Last week's molecule was N-acetylmuramic acid (MurNAc) one of the components of the polysaccharide in bacterial cell walls [Monday's Molecule #206]. The winner was Michael Florea. He should contact me by email to collect his winnings.
Today's (Tuesday's) molecule is a new addition to biochemistry textbooks because its structure was only solved a few years ago. There are plenty of hints in the figure. You have to identify the molecule AND each of the seven activities that are labelled. Bonus points for the PDB identification number and the species.
Email your answers to me at: Monday's Molecule #207. I'll hold off posting your answers for 24 hours. The first one with the correct answer wins. I will only post 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.)
It's Ray Comfort and he's going to destroy Richard Dawkins. Bet you can hardly wait to see this movie. PZ Myers is in it. Read what he has to say at: Lie harder, little man.
You can read Max Andrews' blog posting at: Junk DNA Isn’t Junk. Be careful, you might find it very difficult to see the connection between this philosophy student's view of biology and anything you might recognize as real science.
It goes without saying that Max Andrews gets the Central Dogma wrong—many scientists make the same mistake. But here's a taste of what else he gets wrong.
The argument from junk DNA suggests that a designer would be maximally efficient in his use of information. There appears to be some information that does not execute or have any meaningful coding. Darwinism takes this issue and uses it as the result of the prediction that there would be left over information not being used due to natural selection and random mutation. However, it doesn’t appear that all junk DNA is actually junk.
Genome organization is patterned to be maximally informative. The overlapping codes observed are known to be evolutionarily costly, because random mutations will likely have a deteriorating effect, not an instructing role So the complex specified information entailed by any genomic region is orders of magnitude higher than previously suspected by, say, Dembski. Any seemingly random aspect of chromosome sequence arrangement is not. A case in point involves endogenous retroviruses (ERV’s). This implies that the taxonomically-specific formatting, indexing, punctuation, etc., of genomes were precisely written. Morphogenetic information is not reducible to the genotype—though it is strongly dependent upon it. Therefore, changes in DNA do not equal changes in the information that structures the body plan.
I wonder who his supervisor is? Maybe Dan or I could be external reviewer on his Ph.D. oral?
Dan Graur is fed up with journalists who don't know the difference between the "genetic code" and the sequence of a genome. He's not alone. But, unlike the rest of us, Dan has a solution. It may be a little difficult to enforce ...
See: An Artistic Inspiration for Putting an End to the Misuse of the Term “Genetic Code”.
Quite a few people think that there's going to be a serious debate about junk DNA at the SMBE meeting in Chicago next week. One of the sessions has a provocative title, "WHERE DID 'JUNK' GO?", but if you look at actual session titles it doesn't look like there's going to be much of a debate.
It's true than the session organizer, Wojciech Makalowski, advertised the session as a dicussion about junk DNA ....
Nick Matzke is going to the SMBE (Society for Molecular Biology and Evolution) meeting in Chicago next week. He's created a T-shirt for supporters of junk DNA [KEEP CALM and ASK ABOUT ONIONS].
John Mattick is a Professor and research scientist at the Garvan Institute of Medical Research at the University of New South Wales (Australia). He received an award from the Human Genome Organization for ....
The Award Reviewing Committee commented that Professor Mattick’s “work on long non-coding RNA has dramatically changed our concept of 95% of our genome”, and that he has been a “true visionary in his field; he has demonstrated an extraordinary degree of perseverance and ingenuity in gradually proving his hypothesis over the course of 18 years.”
Theme
Better BiochemistryWhile I was collecting posts on biochemistry, I came across one that I wrote almost five years ago. It was about a new record for catalytic proficiency. As you know, enzymes speed up reactions that occur naturally and spontaneously. The difference between the spontaneous rate and the rate catalyzed by an enzyme is called the catalytic proficiency.
That old post [Enzyme Efficiency: The Best Enzyme] had a nice graphic showing the spontaneous rates of some reactions that take place quickly inside a cell.
Here it is ....
And here's how the information in that 2008 post got incorporated into the latest edition of my textbook.
This is a "Theme" post where I collect all previous posts on teaching biochemistry and molecular biology.
March 22, 2015
On the handedness of DNA
March 5, 2015
Don't misuse the word "homology"
January 28, 2015
Vision and Change
January 28, 2015
Evidence-based teaching
January 15, 2015
The Nature of Science (NOS)
January 11, 2015
Why can't we teach properly?
January 8, 2015
Evolutionary biochemistry and the importance of random genetic drift
January 3, 2015
Thinking critically about the Central Dogma of Molecular Biology
December 9, 2014
On the meaning of pH optima for enzyme activity
December 9, 2014
On the specificity of enzymes
December 4, 2014
How to revolutionize education
October 20, 2014
How not to teach biochemistry
October 3, 2014
Metabolism first and the origin of life
September 11, 2014
The mystery of Maud Menten
August 8, 2014
Historical contingency and the evolution of the glucocorticoid receptor
July 28, 2014
Finding the "perfect" enzyme
Jun 2, 2014
"Flipping the classroom": what does that mean?
April 25, 2014
ASBMB Core Concepts in Biochemistry and Molecular Biology: Molecular Structure and Function
April 24, 2014
ASBMB Core Concepts in Biochemistry and Molecular Biology: Biological Information
March 21, 2014
ASBMB Core Concepts in Biochemistry and Molecular Biology: Homeostasis
March 5, 2014
The crystal structure of E. coli RNA polymearse σ70 holoenzyme
January 10, 2014
How not to teach biochemistry at memorize.com
December 9, 2013
Monday's Molecule #226
December 6, 2013
Die, selfish gene, die!
December 6, 2013
Do you understand this Nature paper on transcription factor binding in different mouse strains?
December 2, 2013
Monday's Molecule #225
November 12, 2013
David Evans Says, "Teach What the Vast Majority of Scientists Affirm as Settled Science"
November 5, 2013
Stop Using the Term "Noncoding DNA:" It Doesn't Mean What You Think It Means
October 30, 2013
Time to Re-Write the Textbooks! Nature Publishes a New Version of the Citric Acid Cycle
October 29, 2013
The Khan Academy and AAMC Teach Evolution in Preparation for the MCAT
October 29, 2013
The Khan Academy and AAMC Teach the Central Dogma of Molecular Biology in Preparation for the MCAT
October 29, 2013
The Khan Academy and the Association of American Medical Colleges (AAMC) Team Up to Teach Evolution and Biochemistry for the New MCAT
October 24, 2013
ASBMB Core Concepts in Biochemistry and Molecular Biology: Matter and Energy Transformation
October 15, 2013
ASBMB Core Concepts in Biochemistry and Molecular Biology: Evolution
October 14, 2013
Fundamental Concepts in Biochemistry and Molecular Biology
October 11, 2013
ASBMB Promotes Concept Driven Teaching Strategies in Biochemistry and Molecular Biology
Another curious aspect of the theory of evolution is that everybody thinks he understands it. I mean philosophers, social scientists, and so on. While in fact very few people understand it, actually, as it stands, even as it stood when Darwin expressed it, and even less as we now may be able to understand it in biology. Jacques Monod (1974)October 8, 2013
On the Importance of Defining Evolution
October 6, 2013
Teaching Biochemistry from an Intelligent Design Creationist Perspective
October 1, 2013
The Many Definitions of Evolution
September 30. 2013
The Problems With The Selfish Gene
September 18, 2013
Breaking News!!! Wikipedia Is Wrong! (about the Central Dogma)
September 13, 2013
Sean Carroll: 'What Is Science?"
September 13, 2013
Better Biochemistry: Teaching ATP Hydrolysis for the MCAT
September 12, 2013
Better Biochemistry: Teaching to the MCAT?
June 27, 2013
The Best Enzyme
April 16, 2013
Where Do Organisms Get Their Energy?
April 10, 2013
Spontaneous Degradation of DNA
March 18, 2013
Estimating the Human Mutation Rate: Biochemical Method
Last week's molecule was myricyl palmitate, the major component of beeswax [Monday's Molecule #205]. The winner was Bill Chaney. There was no undergraduate winner.
Today's molecule is a very common molecule shown in a somewhat unusual conformation. (It's the conformation of the molecule when it's bound to a certain enzyme.) Identify the molecule (common name only). Can you describe the conformation?
Email your answers to me at: Monday's Molecule #206. I'll hold off posting your answers for 24 hours. The first one with the correct answer wins. I will only post 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.)
Laurence Hurst is a Professor of Evolutionary Genetics in the Department of Biology and Biochemistry at The University of Bath (United Kingdom). He did his graduate studies under W.D. Hamilton at Oxford so it's safe to assume that he has adaptationist leanings.
Hurst wrote a comment in BMC Biology where he criticized the logic employed by those of us involved in the junk DNA debate [Open questions: A logic (or lack thereof) of genome organization]. Here's part of what Hurst says about logic ...
As a graduate student I was advised that if you don’t understand why an animal does what at first sight looks like behavior contrary to its best interests, then you should presume that it is you, not the animal, that is stupid. Look harder, the wisdom goes, and you will discover natural selection’s cunning logic.
That's bad advice, as Stephen Jay Gould and Richard Lewontin pointed out 35 years ago [The Spandrels of San Marco and the Panglossian Paradigm: A Critique of the Adaptationist Programme]. But, like many adaptationists, Hurst is willing to concede that this kind of reasoning may not apply at the molecular level.
While this may be good advice to those studying organismic behavior or anatomy, when we approach genomic anatomy and behavior it will not do.
Indeed, typically when thinking about genomes people often make the opposite presumption. Intergenic DNA was dismissed as irrelevant junk and many transcripts are presumed to be just so much noise. Synonymous mutations have been assumed to be neutrally evolving and where in a genome a gene sits is considered to be largely irrelevant. But are these assumptions more witness to a lack of understanding rather than robust statements about how genomes function and evolve? You are, after all, alive reading this, testament to the fact that your genome is doing something right.
So then, what features of our and other genomes are functionally relevant and which just so much noise? More importantly, when selection does act, why is it acting?
Hurst seems to be assuming that we know nothing about most of the genome and he makes the erroneous assumption that junk DNA advocates dismiss all intergenic DNA as junk. These are the hallmarks of someone who is uniformed about the debate over junk DNA. There is strong positive evidence for junk and those arguments need to be addressed (e.g. genetic load, C-Value Paradox). There is also strong evidence for functional intergenic sequences (origins, centromeres. telomeres, SARs, regulatory regions, etc.) and that evidence is part of the debate. None of the advocates of junk DNA claim that all intergenic DNA is junk.
We know that half of our genome is composed of bits and pieces of defective transposons. That's not ignorance. Broken genes are ... broken genes. They don't work. They are junk. We know enough about genes to recognize the difference between active functional transposons and those that carry lethal mutations of are missing large pieces of their coding region. It's logical to conclude that about half of our genome is junk based on those facts alone.
We know enough about transcription to know that spurious transcription and production of junk RNA transcripts are an inevitable consequence of the basic biochemistry of DNA binding proteins. That's not ignorance.
We know enough about nearly neutral mutations and molecular evolution to know the the existence of an approximate molecular clock means that most synonymous mutations and amino acid substitutions are fixed by random genetic drift. That's not due to a lack of understanding. Hurst has published evidence that some of these seemingly neutral mutations affect function but he ignores the evidence that most behave as if they were neutral.
The fact that you are alive does, indeed, mean that your genome is doing something right. It's good enough for survival of our species. It does not mean that all of your genome is functional.
To his credit, Hurst recognizes that the ENCODE scientists were wrong and that the null hypothesis is NOT natural selection.
The challenge is difficult. Assuming that sites involved in interactions are all functional isn’t good enough. By this, the logic employed by ENCODE, following a collision between a car and a pedestrian, a car’s bonnet would be ascribed the 'function' of projecting a pedestrian many meters and the pedestrian would have the 'function' of deforming the car’s bonnet. Similarly, we expect, for example, accidental transcription factor-DNA binding to go on at some rate, so assuming that transcription equals function is not good enough. The null hypothesis after all is that most transcription is spurious and alternative transcripts are a consequence of error-prone splicing. Conversely, assuming unbound sequence, such as nucleosome-free regions, to be lacking in function can mislead, as they can be critical for the proper control of gene expression.
I get the feeling that Hurst is uncomfortable with the idea that most of our genome is junk [see Hacking the Genome] but he's at least on the right track when he recognizes that there's still a legitimate scientific debate.
Hat Tip: Dan Graur: Laurence Hurst’s Error: The Inability to Distinguish between a Stupid Animal, a Dead Animal, and the Elephant in the Room
