theories on how life evolved and enjoy the North American premiere of one the world's most celebrated photography exhibits. Think speed-dating - Darwin-style!
Speakers include:
Mark Borrello <---- Teaches on the history of evolution, and is an anti-creationist superhero
Sehoya Cotner <---- Teaches about Sex and evolution, dont tell the Georgia state legislature
Mark Decker <---- Teaches, Writes, Teaches, Skydives, oh and strives to improve Teaching (Plus he doesn't snarf your scotch when you are off teaching.)
Greg Laden <---- Not sure about this guy, does something or other someplace
Keith Olive <---- A physicist! Clearly, a late addition to make the biologists feel inadequate...or maybe I'm transferring.
BTW its a birthday party. There will be cake!
Bats: are belfries their only option?
Small mammals are dying and we don't know why! Does it matter? I've posted why it does and what we know previously. Well it looks like white-nose syndrome is spreading from a couple of caves in NY 2 years ago to 6 states already this year....this is not a good thing.
Mexican free-tailed bats © Lynn McBride (JPG)
One thing that stills concerns me is that researchers are trying to find ways to combat the Geomyces fungus, which is infecting the bats and is the white in white-nose. This is good, however I still have not seen definitive cause-effect data that suggests that fungus is the problem and not a symptom. I hope research is still being done to determine why bats are coming down with these fungal infections.
Possibilities:
1. This is an emerging pathogen that has developed virulence properties. While these fungi do not grow at human body temperature, Im not a cheerleader of emerging mammalian infectious agents.
2. Environmental toxins are screwing up the bats immune system or physiology.
3. A virus is acting similarly to the environmental toxin example (analogous to HIV in people).
4. Others I have yet completed the thought on.
How to make a virus
There was a pretty good seminar I saw on the subject of virology, which is not my area of expertise nor necessarily of interest. However, the presentation and work done was explained well and was done in an engaging way, such that even though this is an area I am not particularly concerned with, I enjoyed immensely.
(Aside: These leads to a particular rant I have. I see that many lab heads avoid departmental seminars unless said seminar is directly related to their particular field. I understand this mindset, because we are all extremely busy, we have many seminars, meetings, and duties beyond research and teaching that vie for our time. However, this mindset is being passed down to the post-docs and, more importantly, the students in these labs. Over the course of several years of this, the end result is a batch of students with little breadth beyond their specific research area, students who are unaware of technical or intellectual advances in other fields that may in fact aid their research, and students who may not have the skills to succeed on their own. /Aside)
The specific seminar I attended was on Hantavirus. Like all organisms, even pseudo-organisms like viruses, there are interesting biological problems and questions associated with them. One thing of interest with the Hantavirus, and other viruses of the Bunyaviridae family, is that it has a segmented genome. This is similar to us, our genome is comprised of 23 individual chromosomes (2 copies of each). Thus, our genome is segmented. This can be contrasted to many, but not all, bacterial species, which have their genomes comprised on a singular circular chromosome. So, the Hantavirus genome is comprised of 3 segments. If you click on the picture, which is from the CDC, you can actually see some of the strands in the viruses that are the RNA segments that comprise the genome. In answer to your question, yes RNA! These viruses maintain their genome as RNA, not DNA. So the discovery of the virus, seeing it inside of cells, analysis of its genomic structure is all basic biology that was worked out over the last few decades.
So what is the profoundly interesting thing here? Well, its a question I do not know the answer to, nor am I sure anyone does in this particular case. However, it does represent an interesting biological problem. A bit more background, when a virus infects a cell, the genome regardless of RNA or DNA is uncoated, in other words freed from the protein shell it travels around in. This allows the virus to replicate, make messages, and make all the proteins necessary to make more viruses. Now once all these new viral genomes are made, they have to be packaged into new shells before leaving the host cell. (Free nucleic acid in the environment usually gets eaten.) For a virus with a single bit of RNA or DNA that gets packaged, you can simply have a protein that grabs one end of the genome and nucleates shell formation or you simply make a bazillion protein shells along with a bazillion genomes and simply play the odds: some shells will be empty but many will not be.
However, our organism of interest, Hantavirus, has a segmented genome. The virus requires all 3 pieces of its genome to be in a shell to have a productive virus. Our previous 2 approaches no longer work so well. In the first approach we need 3 proteins, one for each genomic segment. We could use the same protein 3 times, but how can you ensure all three segments are in each shell and not simply segment 1 and its associated protein 3 times. We could have 3 different proteins, 1 for each segment. The problem here is that Hantavirus only encodes for 3 different proteins total: the shell protein, the RNA polymerase, and an RNA binding protein that does several different things. So we don't appear to have the information necessary to take this approach.
The second approach tends to fail as well. If we make a bazillion shells and a bazillion of each segment. If there is an 80% chance a given segment randomly ends up in a shell then we have a 0.8 x 0.8 x 0.8 = 51% chance of a shell getting all 3 segments, so 0.5 bazillion. That doesnt sound so bad, but I did just make up the 80% number, what if its 50%? then ~12.5% of the shells will have all 3 segments. Is that enough to maintain a viable infection? I don't know, but its knowable and interesting to think about. This issue is more complicated, because we have assumed that once a given segment gets in, the same segment won't get in again. If we abandon this assumption, then our 80% chance of a given segment to get in isn't 51% but 11% (.8 x (.8 x 2/3) x (.8 x 1/3)) We could help our scenario out by making the shells large enough to hold more than 3 segments worth of material. If a shell can hold 5 segments worth of material, then we dramatically increase our chance of getting all 3 segments in.
So what does Hantavirus do? Well based on the seminar, that is still a question that needs answering. Maybe one of the above approaches is right or maybe the 3 segments are not truly separate but tethered together with 1 or more of their proteins or host proteins that the virus coopts for its own devices or maybe its something else even more interesting! Regardless, this is why biology and science in general is cool. We have an obvious problem an organism (Im using the term loosely) needs to solve, how does it do it? By the way, his isn't simply fun for the sake of fun, in the case of Hantavirus, if we know how packages its genome maybe we can develop ways to stop it and effectively combat Hantavirus it or similar viruses.
(Aside: These leads to a particular rant I have. I see that many lab heads avoid departmental seminars unless said seminar is directly related to their particular field. I understand this mindset, because we are all extremely busy, we have many seminars, meetings, and duties beyond research and teaching that vie for our time. However, this mindset is being passed down to the post-docs and, more importantly, the students in these labs. Over the course of several years of this, the end result is a batch of students with little breadth beyond their specific research area, students who are unaware of technical or intellectual advances in other fields that may in fact aid their research, and students who may not have the skills to succeed on their own. /Aside)
The specific seminar I attended was on Hantavirus. Like all organisms, even pseudo-organisms like viruses, there are interesting biological problems and questions associated with them. One thing of interest with the Hantavirus, and other viruses of the Bunyaviridae family, is that it has a segmented genome. This is similar to us, our genome is comprised of 23 individual chromosomes (2 copies of each). Thus, our genome is segmented. This can be contrasted to many, but not all, bacterial species, which have their genomes comprised on a singular circular chromosome. So, the Hantavirus genome is comprised of 3 segments. If you click on the picture, which is from the CDC, you can actually see some of the strands in the viruses that are the RNA segments that comprise the genome. In answer to your question, yes RNA! These viruses maintain their genome as RNA, not DNA. So the discovery of the virus, seeing it inside of cells, analysis of its genomic structure is all basic biology that was worked out over the last few decades.So what is the profoundly interesting thing here? Well, its a question I do not know the answer to, nor am I sure anyone does in this particular case. However, it does represent an interesting biological problem. A bit more background, when a virus infects a cell, the genome regardless of RNA or DNA is uncoated, in other words freed from the protein shell it travels around in. This allows the virus to replicate, make messages, and make all the proteins necessary to make more viruses. Now once all these new viral genomes are made, they have to be packaged into new shells before leaving the host cell. (Free nucleic acid in the environment usually gets eaten.) For a virus with a single bit of RNA or DNA that gets packaged, you can simply have a protein that grabs one end of the genome and nucleates shell formation or you simply make a bazillion protein shells along with a bazillion genomes and simply play the odds: some shells will be empty but many will not be.
However, our organism of interest, Hantavirus, has a segmented genome. The virus requires all 3 pieces of its genome to be in a shell to have a productive virus. Our previous 2 approaches no longer work so well. In the first approach we need 3 proteins, one for each genomic segment. We could use the same protein 3 times, but how can you ensure all three segments are in each shell and not simply segment 1 and its associated protein 3 times. We could have 3 different proteins, 1 for each segment. The problem here is that Hantavirus only encodes for 3 different proteins total: the shell protein, the RNA polymerase, and an RNA binding protein that does several different things. So we don't appear to have the information necessary to take this approach.
The second approach tends to fail as well. If we make a bazillion shells and a bazillion of each segment. If there is an 80% chance a given segment randomly ends up in a shell then we have a 0.8 x 0.8 x 0.8 = 51% chance of a shell getting all 3 segments, so 0.5 bazillion. That doesnt sound so bad, but I did just make up the 80% number, what if its 50%? then ~12.5% of the shells will have all 3 segments. Is that enough to maintain a viable infection? I don't know, but its knowable and interesting to think about. This issue is more complicated, because we have assumed that once a given segment gets in, the same segment won't get in again. If we abandon this assumption, then our 80% chance of a given segment to get in isn't 51% but 11% (.8 x (.8 x 2/3) x (.8 x 1/3)) We could help our scenario out by making the shells large enough to hold more than 3 segments worth of material. If a shell can hold 5 segments worth of material, then we dramatically increase our chance of getting all 3 segments in.
So what does Hantavirus do? Well based on the seminar, that is still a question that needs answering. Maybe one of the above approaches is right or maybe the 3 segments are not truly separate but tethered together with 1 or more of their proteins or host proteins that the virus coopts for its own devices or maybe its something else even more interesting! Regardless, this is why biology and science in general is cool. We have an obvious problem an organism (Im using the term loosely) needs to solve, how does it do it? By the way, his isn't simply fun for the sake of fun, in the case of Hantavirus, if we know how packages its genome maybe we can develop ways to stop it and effectively combat Hantavirus it or similar viruses.