A new online collaborative learning space, and a scholarship opportunity

Via email from the Nature Publishing Group I just got word of a new online resource they've developed to help students learn genetics, and perhaps for teachers to teach the subject as well. Scitable is the NPG's new collaborative learning space for science, bringing together a library of scientific overviews with a worldwide community of scientists, researchers, teachers, and students. What's more, Scitable is even (for the moment, I hope forever) free! The first topic area with substantial content now online there is Genetics. Given how much time I spend on population genetics in my Evolution class, this promises to be a good resource for students needing a refresher to keep up with the class. And perhaps my colleagues teaching Genetics will find it useful as well.

And for students checking it out right now, there is also a scholarship being offered:

As a way of introducing students to Scitable, we are running a "Portrait of My DNA" contest that allows students to compete for one of three scholarships. ...

If the first place student is referred by you, your department will receive an additional scholarship of equal value to give to the student of your choice. You can learn more about the contest at http://www.nature.com/scitable/study-center.

So students, if you are still reading this blog even though the semester is over (for you anyway, although I'm still grading!), check the website out, and throw your hat in for the scholarship.

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Adaptationist hypotheses are sexy, but don't forget the null hypothesis!

Just because a trait exists, or some process happens, and I can come up with an adaptationist just-so-story to explain its significance, doesn't necessarily mean that that trait or process actually has any functional, adaptive significance! That old lesson, hammered into behavioral ecologists like me by Gould and Lewontin's classic paper from 30 years ago, it seems, must be learned all over again by a new generation of genomic biologists! So argues Michael White in this must-read essay on the fascinating phenomenon of Genomic Junk and Transcriptional Noise:

With hot, new technologies, biologists are taking higher-resolution snapshots of what's going on inside the cell, but the results are stirring up controversy. One of the most interesting recent discoveries is that transcription is everywhere: DNA is transcribed into RNA all over the genome, even DNA that has long been thought to have a non-functional role. What is all of this transcription for? Does the 'dark matter' of the genome have some cryptic, undiscovered function?

Unfortunately, in all of the excitement over possible new functions, many biologists have forgotten how to frame a null hypothesis - the default scenario that you expect to see if there is no function to this transcribed DNA. As a result, the literature is teeming with wild, implausible speculation about how our excess DNA might be beneficial to us.

So here, let's step back and look at what we expect from DNA when it's playing absolutely no functional role; in other words, let's look at the null hypothesis of genomic junk and transcriptional noise. We can then take our null hypothesis and use it to look at a fascinating new study of how genomic parasites sculpt transcription in our cells.

There is no such thing as inert DNA

What bothers me most about the recent hullaballoo over pervasive transcription is the tacit assumption that non-functional DNA has to be inert. This is a terrible assumption from both a biochemical and an evolutionary viewpoint. We have every reason to expect non-functional DNA to be noisy.

...

[via Genomic Junk and Transcriptional Noise]

Now, I don't know a whole lot about what goes on inside cells and the intricacies of DNA transcription - so it is still news to me that there is so much more transcription going on than is actually "needed", a whole lot of transcriptional noise from non-coding regions of our genomes! But, as White argues so well, just because this non-coding DNA is getting transcribed doesn't mean it is no longer "junk" - all this transcription may simply be a result of basic biochemistry. Throw together a whole bunch of DNA and RNA polymerases, within the confined quarters of, say, a typical mammalian cell, and some of this stuff is bound to happen. So my genome-studying friends - excited as you are about the huge volumes of data you are drowning in and all these new discoveries, pause a moment to reflect on what it all means, and stop seeing function everywhere. Remember the NULL hypothesis, which, in this case, predicts transcriptional noise to occur all the time.

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Just little bit of G, T, C, A ...

An ass-shaking jam, indeed, from Bio-Rad, courtesy of Dr. Isis the Scientist!

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How the influenza virus can drift and shape-shift to keep us on our toes

As you may have read by now, the new swine flu virus, this new strain H1N1 which is threatening to turn into a pandemic according to the WHO (even though there is much confusion about the actual number of infected/dead victims confirmed to have this strain), is actually an interesting genetic mixture, a chimera if you will with a potpourri of genes from different influenza strains: these may be from multiple host taxa — birds (thought to be the original source of all influenza viruses), humans, and, of course, pigs (from North America and Asia!) — or perhaps all from pigs (the picture is still cloudy). In any case, if you are wondering how such reassorted viruses form, the following video paints a cartoon picture to help you understand. The key thing to remember is that viruses, like many other microbes, are rather promiscuous when it comes to swapping bits of DNA - even across "species" - and such lateral transfer can allow new strains to evolve, even drug-resistant ones, much more rapidly. Here's how influenza may be able to shift the shape of its antigens, and potentially jump between host species:

But, that is not the only trick up this virus' sleeve. Ever wonder why, unlike with other vaccinations which are often a once-in-a-lifetime deal, you've got to take that flu shot over every single year? Because, even in the absence of opportunities to hook-up and swap genes with other viruses, i.e., even when a host is infected by just a single strain of the flu, the virus is constantly changing shape. Mutations arise all the time, and those that change the shape of the antigen such that it is no longer recognized by host antibodies will be naturally selected. Antigen shape therefore drifts around constantly, making it a much more fun game for the host immune system - and our vaccines - to keep up with the flu! It's evolution in action, right within our own bodies and those of animals we cohabit with! You didn't think we had quite liberated ourselves from the clutches of evolutionary processes now, did you? As you ponder that, here's another cartoon depicting antigenic drift:

[Hat-tip: GrrlScientist for finding the videos]

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Applying phylogenetics: Did the California H1N1 swine flu come from Ohio?

Just as we (in Biol 105) finish up studying how phylogenetic trees are estimated, and how they might be used to answer interesting questions, comes this highly topical example - microbiologist and science blogger Sandra Porter spent a happy afternoon applying phylogenetic analyses to try and answer the health scare du jour:

This afternoon, I was working on educational activities and suddenly realized that the H1N1 strain that caused the California outbreak might be the same strain that caused an outbreak in 2007 at an Ohio country fair. Here's the data.

Once I realized that the genome sequences from the H1N1 swine flu were in the NCBI's virus genome resources database, I had to take a look.

And, like eating potato chips, making phylogenetic trees is a little bit addictive. Or maybe it was just the adrenaline rush that hit when I realized that every tree was telling me the same thing.

What did those trees say?

Read the full blog post to study the results yourself, and see what you think of the remarkable concordance between the trees, providing a plausible answer to the question of where this virus may have originated.

In the process, Dr. Porter has also given us all a glimpse at the working product of a fresh analysis - raw results hot off the computer before they are published in a peer-reviewed journal! Is this a first for the blogosphere? I don't know, but given the high level of public interest, I can see why one might want to get the results out quickly. Surely some top science journal would be interested in publishing this quickly as well?

Thanks to Porter's blog, we all get to see how genomic data available in the public domain can be used to help address problems that might affect us in real time! How cool is that?! As I try to impress upon my students every time we discuss the subject: Phylogenies are not just static graphic depictions of inferred relationships between organisms long gone - trees of dead wood, so to speak: they also serve as working models of ongoing evolutionary processes! And often enough, they help us pinpoint the origins of new diseases, in turn helping us develop treatment strategies before the outbreak gets too far out of hand. And how is that for putting those phylogenetic trees to work?

Meanwhile, Tara Smith, of Aetiology (also on ScienceBlogs) following up on Porter's big discovery, notes that the peer-reviewed paper describing the Ohio swine flu strain came out only recently. And here's the bit that really raises the eyebrow, if not the hair on your head:

I also assume this is where the human-avian-swine reassortant claim came from. The authors note that:

The H1N1 viruses contain the HA and NA from the classical swine virus and the internal genes from the triple reassortant H3N2 viruses (rH1N1); the H1N2 viruses contain the HA from the classical swine virus and the NA and internal genes from the triple reassortant H3N2 viruses (Karasin et al., 2002; Webby et al., 2004). Contemporary triple reassortant viruses were demonstrated to have acquired a PB1 gene of human virus origin; PA and PB2 genes of avian virus origin; and the remaining internal genes, M, NS, and NP, of swine virus origin, thus giving rise to the triple reassortant designation (Zhou et al., 1999).

So what it looks like to me is that this isn't a *new* reassortant virus, but is closely related to one that had already been identified in swine--and that had already caused an outbreak in humans right here in the US.

So why is the virus getting so much more media attention this time around? Is the strain in Mexico really the same or different? And if it is the same (or close) how did it get from Ohio to Mexico City and back to Texas and California? Gotta love that globalization, eh!

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Regulatin' Genes is where its all at! Evo-Devo!!

Go Evo-Devo!! I guess I can skip the evo-devo lecture in the evolution class now, eh?

[Hat-tip: Pharyngula]

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Do you have a bit of Neandertal in you?

Of course, we undoubtedly share the bulk of our DNA sequence with our long-lost cousins, the Neanderthals. But more interesting is the question of whether our direct ancestors actually ever got it on with the Neanderthals! Was there any nookie... er... horizontal transfer of genetic material between them? That could get really interesting, no? Well, it appears we're getting closer to finding out:

The entire genome of a 38,000-year-old Neanderthal has been sequenced by a team of scientists in Germany. The group is already extracting DNA from other ancient Neanderthal bones and hopes that the genomes will allow an unprecedented comparison between modern humans and their closest evolutionary relative.

The three-year project, which cost about €5 million (US$6.4 million), was carried out at the Max Planck Institute for Evolutionary Anthropology in Leipzig. Project leader Svante Pääbo will announce the results of the preliminary genomic analysis at the American Association for the Advancement of Science annual meeting in Chicago, Illinois, which starts on 12 February.

[via Neanderthal genome to be unveiled : Nature News]

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On Human Evolution

Is our species, Homo sapiens, still evolving? No doubt all of you have wondered about this at some point (unless you don't believe in evolution, in which case you have a different puzzle to scratch your heads over). And with human technology constantly coming up with ways to allay any selective pressures, it is easy to think that we've stopped evolution in its tracks as far as our own species is concerned. But have we, really? Is it even possible to pause evolution? Last month, Seed magazine had an interesting article, "How We Evolve" describing the state of current knowledge about human evolution and how modern genomics tools are helping to shed light on this question:

When the previous generation of life scientists was coming up through the academy, there was a widespread assumption, not always articulated by professors, that human evolution had all but stopped. It had certainly shaped our prehuman ancestors — Australopithecus, Paranthropus, and the rest of the ape-men and man-apes in our bushy lineage — but once Homo sapiens developed agriculture and language, it was thought, we stopped changing. It was as though, having achieved its aim by the seventh day, evolution rested. "That was the stereotype that I learned," says population geneticist and anthropologist Henry Harpending. "We showed up 45,000 years ago and haven't changed since then."

The idea makes a rough-and-ready kind of sense. Natural selection derives its power to transform from the survival of some and the demise of others, and from differential reproductive success. But we nurse our sick back to health, and mating is no longer a privilege that males beat each other senseless to secure. As a result, even the less fit get to pass on their genes. Promiscuity and sperm competition have given way to spiritual love; the fittest and the unfit are treated as equals, and equally flourish. With the advent of culture and our fine sensibilities, the assumption was, natural selection went by the board.

So what can genomics tell us?

John Hawks started out as a "fossil guy" studying under Milford Wolpoff, a paleoanthropologist who is the leading proponent of the faintly heretical multiregional theory of human evolution. Coming to genetics from such a background has perhaps given Hawks the stomach to wield unfashionable hypotheses. In December of last year, he, Harpending, and others published a paper whose central finding, that evolution in humans is observable and accelerating, would have been nonsensical to many geneticists 20 years ago. Up to 10 percent of the human genome appears to be evolving at the maximum rate, more quickly than ever before in human history.

Go read the rest of the story. Especially the frightening scenarios towards the end.

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When a Cutthroat meets a Rainbow

Submitted by Christopher Clapp for the Evolution class.

The introduction of a known species of rainbow trout into a native population of cutthroat trout and the consequences of their contact within their environments is the focus of this study. The interaction of these two species has resulted in their study of subsequent progeny shows hybridization of the two, and thus a decline of the natural populations of cutthroat trout. The implications of this hybridization will show throughout subsequent generations, considering what is known of the native species. Metcalf uses mitochondrial and nuclear markers to determine the levels of crossing of the two species based on the nature of homozygous or heterozygous allele category. These populations of hybridization were evaluated due to the known history of the streams being studied. Trout being separated by natural geographic restrictions such as natural waterfalls or by human chemical treatment conducted in the past forms for a basis of evaluation.

The successful progeny of hybridization between the two locations is evident; however there are differences between the chemically treated streams and the naturally restricted. Interestingly enough, results show that there is a trend of the cutthroat nuclear trout alleles being more prevalent beyond the upstream barrier as expected. The mitochondrial alleles were more prevalent within the hybrid or rainbow species within the areas that direct contact has been introduced within the natural barrier stream. Our study supports the notion that natural waterfall barriers provide a refuge for pure native cutthroat trout genomes across their range (Metcalf et al 2008). In the Cony Creek population, which was subject to chemical treatment in 1984, the nuclear markers were more prevalent within the cutthroat species. This bias toward the pure cutthroat is speculated to be due to the chemical treatment of the streams to eradicate the rainbow trout populations amidst restocking the cutthroat population (Rosenlund et al. 2001). Why is the case? The allele frequency distributions and disequilibrium values suggest that hybridization has been underway for longer in Cony Creek than in Graneros Creek according to Metcalf, et al (2008). I seem to feel that introducing a chemical treatment to an environment that focuses directly on one specific species allows for a re-founding of the native species. However, there findings show the invasiveness nature of the rainbow species. Over time the cutthroat nativity would be eradicated regardless of natural barrier or chemical treatment. This poses two major problems for the environment with regard to the natural species, and the changes of fish populations within streams. The introduction of new fishes for conservation strategies not only directly affect the native population, it affects the ecosystem among other animals within the environment as well. If an aggressive population of trout that is more successful than the native, the impact on resources for the community will also be affected; the environment will be in disequilibrium.

We seem to have two intrusions of the human hand into an environment, one for the introduction of the rainbow, and one to eradicate the rainbow trout species. The study shows that there is greater fitness among the hybrids. The cross between a rainbow trout female and a cutthroat male resulted in a shorter time to hatching and the progeny had a faster growth rate and a greater abundance of yolk at hatch and emergence than the hybrids of the reciprocal cross (Hawkins and Foote, 1998). Nevertheless, the two species form a system of fertility to study the hybrid selection based on natural selection and/or the effects of human based effects in the form of conservation strategies. What is this to say for the natural selection of the hybrid species or the difference between the two, and what are the effects of the introduction on the environment? Historically fishless lakes and streams have been associated with declines in amphibians, changes in invertebrate communities and changes in nutrient cycling (Knapp and Matthews, 2000). However, there is always something to be learned from the development of a new species. The selection and fitness over such a short amount of time is interesting to evaluate within the two species.

It seems to be that the rainbow trout are invading the natural species of cutthroat, and have an effect on the native species. Why are the rainbows so successful at invading this species? What are we to learn of the intrusion of populations by human hands? Either way, I agree with Metcalf in the capacity that the evaluation of the new hybrid species will give insight into long-term conservation strategies. It seems that if we limit the studies and only hold them as individuals there will always be contradiction of the results. Conservation methods and steps may be a bit naïve if you only consider one method to achieve one result. By not considering the whole picture, we are increasing our opportunity cost, and thus the potential for loss.

References:

Denise K. Hawkins, Chris J. Foote (1998). Early survival and development of coastal cutthroat trout (Oncorhynchus clarki clarki), steelhead (Oncorhynchus mykiss), and reciprocal hybrids Canadian Journal of Fisheries and Aquatic Sciences, 55 (9), 2097-2104 DOI: 10.1139/cjfas-55-9-2097

Roland A. Knapp, Kathleen R. Matthews (2000). Non-Native Fish Introductions and the Decline of the Mountain Yellow-Legged Frog from within Protected Areas Conservation Biology, 14 (2), 428-438 DOI: 10.1046/j.1523-1739.2000.99099.x

J. L. Metcalf, M. R. Siegle, A. P. Martin (2008). Hybridization Dynamics between Colorado's Native Cutthroat Trout and Introduced Rainbow Trout Journal of Heredity, 99 (2), 149-156 DOI: 10.1093/jhered/esm118

Rosenlund BD, Kennedy C, Carnowski K. 2001. Fisheries and the Aquatic management of Rocky Mountain National Park. (US Dept. of the Interior).

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Darn those scientists, confounding our politics again!

Unbelievable!! This is the leadership we are supposed to look forward to?!

As someone who came to the US because of the opportunities this country offered to pursue scientific research, and having seen science get bipartisan lip service (at least) over the past 4 presidential election cycles (when I have been here), despite the decline in science funding over the past 8 years, I find it really bizarre to see this "team of mavericks" tilting against the windmills of science in this fashion! First it was McCain railing against "pork-barrel" earmark funding to study the genetics of grizzly bears (a very successful project, btw, that he had actually voted for, before turning it into a convenient flogging-horse on the campaign trail), and now Palin takes on the iconic model organism of modern genetics, Drosophila!! Talk about clueless chutzpah, bashing research on the very organism which has yielded, among myriad other insights, important clues about autism, the cause she claims she would fund by cutting off these "earmark" projects!! But, as has been clear from the day she joined the ticket, and as Rachel Maddow demonstrates yet again, this hockey-mom continues to operate in a completely irony-free zone - how can one make fun of her when she embodies the joke so completely? (remember how people chuckled when someone initially suggested that she had foreign policy expertise because of Alaska's proximity to Russia; until she actually took that line seriously and ran with it?)

Science - cutting-edge basic science - has surely been one of the defining characteristics of this country's global leadership over the past half-century or more, no?! Why do these "mavericks" now suddenly think it is ok to throw that away, and that they will win more votes if they bash science and scientists? I've wondered about the curious dichotomy in this culture, where science and technology provide the basis of so much of everyday life, yet science and scientists, and intellectuals in general, are feared/reviled as nerds/dangerous elitists. Is the anti-intellectual strain in this society so strong that McCain/Palin can drum up a few more votes to win this election by continuing to bash science, and further entrench the age of american unreason? Please tell me that is not the case, that things haven't gone that far wrong... or should I be packing my bags as another soon-to-be-unwanted scientist who has been wasting his life and taxpayer money studying birds??!! While remaining a foreigner, to boot!!

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A gene to save us from HIV?

Sandra Porter, over at Discovering Biology in a Digital World has a very interesting post up reviewing recent research on a gene that might protect us from HIV and other retroviruses. Well worth reading, given our recent classroom discussions of HIV, and the upcoming lectures where we will address resistance genes, fairly soon! Besides this post is also an excellent model for you to shoot for when writing your own critique/commentary/synthesis for this class!

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A more substantial discussion about biology and theology on campus today

At least I expect it to be more substantial than the other stuff that's been going on around here lately. The last lecture of the Ethics Center's spring seminar series will be by Ted Peters, a theologian who has published extensively on the connections between science and religion and ethics.

In today's lecture "The Stem Cell Controversy: Who is Fighting Whom About What?" Peters will discuss religious and ethical issues that arise in the context of debates about stem cell research and biotechnology. This talk will be based in part on Peters’ recent book, The Stem Cell Debate.

The lecture will be at noon in the Alice Peters Auditorium at the University Business Center.

Ted Peters is Professor of Systematic Theology at Pacific Lutheran Theological Seminary and the Graduate Theological Union in Berkeley, California. His recent books include: Science, Theology, and Ethics, Playing God? Genetic Determinism and Human Freedom and the forthcoming Sacred Cells?: Why Christians Should Support Stem Cell Research. Peters also serves on the Scientific and Medical Accountability Standards Working Group for the California Institute for Regenerative Medicine (CIRM).

Andrew Fiala reminds me to add that Peters will also be meeting with students in the philosophy club from 2-3 in USU 311, where he will lead an informal and general discussion of religious studies, theology, science, free will and determinism, and whatever else students want to talk about. Faculty and students are welcome to attend.

And students, if you attend, consider submitting your impressions/reflections on the talk and the general topic of stem cell ethics for this class blog.

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Those disorganized cellular filing cabinets we call chromosomes

Dear readers who were subjected to last night's dumb version of science, your reeducation must begin now, starting with the basics! And, by an amazing coincidence, there happens to be an excellent new post on Pharyngula today, addressing a basic question: how can chromosome numbers change? Go read it, and bookmark it for future reference. If you haven't yet had someone throw that question at you as a "gotcha" about how new species couldn't possibly evolve, you will likely find it flying at you one of these days - and if you read this post, you'll be ready!

PZ makes the nucleus sound rather like my office: lots of disorganized information stashed in bundles everywhere... I need a linkage map to find stuff; or perhaps I could just induce some mutations to make chunks of it go away or something! You better hope I don't end up with rearrangements of your term papers, eh? Might be entertaining, though... :-)

[From Pharyngula: Basics: How can chromosome numbers change?]

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An ancient reptile challenges some modern hypotheses about molecular evolution rates

Student post submitted by Nathan S. Sunderson.

A recent study by Jennifer Hay and colleagues at the Allan Wilson Centre for Molecular Ecology and Evolution in New Zealand has found that unexpectedly, the Tuatara (Sphenodon punctatus ) may have some of the fastest rates of molecular evolution seen in the animal kingdom. The two species of tuatara have long been a fascination in the realm of herpetology because they have changed little since the time of the dinosaurs and are the sole living members of a sister clade to the familiar squamata (snakes and lizards). Tuataras have many “primitive” characteristics such as low metabolism, slow growth, and slow reproduction: all of which are expected to correspond to slow mutation rates. How can an animal with such historically slow morphological evolution have high rates of molecular evolution?

By sequencing the mitochondrial DNA hypervariable regions (HVRs) of the control region of modern and fossilized tuataras and radiodating the fossils examined, the group calculated an evolution rate of 1.56 (0.83-2.34) substitutions per nucleotide per million years. This is the highest rate seen among the 10 animal species studied to-date using similar statistical techniques.

These findings contradict the assertions that: 1) there is an inverse relationship between generation time and molecular evolution rate, 2) rate of evolution corresponds to body size, and 3) there is a direct correlation between metabolic and evolutionary rates. The most important implication of this study is that the rates of neutral molecular and phenotypic evolution may be decoupled. Indeed, previous studies on other living fossils (coelacanth and horseshoe crab) suggest that they may similarly have high evolutionary rates. The group has suggested that perhaps genome structure and replication processes (not metabolism, body mass, and generation time) are the key to understanding the diversity of evolutionary rates among animals.

Reference:

HAY, J., SUBRAMANIAN, S., MILLAR, C., MOHANDESAN, E., LAMBERT, D. (2008). Rapid molecular evolution in a living fossil. Trends in Genetics, 24(3), 106-109. DOI: 10.1016/j.tig.2007.12.002

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In other news...

If only things were the other way around...

glumbert - Gay scientists isolate Christian gene

[Hat-tip: Onegoodmove]

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Time to Fight HIV in Our Genes

A lot of scientists are aware of the CCR5 gene and the mutant form of this gene that has a base pair deletion at position 32. The normal CCR5 gene codes for a receptor protein that gets HIV into the cell and people with the mutant form are resistant to HIV because the virus is unable to enter into the cell. It is an exciting time in the medical community because researchers have discovered a new promising gene that could potentially prevent the virus from forming. HIV is a rapidly mutating virus that is hard to stop with vaccines and cocktail drugs. It has been scientists’ objective to find new ways of fighting HIV despite its constant evolution, and they might have discovered a way to fight it naturally.

So what is this magical gene that is located in every cell of our body? It is called the TRIM22 gene and it has the amazing ability to prevent the assembly of the virus in our cells. A team of Canadian researchers at the University of Alberta discovered this gene and are excited to continue doing experiments to see how it works exactly. When the gene was placed into cells it actually prevents the virus from forming and intern prevents the onset of AIDS. In another experiment, the research team prevented cells from turning on the TRIM22 gene which caused the coordinating interferon to become ineffective at blocking the HIV infection. Under normal conditions this interferon coordinates attacks by the TRIM22 gene against infections. This means the TRIM22 gene is a crucial part of our defense against HIV. These research findings can be found in the public library of science pathogens.

Further research is necessary to answer more questions about this gene and its ability. For instance, the TRIM22 gene does not work in people who are already infected with HIV. Reasons for this are still unknown and mind boggling to scientists. Other studies are being done to see what other viruses the TRIM22 gene can fight. The tests done here were conducted using computer analysis and cell cultures, so it will be interesting to see what happens when they test the genes on model organisms.

The prospects of this research are promising and scientist hope to use this natural means for fighting the HIV virus to synthesize drugs that mimic the TRIM22 gene. Science and technology are allowing medicine to go in directions that it has never gone before. With dedicated scientists and proper funding it is possible that we will find a cure to HIV in the next few decades.

[contributed by Sheena Edmonds]

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Let the Training Begin (reflections on Bush's lecture)

Dr. Bush gave a fascinating lecture today on stem cell research; how far we have come and how far we have left to go. The first mouse embryonic stem cells were cultured in 1981, and the first human embryonic stem cell was cultured in 1998. Just a decade later, scientists are able to transform these and other stem cells into any tissue in the body. A technique done regularly among researchers is somatic cell nuclear transfer. This is when the nucleus is removed from an unfertilized egg cell and replaced with the nucleus from a patients somatic cell (heart cell, liver cell, etc.). This ultimately puts the genetic material of the patient into cells that can become any part of their body. This is exciting because whenever tissue is transplanted into a human being there is always the risk of rejection, but this method minimizes that risk because the cell contains instructions for life, unique to the donor.

Some might ask how the undifferentiated stem cells become destine for specific tissue types. One way scientists are doing this is by treating stem cells with different “cocktails” of growth factors that will determine their final destination. One example Dr. Bush gave was the experiment where mouse cells were treated with two different growth factors which caused them to become cardiac muscle cells. He showed a brief video of these cells and they were actually beating! He said they are now even able to take cells that are already at there terminal state, like skin cells, and make them into stem cells. We saw an example of this in class when Dr. Katti showed us how they took skin cells, turned them into stem cells, which became red blood cells that were placed in a mouse with sickle cell anemia and ultimately cured the mouse of this disease.

It is truly amazing what these cells and this research is capable of. There are some set backs for those doing stem cell research. For example, the federal government will only provide funding for research done on 21 cell lines that have been approved. However, this does not stop private funding from taking place. Dr. Bush believes that we are about five to ten years away from seeing stem cells used in medicine. In July of this summer, Dr. Bush is going to have a workshop for university professors showing them how to culture stem cells so that, in the future, college courses can be designed to teach students these methods.

From the stand point of evolution, will stem cells and their potential in medicine ultimately have adverse effects on the human population? Futuristically speaking, if we eliminate disease are we eliminating natural selection on our species? Will this cause the human population to rapidly overshoot its carrying capacity because everyone is living healthy lives without terminal illnesses? Or on the other hand, will new diseases arise from strains of mutant stem cells? As much as it is exciting to find cures to Parkinson’s, liver disease, and sickle cell anemia; it is equally frightening to ponder the repercussions of this new wisdom.

Check out these websites for additional news regarding stem cells:

Somatic Cell Nuclear Transfer (Therapeutic Cloning)

California Institute for Regenerative Medicine

Chemical Turns Stem Cells Into Beating Heart Cells

[contributed by Sheena Edmonds]

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On junk DNA

While we talk about the quirks of DNA and mutations in class this week, here's a good review of junk DNA that you might enjoy spending a few minutes reading. Here's how it begins:

The instructions for "life as we know it" are coded in DNA, but it appears that only a fraction of our DNA is ever used. (This is probably not true of our brains, myths notwithstanding.) At least, only a fraction of it is ever translated into proteins such as enzymes. Some of the untranslated (noncoding) DNA has known functions, such as coding for the RNA part of the ribosomes that translate messenger RNA into protein, but much appears to be junk. Much of the junk is multiple copies of transposons, bits of unusually selfish DNA that reproduce like rabbits and burrow into the chromosomes, sometimes presumably disrupting functional DNA.

But if the noncoding DNA is mostly useless junk, why has some of it apparently been preserved by natural selection?

Go read the whole thing on This Week in Evolution, a blog I hope is becoming part of your weekly wander through the blogosphere.

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Reprogramming our cells to fix those darn mutations

Yes, we seem to be approaching that brave new world where we can fix mutations in our genomes to treat certain genetic diseases. The technology has already reached the point where it can handle at least point mutations as seen in this astonishing piece of recent research where they were able to reprogram cells in mice to treat sickle-cell anemia. You can find a nice description of the work with some background to put it into context in this essay on "Not Exactly Rocket Science", a blog I discovered while updating the bit about sickle cell in my lecture on mutations for today's class. It looks like a blog well worth reading on a regular basis, and has a number of other good examples of commentary on peer-reviewed articles you might emulate for your blogging for this class!

And as you absorb this paper, and marvel at how we might, someday soon, be able to fix some of our genetic defects, ponder the ethical implications of acquiring this ability to tinker with our genes at this level!

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