Nothing could be wrong until you realize that Science writer editor Elizabeth ("Liz") Pennisi is behind it. That changes things entirely.
To find out why you have to read Dan Graur's latest at: A Dog on the Cover of @ScienceMagazine: Sins of Omissions.
At some point, the big bosses at Science magazine are going to have to wake up to the fact that they're publishing a lot of bad papers and commentaries. Something is seriously wrong.
David Klinhoffer likes Elizabeth Pennisi: Shooting the Messenger: Elizabeth Pennisi. He says ...
As we frequently hasten to emphasize about daring writers and researchers in science, I have no reason to think Pennisi is a Darwin skeptic much less a proponent of ID. Still, she's a reporter who is open to promoting "evolution heresy." She's unafraid to challenge the old guard. More than once she has stuck her finger in the eye of ancient régime. Now you know why she ticks off guys like Graur and Moran.
Yep. He got that right. Graur and I are definitely part of the old regime and we don't like people who promote evolution heresy ... or their sycophants.
Claudiu Bandea is a frequent commenter on this blog. Whenever the subject of junk DNA comes up he reminds us that he had a theory over twenty years ago. Now he has published(?) an advertisement at: On the concept of biological function, junk DNA and the gospels of ENCODE and Graur et al.. Here's the abstract ...
In a recent article entitled “On the immortality of television sets: "function" in the human genome according to the evolution-free gospel of ENCODE”, Graur et al. dismantle ENCODE’s evidence and conclusion that 80% of the human genome is functional. However, the article by Graur et al. contains assumptions and statements that are questionable. Primarily, the authors limit their evaluation of DNA’s biological functions to informational roles, sidestepping putative non-informational functions. Here, I bring forward an old hypothesis on the evolution of genome size and on the role of so called ‘junk DNA’ (jDNA), which might explain C-value enigma. According to this hypothesis, the jDNA functions as a defense mechanism against insertion mutagenesis by endogenous and exogenous inserting elements such as retroviruses, thereby protecting informational DNA sequences from inactivation or alteration of their expression. Notably, this model couples the mechanisms and the selective forces responsible for the origin of jDNA with its putative protective biological function, which represents a classic case of ‘fighting fire with fire.’ One of the key tenets of this theory is that in humans and many other species, jDNAs serves as a protective mechanism against insertional oncogenic transformation. As an adaptive defense mechanism, the amount of protective DNA varies from one species to another based on the rate of its origin, insertional mutagenesis activity, and evolutionary constraints on genome size.
It's not a good idea to attack someone who; (a) is an expert in the field, (b) is intelligent and outspoken, and (c) has a blog. But that never stopped Claudiu Bandea before so why should it now?
Here's part of how Dan Graur responds at: A Pre-Refuted Hypothesis on the Subject of “Junk DNA”. There's more, read it all.
The first problem with this hypothesis is that big eukaryotic genomes consist mostly of very few active transposable elements and numerous dead transposable elements. So, big genomes seem to need little protection. Moreover, a positive correlation exists between genome size and number of transposable elements. In 2002, Margaret Kidwell published a paper entitled “Transposable elements and the evolution of genome size in eukaryotes.” In it, she showed that an approximately linear relationship exists between total transposable element DNA and genome size. Copy numbers per family of transposable elements were found to be low and globally constrained in small genomes, but to vary widely in large genomes. Thus, the major characteristic of large genomes is the absence of selective constraint on transposable element copy number.
Given that the vast majority of transposable elements are dead, the most parsimonious explanation is that the continuous accumulation of dead transposable elements is the reason for genomes becoming large. Let me spell it out: the “large” part in “large genomes” is made of transposable elements. Genome do not become large first and then protect genetic information by becoming sinks of transposable elements.
The other problem with the protection-from-mutation hypothesis is that it assumes selection on mutation to be effective. Selection on mutation is referred to in population genetics as second-order selection. The reason is that this type of selection is anticipatory. It protects against a possibility, not an actuality. Second-order selection on mutation (mutability) requires huge effective population sizes, so huge in fact that they are only found in a few bacteria and viruses. Unfortunately for the protection-from-mutation hypothesis, genome size is known to be inversely correlated with effective population size. In other words, huge genomes are found in species that have very small effective population sizes. So small, in fact, that even regular selection (first-order selection) is not very effective.
Thomas Huxley was proven right again: "The great tragedy of Science is the slaying of a beautiful hypothesis by an ugly fact." Several ugly facts in this case.
I can't count the number of people who have tried to explain to Claudiu Bandea that his idea is ridiculous. Hopefully, this last embarrassment will silence him.
Naturally, the Intelligent Design Creationists are all over it [Another response to Darwin’s followers’ attack on the “not-much-junk-DNA” ENCODE findings].
For some reason the title reminds me of "What Does the Fox Say." Oh well, PZ Myers is desperately interested in knowing which way Darwin walked when he took a stroll on the Sandwalk [An important historical question!].
I know which way PZ walked 'cause I led him!
I first became aware of Syvlia Brown when I saw her on Larry King Live ten years ago [Interview with Sylvia Browne]. As most of you know, Larry King is a real sucker for quacks of all types and he used to let psychics like Sylvia Browne respond to listeners who called in to the show. It was always good for a laugh.
In the middle of that part of the show we have this exchange.
KING: OK. Do you know when you're going to die?
BROWNE: Yes. When I'm 88.
Later on I was happy to post a link to Anderson Cooper's debunking of Sylvia Browne on CNN [Psychic Sylvia Browne Is Nothing but a Con Artist and a Fake].
Sylvia Browne died yesterday [Psychic Sylvia Browne, famous for TV appearances, dies at 77]. She was 77 years old. Only off by 11 years.
[Hat Tip: PZ Myers: Didn’t see that one coming]
R. Ford Denison has an excellent blog called This Week in Evolution. He recently posted an article about the evolution of multicellularity [Evolving-multicellularity lab exercises]. That post contains a link to a paper he recently published with a former student (Ratcliff et al., 2013). Here's the abstract.
Multicellularity was one of the most significant innovations in the history of life, but its initial evolution remains poorly understood. Using experimental evolution, we show that key steps in this transition could have occurred quickly. We subjected the unicellular yeast Saccharomyces cerevisiae to an environment in which we expected multicellularity to be adaptive. We observed the rapid evolution of clustering genotypes that display a novel multicellular life history characterized by reproduction via multicellular propagules, a juvenile phase, and determinate growth. The multicellular clusters are uniclonal, minimizing within-cluster genetic conflicts of interest. Simple among-cell division of labor rapidly evolved. Early multicellular strains were composed of physiologically similar cells, but these subsequently evolved higher rates of programmed cell death (apoptosis), an adaptation that increases propagule production. These results show that key aspects of multicellular complexity, a subject of central importance to biology, can readily evolve from unicellular eukaryotes.
Here's the problem. Most fungi are multicellular and Saccharomyces cerevisiae (budding yeast) almost certainly evolved from an ancestor that could form hyphae. In fact, wild-type diploid strains or Saccharomyces cerevisiae will form multicellular filaments (pseudohypha) in response to starvation for nitrogen (Liu et al., 1996).
Many of the common lab strains have lost the ability to form multicellular pseudohyphae because they carry a nonsense mutation in the FLO8 gene (Liu et al., 1996). Presumably, those strains have been selected by bakers and brewers over the past several thousand years.
In their discussion, Ratcliff et al. (2012) say ...
Although known transitions to complex multicellularity, with clearly differentiated cell types, occurred over millions of years, we have shown that the first crucial steps in the transition from unicellularity to multicellularity can evolve remarkably quickly under appropriate selective conditions.
I don't this this is quite fair since the yeast strain is just reverting to a primitive condition. This might only have required one or a few mutations. It's not a very good model for de novo evolution of multicellarity.
The work from Gerry Fink's lab (e.g. Liu et al. 1996) is a good example of why we should be cautious using yeast as a model for anything. The yeast strains used in the lab have been selected for specific characteristics since bread-making and beer-making were first invented over 4000 years ago. We need to be cautious about drawing general conclusions based on work with lab yeast strains.
The lab exercise based on the Ratcliff et al. (2012) paper [Experimental Evolution of Multicellularity] may be interesting but it's also misleading. The description of that experiment implies that students are reproducing the ancient evolution of multicellularity from single-cell organisms. Instead, what students are actually looking at is the reversion of a derived, exclusively single-cell strain, to the more primitive multicellular state. That's not the same thing.
[Photo Credit: That's Ford at a rally in Ottawa where we were protesting the Conservative government's clamp-down on science in Canada. He took advantage of the audience to advertise his book. 
Liu, H., Styles, C.A. and Fink, G.R. (1996) Saccharomyces cerevisiae S288C has a mutation in FL08, a gene required for filamentous growth. Genetics 144:967-978. [PDF]
Ratcliff, W.C., Denison, R.F., Borrello, M. and Travisanoa, M. (2012) Experimental evolution of multicellularity. Proc. Natl. Acad. Sci. (USA) 109:1595-1600. [doi: 10.1073/pnas.1115323109]
There are a lot of myths surrounding the influence of the Texas Board of Education on the content of biology textbooks. Most people seem to think that major publishers have watered down or eliminated evolution in response to pressure from the Texas board. There's very little evidence to support that claim.
In any case, the situation has changed as reported by Josh Rosenau on the NCSE website [What’s the Future of Texas Textbook Battles?].
The adoption process ending this week will be the first science textbook adoption in a decade. Creationists on the board opened the door to abuses with the standards they passed in 2009, and lame duck board members after the 2012 elections snuck in ideologically-driven textbook reviewers. This summer, these reviewers attacked evolution and climate change in biology textbooks, looking to influence publishers and the board. The hope was that the board’s influence over purchasing decisions would be powerful enough to compel publishers to undercut the science.
But publishers are stronger now. A 2011 law (passed in response to the absurd process in 2009 and 2010) allows local districts to buy any book they want, whether or not it’s on the board’s approved list. Districts are still going to prefer an approved textbook, but if the board goes too far, local districts can opt for a book not on the list, which means the publishers can walk away from the adoption process rather than weaken their textbooks. This science standards adoption is the first under the new law, a test case for battles to come (especially next year’s social studies textbook adoption).
So far, the publishers are standing strong. Creationists pushed them to water down evolution coverage, but they seem to be finding ways around the reviewers’ suggestions. As Ron Wetherington (who won a Friend of Darwin Award from NCSE in honor of his work on the 2009 standards) told the Dallas Observer "I reviewed the publisher’s response to this. In this particular case, the publisher said, ‘Up yours, we’re not going to change anything.’" We don’t yet know whether the state education agency will accept that response and recommend these textbooks for adoption.
Here's the view from TFN Insider [Important News: Publishers Are Resisting Pressure to Dumb Down Their Biology Textbooks for Texas].
We have now had our first look at changes publishers have submitted in response to objections — many of them attacks on evolution and climate change science — raised by official state review teams evaluating new science textbooks for Texas. And we have very encouraging news:
All 14 publishers are refusing to water down or compromise instruction on evolution and climate change in their proposed new high school biology textbooks.
These publishers deserve our thanks for standing up to pressure from right-wing politicians and activists working to corrupt the science in our children’s textbooks.
Contrast this with the question asked by Paul Waldman a few months ago [The Missing Piece in Coverage of Texas Evolution Controversies].
So here's the missing piece: what about the textbook companies? When this issue is discussed, the publishers are talked about as if they have no agency, no ability to affect the outcome of these events. But they're morally culpable for participating in these farces. If they wanted, they could stand up to the state of Texas. So how can the people who work at a publisher in good conscience agree to write a biology textbook that treats evolution as a wild, unsupported idea? What if the Texas Board of Education demanded that their books discuss the "controversy" about whether the Earth travels around the sun or vice-versa, or the "controversy" about whether earthquakes happen because the turtle on whose back the world sits is scratching an itch, or the "controversy" about whether stars are actually faeries winking at us from up in the sky? Would the publishers say, "OK, if that's what you want, we'll write it and print it"? Someone should ask them where they draw the line on their integrity.
This was gleefully cross-posted to Jerry Coyne's blog website [Textbooks and Texas] where his sycophants jumped all over me for suggesting that publishers were not actually modifying their textbooks in any significant way.
Here's an excerpt from Jerry Coyne's latest post [Creationism on life support at the Texas Board of Education].
This week the Texas Board of Education will consider which biology texts to “recommend” for Texas public-school students. I say “recommend” rather than “adopt” because the rules have changed. The list of approved books, from which all school districts were once required to choose, is now gone, and the Board can only recommend books. Texas school districts can now choose whichever books they want to use, including material from the Internet. That’s a huge bonus to publishers, who used to have to rewrite many of their biology and history books so they’d be acceptable to Texas, largely purging them of evolution and giving a more conservative point of view on American history. Now they won’t have to do that, and publishers are beginning to resist such changes anyway. If all the publishers resisted, Texas wouldn’t have any books to buy!
I still think it's misleading to say that publishers "used to have to rewrite many of their biology ... books so they’d be acceptable to Texas, largely purging them of evolution." I've got copies of Miller & Levine's biology textbooks, for example, and they cover evolution quite well. I could be wrong but I don't think the Texas Board of Education ever rejected a biology textbook. They were all on the list of "approved" textbooks even though they covered evolution.
From Tressie McMillan Cottom at tressiemc [The Audacity: Thrun Learns A Lesson and Students Pay].
Sebastian Thrun, founder of Udacity, one of the most high-profile private sector attempts to "disrupt" higher education discovered inequality this week. Thrun has spent the last three years dangling the shiny bauble of his elite academic pedigree and messianic vision of the future of higher education before investors and politicos. He promised nothing short of radically transforming higher education for the future by delivering taped classroom lessons of elite professors through massive open online courses. So what went wrong?
After low performance rates, low student satisfaction and faculty revolt, Thrun announced this week that he has given up on MOOCs as a vision for higher education disruption. The "godfather of free online education" says that the racially, economically diverse students at SJSU [San Jose State University], "were students from difficult neighborhoods, without good access to computers, and with all kinds of challenges in their lives…[for them] this medium is not a good fit." It seems disruption is hard when poor people insist on existing.
Thrun's goal was to market lectures by "elite" professors at places like Sanford1. His new company, Udacity, was going to make tons of money by selling lists of successful students to private companies who are looking for talent. Guess what? It turns out that there are lots of disadvantaged students in introductory courses at SJSU who don't learn from lectures given by elite Stanford professors. Who would have guessed?
In case you've forgotten the hype that Sebastian Thrun created when he formed Udacity, read: Sebastian Thrun Will Change Education. And watch the video.
1. My position on this is that the professors at Harvard and Stanford are not necessarily the best teachers. In my field of biochemistry, for example, we have direct evidence that professors at MIT do a horrible job of teaching biochemistry [Where Are the Best University Teachers?]. In my experience, the best biochemistry teachers are often located at small colleges where they pay attention to the latest pedagogical literature and actually read the textbooks they use in class.
BBC News is reporting that Fred Sangerhas died [Frederick Sanger: Double Nobel Prize winner dies at 95]. Sanger is one of the few people to win two Nobel Prizes. His first was for sequencing insulin and his second was for developing a technique for sequencing DNA (Sanger sequencing).
Most people, even most scientists, have no idea how much he influenced molecular biology. Sanger worked at Cambridge (UK). When Francis Crick first arrived at Cambridge in 1947 he soon met a number of important scientists. Here's how Horace Freeland Judson describes Sanger in The Eight Day of Creation (pp. 88-89).
One of these in particular, the biochemist Frederick Sanger, came to have great intellectual importance in Crick's thinking and then to molecular biologists generally as the field developed. Sanger is temperamentally and in scientific style Crick's opposite. Where many scientists, Crick among them, flower at conferences and do a great deal of their science by talking, Singer is a quiet man—reticent, even shy, a man who worked with his hands, at the bench. He almost never talked to the press, never despite the editor's importuning wrote the big article for Scientific American. One might spot him bicycling to work on a spring morning, in a drab brown coat, in the rain. Once I stopped to talk with him in the corridor of the laboratory building, where he was waiting in the queue for his turn at the ultraviolet-light box, in order to illuminate the spots on a sheet of chromatography paper he was holding. Sanger is a Quaker by upbringing, and stayed at Cambridge through the second world war; holding only a junior fellowship in the biochemistry department, and even when the war dried up the usual sources of research funds, with family money he was able to keep going. In the course of nearly a decade, beginning in the mid-forties, Sanger settled upon the new techniques of chromatography to determine the amino-acid sequences of the two chains of the bovine insulin molecule. He proved that the sequences are unique and always the same, meaning that every molecule of insulin in every cow is exactly like every other. Yet the sequences show no general periodicities: they are not predictable from ordinary chemical rules.
Sanger published very rarely. His papers came to be red with heart in mouth by other scientists, for they are technically brilliant. Even as he worked, though, the news slowly spread and the implications sank in. For one thing, his department held a biochemistry tea club where perhaps once a month research that was relatively finished, though not yet submitted for publication, was presented. Brigitte Askonas, later an important figure in immunology in England, came to Sanger's lab as a doctoral student late in 1948, staying on into 1952. "Even then, Fred had only a minor fellowship—and some had wanted to kick him out," she told me once. "When one would ask him how his work was going, he would say very little. 'Oh, I've got another peptide.'" Then at a lab meeting he would bring a stack of cards showing overlapping short sequences, and slowly, diffidently, build up his latest segment of the molecule. "Crick always came to the tea club," Askonas said. "And he always asked awkward questions. Enfant terrible questions. And then he would explain, somewhat disingenuously, 'You see, I'm just learning.'" Sanger's general conclusion was forceful by 1949, when he went to the annual symposium on quantitative biology at Cold Spring Harbor (his only such visit). In a paper published on the first of June of that year—the earliest of his magisterial series of papers on insulin appearing every odd-numbered year until 1955—he was already able to say that "there appears to be no principle that defines the nature of the [amino-acid] residue" occupying any particular position in a protein. The conclusion was definitive by 1951. For this work and the methods of sequencing he invented to do it, Sanger was awarded the Nobel Prize in chemistry in 1958. (He later turned to the more difficult problem of sequencing nucleic acids, which earned him a share of another Nobel Prize, in 1980. Crick, from his first arrival in Cambridge, new of Sanger's work step by step, months and even years before new steps were published.
The Green Party of Canada is led by Elizabeth May who has a seat in parliament. The Green Party (of Canada) advocates many positions that are anti-science [Do Not Vote for the Anti-Science Green Party].
The National Post is a major Canadian newspaper that leans to the right so it has never been a friend on the Green Party. In spite of this bias, they got something right when they wrote, Elizabeth May’s Party of Science seems to support a lot of unscientific public policies.
The article was written by Tristin Hopper. Here's what he says in the opening paragraphs.
Two months ago in Halifax, Green Party leader Elizabeth May appeared at a Stand Up For Science rally; one of many demonstrations held across the country to protest, among other things, a Canada-wide “muzzling” of government scientists.
“You may not like the opinions you get from science, but you have to listen to science,” Ms. May told Halifax radio.
Only a week before, however, Ms. May had been at a town hall meeting in her Saanich, B.C. riding telling her constituents not to trust federal science — albeit from a different agency than the ones being defended on the streets of Halifax.
“Agriculture Canada is increasingly a corporate model for profits, for Monsanto and Cargill, and certainly not to help farmers and certainly not to ensure safe food for Canadians,” said Ms. May.
The point needs emphasis. There's really no serious scientific debate over the safety of GM food. It is safe to eat. That does not mean that every single scientific paper that has ever been published proves that GM food is safe. You can always find some paper somewhere that backs up your preferred view of a scientific issue. Most Sandwalk readers know that real science is determined by the consensus views of the experts in the field and not by the rogue scientists who disagree. If you've been reading my blog, you will also know that in any debate that involves science both sides have to appear to have science on their side because, if you don't have science on your side in the 21st century, you've lost the debate.
Here's how Michael Kruse puts it. (He is quoted in the National Post article.)
“I really think the Green Party is just doing the same things everybody else does, which is to make up an idea that matches with your ideology, and then go looking for evidence to support it,” said Michael Kruse, chair of Bad Science Watch, a non-profit devoted to rooting out false science in public policy.
Michael has it right. The Green Party is doing exactly what a long list of groups do when their favorite beliefs aren't supported by the scientific consensus. They cherry-pick. Then they make up conspiracy theories to explain why climatologists, evolutionary biologists, nutritional scientists etc. are misleading the general public about the real science in their field.
In a July essay, Aaron Larsen, a Canadian-born Harvard post-doctoral fellow publicly called out the Green Party—his preferred choice at the ballot box—for its platform declaring that genetically-engineered crops are a “potentially serious threat to human health and the health of natural ecosystems.”
“Just to be clear, there has never been a single reputable, peer-reviewed study that has found any link between the consumption of genetically modified foods and adverse health effects,” he wrote.
That's why the Green Party is anti-science. There are many other examples of Green Party policies that are anti-science. You should not vote for the Green Party if you value science. I hate to think what might happen to science if it ever became the governing party of Canada.
[Hat Tip: Canadain Atheist]
My philosopher friend, Chris DiCarlo, and I are trying to teach our students how to think critically. We use the evolution/creation debate as an example of how to make valid arguments (and how not to make them). Two of the important points we emphasize are that you should try to avoid the strawman fallacy and you should try very hard not to misrepresent your opponent's point of view. (These are related.)
I tell my students that it's important to understand what your opponents are arguing—you must try and walk in their shoes, so to speak. This is crucial. You may decide that their arguments are completely wrong and ridiculous but you must make sure you interpret them correctly or you are guilty of several sins.
You might recall that I recently posted a comment about David Evans, Executive Director of the National Science Teachers Association (NSTA) [David Evans Says, "Teach What the Vast Majority of Scientists Affirm as Settled Science"]. I liked the idea that we should teach what the "vast majority of scientists affirm as settled science." When it comes to teaching, you have to make a decision about what is good science and what is bad science and it seems reasonable to NSTA (and to me) that the consensus among the experts is a good criterion to use. If you read the comments in that post you'll see that it's not always easy to decided what that consensus is, but that's not the main point.
Last week's molecule was a Holliday junction, one of the key intermediates in recombination. It's named after Robin Holliday who has since retired from science to concentrate on being a sculptor. He has produced several "biological" sculptures including "DNA Structure" (top) and "Cross Over" (bottom). The winner is Caroline Josefsson from British Columbia. The undergraduate winner is Andrew Wallace but since he lives in Australia, I suspect he won't be coming to lunch [Monday's Molecule #222].
Today's molecule (below) is not one of my favorite molecules for many reasons. However, it's pretty important in some species. Name the molecule, being as specific as you can without resorting to IUPAC rules. I need the most common name as well as a more detailed name.
Email your answer to me at: Monday's Molecule #223. I'll hold off posting your answers for at least 24 hours. The first one with the correct answer wins. I will only post the names of people with mostly correct answers to avoid embarrassment. The winner will be treated to a free lunch.
There could be two winners. If the first correct answer isn't from an undergraduate student then I'll select a second winner from those undergraduates who post the correct answer. You will need to identify yourself as an undergraduate in order to win. (Put "undergraduate" at the bottom of your email message.)
The mayor of Toronto is an alcoholic, a drug user (cocaine), and many other things that make him unsuitable to hold any political office. The city of Toronto is trying really hard to get him to resign or take a leave of absence but there's not much they can do if he refuses to act in an honorable and responsible manner.
It's really hard to find anything likeable about the man but I did notice that he likes Tim Hortons coffee. Look at what's in his hand as he walks down Danforth Street in drunken stupor! He can't be all bad, can he?
A recent article in New Scientist made me annoyed. The title in the print edition is Cure for Baldness Finally Cuts It. It starts off with ...
We may be a hair's breadth away from a cure for baldness.
Baldness is not a disease so it doesn't need to be cured.1 Gray hair is also not a disease and neither are the wrinkles that appear on your face as you get older.
You may choose to disguise baldness with hair transplants or paint your white hairs to make it look like you don't have them. You can even inject botox to hide wrinkles. If you do this, the only disease you have is vanity. And stupidity, for letting the cosmetic industry trick you into feeling guilty about a perfectly natural phenomenon.
I'm never going to let my tax money pay for your vanity "cure." Don't even ask if it should be covered by our public health insurance.
1. Don't quibble. You know that what I'm talking about is the normal kind of baldness in men that develops as you get older.
The National Science Teachers Association (NSTA) is responsible for The Adaptation Assessment Probe that I criticized last week. It's a remarkably poor question on adaptation—expecially considering that it was designed by teachers.
David Evans1 is the Executive Director of NSTA and he has written about the recent attempts to insert creationism into textbooks in Texas [In Texas, Standing Up for Science]. He says one very good thing in these two paragraphs.
There are many ways that humans come to know, experience, understand and appreciate the world in which we live. Consider, for example, the different realms of religion, science and art. We can all appreciate the beauty of a sunset without understanding that its beauty comes from the energy of a thermonuclear reaction and the refraction of its light in the atmosphere. Likewise, understanding the scientific processes of the sunset does not prevent one from capturing its beauty on canvas or making a spiritual connection.
There are countless differing opinions about how best to educate our children, but presenting non-scientific or religious ideas in science class or in science textbooks is simply wrong and blurs the line about what is and what is not science. This will only confuse and mislead students and does nothing to improve the quality of science education and everything to weaken it. Decisions about what counts as science should not be a popularity contest. No matter how many people object, public schools must teach what the vast majority of scientists affirm as settled science.
I like the way he expresses the idea that we "must teach what the vast majority of scientists affirm as settled science." This avoids getting into definitions about what counts as science. It avoids the "methodological naturalism" trap. Well done!
The next paragraph isn't quite as good. It could have been a lot better. All he had to do was leave out the little phrase that I underline and enclose in brackets. It would not change the meaning but it would properly reflect "what the vast majority of scientists accept as settled science."
Texas students deserve the best science education possible, as do students everywhere. This means teaching them sound science, including evolution [by natural selection] as a major unifying concept in science. It is firmly established as one of the most important and robust principles in science, and is the best and most complete scientific explanation we have for how life on Earth has changed and continues to change. Furthermore, the very foundation of science is grounded in, and based upon, evidence. Classrooms will use the textbooks Texas adopts for years (the last science textbook adoption was a decade ago). Compromising the integrity of science for a whole generation of students to satisfy a few vocal ideologues is simply not acceptable.
1. From the website: "Evans holds a Ph.D. in oceanography from the University of Rhode Island and a bachelor’s degree in mathematics from the University of Pennsylvania. He studied for his teaching certification at Villanova University."
Last week's molecule was D-serine. (Not L-serine.) The winner is undergraduate Zhimeng Yu [Monday's Molecule #221].
I was reminded of this week's molecule by a discussion we are having in an evolution forum and by a comment from a student who took a MOOC on genetics. Does it depict something that should be taught in every introductory genetics course? Is it something that should be discussed in an evolution course? You need to name the structure formed by the blue, gray, and black strands. It has a specific name.
Email your answer to me at: Monday's Molecule #222. I'll hold off posting your answers for at least 24 hours. The first one with the correct answer wins. I will only post the names of people with mostly correct answers to avoid embarrassment. The winner will be treated to a free lunch.
There could be two winners. If the first correct answer isn't from an undergraduate student then I'll select a second winner from those undergraduates who post the correct answer. You will need to identify yourself as an undergraduate in order to win. (Put "undergraduate" at the bottom of your email message.)
