The book is done! It's off to the printer and we should have copies by the end of August. Everyone who posts a comment will get a free copy.1
1. In some parallel universe.
Confession time. Illustrators are people, too. And by that I mean they bring assumptions to the table at the outset of every project. There’s no avoiding it – no matter how educated and experienced you are, you can’t know it all. That is why it is so critical for researchers and editors to be intimately involved in every draft of the drawings they commission and publish. This may sound like a mega no-brainer, especially if you’re an editor or art director in a field other than in the sciences who is accustomed to working intimately with illustrators to get what you want. But in my experience illustrating two popular non-fiction science books, illustrations are treated as icing on the cake and are glossed over by fact checkers and editors who otherwise comb manuscripts for errors. Illustrating Your Inner Fish is a prime example. The manuscript went through four drafts of revisions with at least two specialized scientific editors. And yet this gaffe made it through:I know exactly how she feels but even multiple expert reviewers won't save you. When we're writing a textbook we take care to review the text and figures together and we pay just as much attention to the figures as we do to the text. For the most recent edition—about to be sent to the printer—the pages were reviewed by me, my coauthor Marc Perry, our developmental editor Michael Sypes (University of Arizona), content reviewer Barry Ganong (Mansfield University), and accuracy reviewers Scott Lefler (Arizona State University) & Kathleen Nolta (University of Michigan). That's six pairs of expert eyes that look at every page.
1. I'll post the correct version in a few days.
It seems that first born cell of evolution must have been quite complex, including a vast proteome of hundreds of different proteins. This is just one of many scientific falsifications of evolution’s prediction of simple beginnings.Most intelligent people can see the flaws in Hunter's logic so I won't bother pointing them out. However, I would like to highlight the first comment on Hunter's blog. Thorton said ...
We know you hit the bottom of the barrel with your anti-science nonsense some time ago CH. Now we discover your barrel had a trap door.Very clever. And very appropriate. Well said Thorton.
Today I’m at the State Board of Education hearings on textbook adoption. Or, in other words, the once every-so-often meeting that helps to determine whether or not Texas makes itself a laughingstock with respect to the teaching of evolution. I guess this is sort of my first “live blog,” which is just weird.This provoked a response from some of the main IDiots like Casey Luskin [University of Texas Evolutionary Biologist Andy Ellington Mocks Fellow Texans as "Idiots" and "Laughingstocks" for Doubting Darwin] and Denise O'Leary [Tax dollar alert: Who pays this Texas biology profs salary?]. Don't you just love it when the IDiots voluntarily supply us with evidence of their reasoning ability?
I continue my love / hate relationship with Texas. On the one hand, this board meeting is democracy in action (not necessarily a good thing in a Republic): every idiot gets their say. On the other, their say means very little. The larger forces at work will drive both curriculum and the impact of that curriculum.
The Discovery Institute, largely a spent force both intellectually and politically since Dover, has chosen to take issue with my comments at the State Board of Education. This is especially amusing as the original disputation of their idiocy came many years ago, and has been published via a NSCE publication for quite some time. Indeed, I refer to this publication in my previous testimony, which was and is available to the Discovery Institute. From this, we can conclude that the Discovery Institute is woefully behind the times not only in terms of science, but even in terms of their own shallow attempts to provide a revisionary context to science. Guys, this just can’t be good for your funding posture. Try to keep up.I miss deaddog.
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So, when the DI has a vague, anonymous scientist (apparently the only kind that the DI employs) point out, as they do in their current idiot posting (please note the use of the word ‘idiot,’ as it absolutely applies to the DI for their complete lack of understanding of the extant scientific literature) ...
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The DI claims this all as a teachable moment, saying that “What we see evidence of here is a scientific debate over the origin of life ….” No, actually, the problem with that claim is that science for the most part requires experimentation. You guys don’t do experiments. We do. You guys just carp about our experiments, and you don’t even do that very well.
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Which would you rather see helping to set policies relating to teaching biology, literally millions of scientists who spend their entire careers doing experiments, or a handful of folks at a faith-based think tank whose jobs largely depend on trying to make inconvenient facts go away?
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Well, Casey, I hope this gets your page hit count up somehow. God knows you need it. But really I don’t think that picking a fight about the facts is going to help you guys much in your further, currently grossly unsuccessful attempts to show your relevance. You didn’t even have boots on the ground at the Texas SBOE hearings this time, you just sent a 80 page screed that in the end didn’t change one word in one textbook up for consideration. Sad, really. But, there ya go. Happy trails.
1. Stop digging.
2. It's a rhetorical question. They are IDiots and that's exactly what IDiots do.
ScienceDaily (July 21, 2011) — For decades, scientists have known that DNA consists of four basic units -- adenine, guanine, thymine and cytosine. Those four bases have been taught in science textbooks and have formed the basis of the growing knowledge regarding how genes code for life. Yet in recent history, scientists have expanded that list from four to six.Speaking of textbooks, this amazing discovery couldn't have come at a better time since I'm just wrapping up the final chapters of my introductory biochemistry book. I'd better review what I wrote to see if I can include the 7th and 8th bases. Here's what I've got so far ...
Now, with a finding published online in the July 21, 2011, issue of the journal Science, researchers from the UNC School of Medicine have discovered the seventh and eighth bases of DNA.
These last two bases -- called 5-formylcytosine and 5 carboxylcytosine -- are actually versions of cytosine that have been modified by Tet proteins, molecular entities thought to play a role in DNA demethylation and stem cell reprogramming.
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Much is known about the "fifth base," 5-methylcytosine, which arises when a chemical tag or methyl group is tacked onto a cytosine. This methylation is associated with gene silencing, as it causes the DNA's double helix to fold even tighter upon itself.
Last year, Zhang's group reported that Tet proteins can convert 5 methylC (the fifth base) to 5 hydroxymethylC (the sixth base) in the first of a four step reaction leading back to bare-boned cytosine.
DNA and RNA contain a number of modified nucleotides. The ones present in transfer RNA are well known (Section 21.8B) but the modified nucleotides in DNA are just as important. Some of the more common modified bases in DNA are shown in Figure 18.17. Most of them are only found in a few species or in bacteriophage while others are more widespread.Oh dear. Looks like I've made a serious mistake. I've shown bases #5, #6, #7, #8, #9, and #10 but everyone knows that up until yesterday only six bases were known.
We will encounter N6-methyladenine in the next chapter when we discuss restriction endonucleases. 5-Methylcytosine is a common modified base in mammalian DNA because it plays a role in chromatin assembly and the regulation of transcription. About 3% of all deoxycytidylate residues in mammalian DNA are modified to 5-methylcytidine.
1. One of my sources is Gomers-Apt and Borst (1995). In addition to the modified bases I've shown above they describe three forms of glycosylated hydroxymethyl cytosine (#11, #12, #13), uracil (#14), α-putrescinylthymine (#15), two different sugar substituted forms of 5-dihydroxypentyluracil (#16, #17), a-glutamylthymine (#18), 7-methylguanine (#19), N6-carbamoylmethyladenine (#20), N6-methylcytosine (#21), three versions of glycosylated 5-hydroxycytosine (#22, #23, #24) and β-D-hydroxymethyluracil (#25).
Gommers-Ampt, J.H. and Borst, A.P. (1995) Hypermodified bases in DNA. FASEB 9: 1034-1042 [FASEB]
Ito, S., Shen, L., Dai, Q., Wu, S.C., Collins, L.B., Swenberg, J.A., He, C., and Zhang, Y. (2011) Tet Proteins Can Convert 5-Methylcytosine to 5-Formylcytosine and 5-Carboxylcytosine. Science Published Online 21 July 2011 [doi:10.1126/science.1210597]
The Eighth Day, first published in 1979, is a gift that keeps on giving. It is not the completeness of his history, nor even the vivid prose that imparts its lasting effect. Rather, Judson had the drive and wit to probe until he understood not just who did what, and with what quirks of personality, but why they did it, and how they did it. At each stage he reveals what was at stake, what the crucial alternatives were, and how the problems were solved (or not, as the case may be). Who cares about this past, you might ask, we scientists being neither artists nor composers?Shortly after I read this obituary I was browsing Biology News Net and came across this remarkable opening statement in a press release from Stowers Institute for Medical Research in Kansas City, Missouri, USA.
Could it be that—for scientists as well as composers and artists—the past can be a source of inspiration, and that we ignore it at our peril? Consider the question of how states of gene expression are conveyed from mother to daughters as cells divide. Are instructions passed along by regulatory proteins present in the cytoplasm (so-called “cytoplasmic determinants”), or is the information somehow built into, or attached to, the DNA and transferred along with it? Experiments performed by Francois Jacob and Jacques Monod and their colleagues at the Institut Pasteur in the 1960s distinguish between the models, strikingly supporting the first of these possibilities. These experiments (including the famous “zygotic induction” and “PaJaMa” experiments—see Judson's book) were, of course, performed with bacteria.
I recently spoke with an editor of a major journal that regularly publishes sensational papers on the question as it applies to higher organisms, and learned that s/he, like many of the journal's authors, had never heard of these bacterial experiments! You realize, reading Judson's book, that the challenge is to engage the thought processes of these French scientists, ponder their approaches and results, and design experiments of comparable power and clarity to confirm or refute their conclusions in a different setting. Without that engagement, the new answers are apt to be (and in my opinion usually are) baloney.
Look up “transcription”—the copying of a gene’s DNA into RNA intermediaries—in any old molecular biology text book, and it all seems very simple: RNA polymerase II, the enzyme that catalyzes the reaction, assembles at the start site and starts motoring down the strand, cranking out the RNA ribbon used to construct proteins. But researchers now know that RNA polymerase II often stalls on DNA strands where it was once assumed to just barrel down.This is a very misleading statement. Back in 1989 I wrote an extensive section on "RNA Polymerase Pauses While Transcribing Some Sequences" in my first textbook. I described the effects of sequence and secondary structure on the rate of elongation and explained how a protein component of the the transcription complex (NusA) promotes pausing in order to enhance transcription termination. The idea that rates of elongation were NOT constant was an important part of most molecular biology textbooks.
A report from the Conaway lab at the Stowers Institute for Medical Research in the July 8, 2011, edition of the journal Cell identifies a switch that allows RNA polymerase to shift gears from neutral into drive and start transcribing. This work sheds light on a process fundamental to all plant or animal cells and suggests how transcriptional anomalies could give rise to tumors.
There is overwhelming evidence that life has evolved over thousands of millions of years. The ancestors of modern organisms, as well as whole groups that are now completely extinct, have been found in great abundance as fossils. The main processes responsible for evolutionary change, such as variation and natural selection, have been repeatedly observed and verified in natural populations and in laboratory experiments. All the features of living organisms, including those discovered in the recent advances in molecular biology, are readily explained by the principles of evolution. Any scientific theory that provides a clear mechanism, offers a broad explanation of natural phenomena, receives strong support from observation and experiment and that is never refuted by careful investigation is usually called a “fact”. The cell theory of organisms, the germ theory of infection, the gene theory of inheritance and the theory of evolution are all facts. Teaching alternative theories as though they had equivalent scientific status is a perversion of education that damages children’s ability to understand the natural world. In particular, creationism is a religious doctrine long since known to be a fallacious account of Earth history that has no scientific standing and cannot be represented as a credible alternative to evolution. Evolution is the single most important principle of modern biology and the foundation of any sound biology curriculum.I don't like this statement because: (1) it implies that the "theory of evolution" is only about variation and natural selection, (2) it confuses evolutionary theory with the facts of evolution, and (3) it confuses creationism with Young Earth Creationism.
Graham Bell
President, Canadian Society for Ecology and Evolution
Li, X., Zhu, C., Lin, Z., Wu, Y., Zhang, D., Bai, G., Song, W., Ma, J., Muehlbauer, G.J., Scanlon, M.J., Zhang, M., and Yu, J. (2011) Chromosome Size in Diploid Eukaryotic Species Centers on the Average Length with a Conserved Boundary. Mol. Biol. Evol. 28: 1901-1911. [doi: 10.1093/molbev/msr011]Here's the challenge. Read the abstract and try and guess what important scientific point the authors are making that deserves publication in a molecular evolution journal. For extra points, read the entire article and see if you can improve your guess. You'll be impressed when you read the discussion and it all becomes clear (not!)
Abstract
Understanding genome and chromosome evolution is important for understanding genetic inheritance and evolution. Universal events comprising DNA replication, transcription, repair, mobile genetic element transposition, chromosome rearrangements, mitosis, and meiosis underlie inheritance and variation of living organisms. Although the genome of a species as a whole is important, chromosomes are the basic units subjected to genetic events that coin evolution to a large extent. Now many complete genome sequences are available, we can address evolution and variation of individual chromosomes across species. For example, “How are the repeat and nonrepeat proportions of genetic codes distributed among different chromosomes in a multichromosome species?” “Is there a general rule behind the intuitive observation that chromosome lengths tend to be similar in a species, and if so, can we generalize any findings in chromosome content and size across different taxonomic groups?” Here, we show that chromosomes within a species do not show dramatic fluctuation in their content of mobile genetic elements as the proliferation of these elements increases from unicellular eukaryotes to vertebrates. Furthermore, we demonstrate that, notwithstanding the remarkable plasticity, there is an upper limit to chromosome-size variation in diploid eukaryotes with linear chromosomes. Strikingly, variation in chromosome size for 886 chromosomes in 68 eukaryotic genomes (including 22 human autosomes) can be viably captured by a single model, which predicts that the vast majority of the chromosomes in a species are expected to have a base pair length between 0.4035 and 1.8626 times the average chromosome length. This conserved boundary of chromosome-size variation, which prevails across a wide taxonomic range with few exceptions, indicates that cellular, molecular, and evolutionary mechanisms, possibly together, confine the chromosome lengths around a species-specific average chromosome length.