Science by press release.

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With apologies to Jonathan Eisen for encroaching on his annoyance specialty, here is yet another case of science via press release.

Big hop forward: Scientists map kangaroo’s DNA

Taking a big hop forward in marsupial research, scientists say they have unraveled the DNA of a small kangaroo named Matilda. And they’ve found the Aussie icon has more in common with humans than scientists had thought. The kangaroo last shared a common ancestor with humans 150 million years ago.

“We’ve been surprised at how similar the genomes are,” said Jenny Graves, director of the government-backed research effort. “Great chunks of the genome are virtually identical.”

The scientists also discovered 14 previously unknown genes in the kangaroo and suspect the same ones are also in humans, Graves said.

The animal whose DNA was decoded is a small kangaroo known as a Tammar wallaby and named Matilda. Researchers working with the government-funded Centre of Excellence for Kangaroo Genomics sequenced Matilda’s DNA last year. Last week, they finished putting the pieces of the sequence together to form a genetic map. The group plans to publish the research next year, Graves said.

Scientists have already untangled the DNA of around two dozen mammals, including mice and chimps, which are closer to humans on the evolutionary timeline. But Graves said it’s the kangaroo’s distance from people that make its genetic map helpful in understanding how humans evolved.

By lining up the genomes of different species, scientists can spot genes they never knew existed and figure out what DNA features have stayed the same or changed over time. Elements that have remained the same are usually important, Graves said.

The research is an important step in the understanding of genomes in general, said geneticist Bill Sherman, an associate professor of molecular ecology and conservation biology at the University of New South Wales.

But another genetic researcher was more skeptical of the project’s significance.

“If you are in Australia and you want to show that you are a major player in genomics, then it’s important,” said Penn State University biology and computer science professor Webb Miller. “But two guys in their garage are going to sequence another marsupial very soon.”

Those “two guys” are Miller and Penn State colleague Stephan Schuster, who are working on a shoestring budget to map the genome of the Tasmanian devil, which is in danger of extinction because of a contagious facial tumor disease. Miller and Schuster said their project could lead to a way to keep the species alive.

But check out the last line for the biggest problem in the story.

This isn’t the first time Australia’s unique wildlife has provided evolutionary clues. Earlier this year, scientists mapped the DNA of a platypus and found that it crosses different classifications of animals.

No. They. Did. Not.


Why do we blog and other important questions.

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I am a member of the Nature Network, though my blog there, Pyrenaemata, has been dormant for some time. That’s largely because I have enough trouble posting (semi-)regularly on this blog and its counterpart at Scientific Blogging (Genomicron 2.0). In any case, there is a forum message at the Nature Network (though I saw it on Sandwalk) that asks a set of questions about blogging that I thought I would answer.

  1. What is your blog about?
    My blog is about science, in particular evolution and genomes. Much of the content of my blog has been about non-coding DNA, and the various myths and misconceptions that this topic entails. I veer into politics infrequently, and I also post some attempts at humour now and then. Unlike several of my favourite blogs (and no doubt to the detriment of my visit count), I do not talk about religion although I do discuss anti-evolutionism.

  2. What will you never write about?
    Never say never — but I made a conscious choice early on to focus on science.

  3. Have you ever considered leaving science?
    Not seriously.

  4. What would you do instead?
    I would probably write. About science.

  5. What do you think science blogging will be like in 5 years?
    I think more professional researchers will join the blogosphere as this becomes socially acceptable. The stigma that poking one’s head out of the ivory tower is not what real scientists do is quickly being replaced by an acceptance that the medium can be useful. I think (ok, hope) that blogs will become a more common source of science news than press releases. That said, I hope there is never any move toward making blogs a venue for actual science, as I believe the peer review system (flawed though it is) is essential.

  6. What is the most extraordinary thing that happened to you because of blogging?
    Nothing extraordinary per se, though more than one interview I have conducted involved the reporter indicating that he/she had found my blog.

  7. Did you write a blog post or comment you later regretted?
    Somewhat. Early on I had an argument with Nick Matzke in which I was a little more adamant than was called for. However, in the end it worked out and we stay in touch. I have also written some posts that I am proud of — the one on Remembrance Day, I have been told, was very moving.

  8. When did you first learn about science blogging?
    My graduate student introduced me to blogs about two years ago. It took a while for me to be convinced to read them (“I’m too busy for that” was probably my mindset), but then I began to see the value for finding information in fields outside my own. Plus, some of them are rather fun. Later, I decided I would try setting up a blog to talk about my research and related work. Voila.

  9. What do your colleagues at work say about your blogging?
    I list my blog in my “service” contributions as I consider this an exercise in public outreach, and that seems to go over ok.

Blogs and teaching.

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There are many beneficial aspects to reading and writing blogs about science. I have found that they are often much better than news feeds (which generally are uncritical repetitions of press releases) for learning about research in areas other than my own specialization. This also makes them very useful for teaching, as new examples that otherwise might be overlooked can be found and added to the course material. Case in point, Not Exactly Rocket Science (a blog you should be reading, btw) has a post about a new paper in today’s Cell in which yeast behave in a cooperative way if they possess a certain “green beard” gene (Smukalla et al. 2008; see also Brown and Buckling 2008). I introduced green beard genes to my upper year evolution course back when I discussed altruism, but it so happens that this afternoon I will be covering major transitions, including the evolution of multicellularity. This paper provides a great way to tie the earlier discussion about altruism to the concept of very basic cooperative cell behaviour, cell adhesion, etc. Plus, I enjoy telling the class “Here is a paper that came out this morning…”.

A frustrating press release (or, adaptation is not random).

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My feeling about science news reports is decidedly mixed. On the one hand, I read most of the main news services in order to keep up with research outside of my own discipline. On the other hand, I would say that about once every two or three days I find a story so silly that it makes me physically uncomfortable. This is one of those.

Evolution’s new wrinkle: proteins with ‘cruise control’ act like adaptive machines

It opens:

A team of Princeton University scientists has discovered that chains of proteins found in most living organisms act like adaptive machines, possessing the ability to control their own evolution.

The research, which appears to offer evidence of a hidden mechanism guiding the way biological organisms respond to the forces of natural selection, provides a new perspective on evolution, the scientists said.

Organisms do not “respond to natural selection”. Natural selection is the differential survival and reproduction of individuals within a population. It is a population level process and it is not interchangeable with “challenges to organism survival”. If all organisms in a population are able to respond to a challenge such that there is no differential survival and reproductive success, then there is no natural selection.

It continues:

The researchers — Raj Chakrabarti, Herschel Rabitz, Stacey Springs and George McLendon — made the discovery while carrying out experiments on proteins constituting the electron transport chain (ETC), a biochemical network essential for metabolism. A mathematical analysis of the experiments showed that the proteins themselves acted to correct any imbalance imposed on them through artificial mutations and restored the chain to working order.

“The discovery answers an age-old question that has puzzled biologists since the time of Darwin: How can organisms be so exquisitely complex, if evolution is completely random, operating like a ‘blind watchmaker’?” said Chakrabarti, an associate research scholar in the Department of Chemistry at Princeton. “Our new theory extends Darwin’s model, demonstrating how organisms can subtly direct aspects of their own evolution to create order out of randomness.”

Adaptive evolution is the result of natural selection — the differential survival and reproduction of randomly varying individuals on the basis of heritable characteristics. This differential survival and reproduction is, by definition, non-random. Again, organisms do not evolve, populations do.

And then it says:

The work also confirms an idea first floated in an 1858 essay by Alfred Wallace, who along with Charles Darwin co-discovered the theory of evolution. Wallace had suspected that certain systems undergoing natural selection can adjust their evolutionary course in a manner “exactly like that of the centrifugal governor of the steam engine, which checks and corrects any irregularities almost before they become evident.” In Wallace’s time, the steam engine operating with a centrifugal governor was one of the only examples of what is now referred to as feedback control. Examples abound, however, in modern technology, including cruise control in autos and thermostats in homes and offices.

The essay is the one presented by Lyell and Hooker to the Linnean Society in 1858, along with one by Darwin. Here is the full paragraph:

Wallace (1858):

The hypothesis of Lamarck—that progressive changes in species have been produced by the attempts of animals to increase the development of their own organs, and thus modify their structure and habits—has been repeatedly and easily refuted by all writers on the subject of varieties and species, and it seems to have been considered that when this was done the whole question has been finally settled; but the view here developed renders such an hypothesis quite unneccessary, by showing that similar results must be produced by the action of principles constantly at work in nature. The powerful retractile talons of the falcon- and the cat-tribes have not been produced or increased by the volition of those animals; but among different varieties which occurred in the earlier and less highly organized forms of these groups, those always survived longest which had the greatest facilities for seizing their prey. Neither did the giraffe acquire its long neck by desiring to reach the foliage of the more lofty shrubs, and constantly stretching its neck for the purpose, but because any varieties which occurred among its antitypes with a longer neck than usual at once secured a fresh range of pasture over the same ground as their shorter-necked companions, and on the first scarcity of food were thereby enabled to outlive them. Even the peculiar colours of many animals, especially insects, so closely resembling the soil or the leaves or the trunks o which they habitually reside, are explained on the same principle; for though in the course of ages varieties of many tints may have occurred, yet those races having colours best adapted to concealment from their enemies would inevitably survive the longest. We have also here an acting cause to account for that balance so often observed in nature,—a deficiency in one set of organs always being compensated by an increased development of some others—powerful wings accompanying weak feet, or great velocity making up for the absence of defensive weapons; for it has been shown that all varieties in which an unbalanced deficiency occurred could not long continue their existence. The action of this principle is exactly like that of the centrifugal governor of the steam engine, which checks and corrects any irregularities almost before they become evident; and in like manner no unbalanced deficiency in the animal kingdom can ever reach any conspicuous magnitude, because it would make itself felt at the very first step, by rendering existence difficult and extinction almost sure soon to follow. An origin such as is here advocated will also agree with the peculiar character of the modifications of form and structure which obtain in organized beings—the many lines of divergence from a central type, the increasing efficiency and power of a particular organ through a succession of allied species, and the remarkable persistence of unimportant parts such as colour, texture of plumage and hair, form of horns or crests, through a series of species differing considerably in more essential characters. It also furnishes us with a reason for that “more specialized structure” which Professor Owen states to be a characteristic of recent compared with extinct forms, and which would evidently be the result of the progressive modification of any organ applied to a special purpose in the animal economy.

Wallace was talking about the consequences of randomly determined variants that had a change in one feature without a compensatory change in some other feature, namely that they would not survive. There is nothing in this that implies that individual organisms are changing in response to challenges or that species are directing their evolution.

It goes on, but I will jump forward:

The research, published in a recent edition of Physical Review Letters, provides corroborating data, Rabitz said, for Wallace’s idea. “What we have found is that certain kinds of biological structures exist that are able to steer the process of evolution toward improved fitness,” said Rabitz, the Charles Phelps Smyth ’16 Professor of Chemistry. “The data just jumps off the page and implies we all have this wonderful piece of machinery inside that’s responding optimally to evolutionary pressure.”

The authors sought to identify the underlying cause for this self-correcting behavior in the observed protein chains. Standard evolutionary theory offered no clues. Applying the concepts of control theory, a body of knowledge that deals with the behavior of dynamical systems, the researchers concluded that this self-correcting behavior could only be possible if, during the early stages of evolution, the proteins had developed a self-regulating mechanism, analogous to a car’s cruise control or a home’s thermostat, allowing them to fine-tune and control their subsequent evolution. The scientists are working on formulating a new general theory based on this finding they are calling “evolutionary control.”

…

Various researchers working over the past decade, including some at Princeton like George McClendon, now at Duke University, and Stacey Springs, now at the Massachusetts Institute of Technology, fleshed out the workings of [ATP], finding that they were often turned on to the “maximum” position, operating at full tilt, or at the lowest possible energy level.

Chakrabarti and Rabitz analyzed these observations of the proteins’ behavior from a mathematical standpoint, concluding that it would be statistically impossible for this self-correcting behavior to be random, and demonstrating that the observed result is precisely that predicted by the equations of control theory. By operating only at extremes, referred to in control theory as “bang-bang extremization,” the proteins were exhibiting behavior consistent with a system managing itself optimally under evolution.

Based on this story, it is challenging to determine just how this is differs from evolution in the usual sense. Looking at the original paper, it appears that what the authors are arguing is that 1) the constituent proteins in the electron transport chain are tuned to an extreme, 2) that this extreme is not related to the function of the proteins as would be “visible” to natural selection on the grounds of electron transport capability, 3) that the proteins in the network are optimized for redox potential, which has no consequences for the organism and therefore cannot have evolved through normal selection, and 4) that something else, i.e. self organization, is involved in producing the extreme features of the proteins. The rest is mathemagic, so someone else can wade through it and see if the argument makes sense if they like.

I am not actually concerned with whether the calculations are correct. As it so often is, the issue is about press releases and the hype and sloppy descriptions of both ideas and history that they (and, too often, the people interviewed) present.

________

Update:

PZ weighs in.

People have been having trouble finding the article. It’s here.

The authors have another paper in the bastion of bad biology, arXiv, that quotes directly from Wallace (here). Don’t blame the story author, these guys lifted that out of context by their own selves.

Quotes of interest — Alu again.

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I discussed the early papers involving the discovery of Alu elements in a previous post in the series. Unlike some transposable elements that are capable of autonomous transposition, Alu elements do not encode the requisite enzymes and depend on those of other sequences such as LINE-1 elements. Alu is restricted to primates, and its origin seems to have been a duplication and reverse transcription of a 7SL RNA gene early in primate evolution. One in ten nucleotides in each human genome is part of an Alu sequence, of which there are more than 1 million copies.

The elucidation of the evolutionary origins of Alu elements came some time after their initial discovery in 1979. Initially, it was thought that the 7SL RNA gene was derived from Alu, but the reverse conclusion was given by Ullu and Tschudi (1984) and was discussed further by authors such as Quentin (1992). As noted, the original papers reporting the existence of Alu elements raised the question about their potential functions. However, the later articles arrived right in the middle of the supposed time when non-coding DNA was dismissed as irrelevant. Once again, the actual literature from the period does not support the notion that such a dismissal ever actually occurred.

Ullu and Tschudi (1984) did not discuss possible function explicitly, but they did note that “these 7SL-specific homologies may reflect a strong functional constraint acting on these sequences.” In an accompanying article in the same issue of Nature, Brown (1984) was more specific about the significance of the results. He stated,

Ullu and Tschudi suggest that Alu sequences represent defective 7SL RNA molecules that have been reverse-transcribed into DNA and inserted into the genome. An analogous origin has been suggested for alpha-globin pseudogenes in the mouse, and the multiple pseudogenes for small nuclear RNAs in man. Pseudogenes are generally thought not to play an important role in the cell. Perhaps those who have argued that Alu, by its very abundance, must have an important function will recognize that this argument has now lost some of its weight.

Two important things are expressed here. One, the assumption that Alu elements are functional because they are abundant (i.e., an adaptationist expectation that they would have been removed otherwise) was apparently common in the early 1980s. Indeed, that’s why the “selfish DNA” idea was proposed (Orgel and Crick 1980; Doolittle and Sapienza 1980). Two, pseudogenes — defunct coding genes — were indeed thought to be non-functional, for obvious reasons. These are the sequences to which the term “junk DNA” originally related.

Additional information regarding the origin of Alu sequences was provided by Quentin (1992), who said,

from the beginning, the Alu progenitor sequences could have retained the capacity to interact with cellular components, suggesting that they are functionally important for the host genome. On the other hand, this RNA secondary structure could have some affinity for reverse transcriptases or other components of the retroposition machinery, and its conservation in the monomeric and Alu dimeric sequences could be related to their mobility. Indeed, this structure is first found in the 7SL RNA sequences that are prone to retroposition, and it is also retained by the progenitor sequences of the Bl family in the rodent genomes. Nevertheless, both hypotheses (secondary structure involved in a cellular function or in the reverse transcription) are not mutually exclusive.

Yet, here is a fairly typical introduction from a recent paper about Alu (Hasler and Strub 2006):

Alu elements, as well as other repetitive elements, were at the origin considered as parasites of the genome that had no major effect on its stability and genic expression. They were thought to be ‘selfish’ or ‘junk’DNA (6,7), but nowadays, several lines of evidence show that the presence of repetitive elements and especially of Alu elements, had a great influence on the human genome, in particular on its evolution. These effects were both negative and positive. On one hand, integration into genic regions that caused gene inactivation might often have been deleterious for the organism. On the other hand, because of their extended sequence homology, Alu elements induced a considerable number of non-allelic recombinations that lead to both duplications and deletions of DNA segments, thereby accelerating evolution by several orders of magnitude. Another function frequently attributed to Alu elements is their ability to provide new regulatory elements to neighboring genes. It was, indeed, reported several times that Alu elements became effectors of gene transcription by providing new enhancers, promoters and polyadenylation signals to many genes.

The only authors cited for the “Alu is just junk” are Orgel and Crick (1980) and Orgel et al. (1980). I have discussed these articles before, but will reiterate one statement from each.

Orgel and Crick (1980):

It would be surprising if the host genome did not occasionally find some use for particular selfish DNA sequences, especially if there were many different sequences widely distributed over the chromosomes. One obvious use … would be for control purposes at one level or another.

Orgel et al. (1980):

In our recent experience most people will agree, after discussion, that ignorant DNA, parasitic DNA, symbiotic DNA (that is, parasitic DNA which has become useful to the organism) and ‘dead’ DNA of one sort or another are all likely to be present in the chromosomes of higher organisms. Where people differ is in their estimates of the relative amounts. We feel that this can only be decided by experiment.

______

Part of the Quotes of interest series.
______

References

Brown, A.L. 1984. On the origin of the Alu family of repeated sequences. Nature 312: 106.

Hasler, J. and K. Strub. 2006. Alu elements as regulators of gene expression. Nucl. Acids Res. 34: 5491-5497.

Orgel, L.E. and F.H.C. Crick. 1980. Selfish DNA: the ultimate parasite. Nature 284: 604-607.

Orgel, L.E., F.H.C. Crick, and C. Sapienza. 1980. Selfish DNA. Nature 288: 645-646.

Quentin, Y. 1992. Origin of the Alu family: a family of Alu-like monomers gave birth to the left and right arms of the Alu elements. Nucl. Acids Res. 20: 3397-3401.

Ullu, E. and C. Tschudi. 1984. Alu sequences are processed 7SL RNA genes. Nature 312: 171-172.

Crankishness.

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As a brief follow up to the post about Dr. Andras Pellionisz’s Google seminar, I cannot help but quote from his website:

Since a US Government-mandated (and taxpayer paid) 4-year study (ENCODE, led by Dr. Collins) established the scientific fact that (at the least a significant part of) formerly “written off” so-called “non-coding DNA” is massively involved in genome function, US government-supported professionals who after the release of ENCODE (reversal of the Establishment in 2007) neglect to to follow Dr. Collins’ mandate that “the scientific community will have to re-think long-held beliefs” are actually liable for a hefty Class Action Lawsuit for Negligence when they disregard the established reversal of protocol and e.g. continue to “write off” investigation of 98.7% of the DNA in cases of grave genomic syndromes.

I really try to be fair with people like this, but woah. Can researchers be charged with negligence for what they don’t study? (Assuming, that is, that there actually was a total dismissal of non-coding DNA, which there wasn’t).

Pellionisz Google Tech presentation.

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Those of you who read this blog or others that discuss non-coding DNA will, for better or worse, be familiar with regular commenter Andras Pellionisz. Many people have concluded that Dr. Pellionisz is essentially a “crank”, though I believe I have tried to give him a fair hearing on this blog (before asking him to stop repeating the same arguments over and over). Whether he has managed to convince anyone of his view that all non-coding DNA is functional is another issue, however. Readers should judge this for themselves. Thus, here are links to his website, a recent article, and a recent Google Tech presentation.

www.junkdna.com (home of the “avant-garde society that formally abandoned ‘junk DNA'”)

Pellionisz, A. 2008. The principle of recursive genome function. Cerebellum 7: 348-359.

Mister Doctor Prof.

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I don’t get too concerned about things such as titles, but I have noticed that this year a more substantial number of students has been sending emails addressed to “Mr. Gregory”. I don’t know if the students this year are unaware that most professors hold a Ph.D. and therefore are “Dr.” and not “Mr.” (or “Ms.” as the case may be), but this seems to be much more common lately. Has anyone else noticed this?

I know this can get a bit confusing, so let me try to explain it, at least as the terms are used in North America.

The title “Doctor” and the abbreviated prefix “Dr.” come from the Latin for “teacher”, and are traditionally bestowed on those who have earned the highest academic degree attainable. The suffix Ph.D. is an abbreviation for Philosophiæ Doctor (L. “Teacher of philosophy”), with “philosophy” from the Greek for “love or pursuit of wisdom”. The Ph.D. is awarded in most academic disciplines, including science. Medical professionals may also hold the title “Doctor” even though they may do little or no teaching, with common degrees being M.D. (Medicinae Doctor, or Doctor of Medicine), D.V.M. (Doctor of Veterinary Medicine), D.D.S. (Doctor of Dental Surgery), and so on.

As a noun rather than a prefix, “Doctor” is usually reserved for medical doctors (“I’m not a doctor but I play one on TV”). Usually, the person teaching your course at a major university is a “Professor” and not a “Doctor” (noun) (“Are you really a mad scientist, professor?”). He or she does, however, use the prefix “Dr.”. Get it?

To make it more complex and Monty Python-ish, the prefix “Prof.” is not used by all professors. “Professor” (noun) is the position, but there are also ranks. In North America, these would be “Assistant Professor”, “Associate Professor”, and “Professor” (or “Full Professor”). In many cases, only full professors use the prefix “Prof.” in situations outside the university. I don’t use “Prof. Gregory” in non-university settings because I am not a full professor. However, I am a professor, not a doctor, although I use Dr. Gregory instead of Prof. Gregory. Right.

Perhaps that’s all too complicated to bother about. Here is the short version: When addressing a professor*, just go with “Dear Dr. So-and-so” unless he or she asks you to call him or her something different.

(*To clarify, this post is mostly for students)

Gamers will detect the problem in this study.

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From New Scientist:

Video games don’t train your brain

Does playing computer games boost your brainpower? Not necessarily, seems to be the answer.

Walter Boot and colleagues at the University of Illinois, Urbana-Champaign, found that non-gamers showed no improvement in memory skills or the ability to multitask after spending more than 20 hours on one of three video games. This appears to contradict previous studies which detected superior mental aptitudes among habitual gamers.

Any gamers care to discuss?

I’m not saying that video games do improve aptitude, but this seems like saying “Weight lifting does not increase muscle mass. Researchers showed no major increase in muscle mass among non-athletes who lifted weights for one week. This contradicts previous results which detected muscle increase in regular weight lifters.”