Attached is Larry Moran’s exit exam for biochemistry and molecular biology. Exit Exam for Biochemistry.
I probably will not get a lot of these right on the first try, but it is a good learning experience. When I don’t know the answer, I can look it up, so this is a good chance to review important concepts.
I will provide answers I think Professor Moran wants students to give, and then I’ll provide my own answers which I think he might dock points for if he were grading. I always try to give the answer the professor is expecting even if I disagree. It shows that I am trying to understanding of what he was trying to teach. It’s not a confession of belief on my part.
For example:
21.How much of your genome is functional?
Answer I think Larry is expecting:
10%, because of the limits mutational load imposes on a genome the size of a human’s and their reproductive excess. But even the 10% number is likely high since the Muller Limit of 1 mutation/person/generation might allow even less than 10% function for the human genome.
My answer:
don’t know, neither does anyone else
Smart Arse Answer:
10% despite the fact ENCODE says 80% because ENCODE are a bunch of “ignoramuses, crooks generating piles of excrement” according to Dr. Moran’s colleague Dan Graur.
Some questions stumped me like:
3.Why can’t you have a lipid monolayer?
Eh? Doesn’t a micelle “layer” count as having a mono layer? Guess not.
I guess the answer is the hypdrophobic tails of the amphipathic phospholipids will generally tend to attach to each other, therefore such lipids are more likely to spontaneously form and remain in the bilayer configuration. But a micelle monolayer associates the hydrophobic tails too, doesn’t it?
Another Question:
17.Why are the amino acids sequences of a typical enzyme different in mice and humans?
Answer I think Larry is expecting:
Enzymatic polymorphisms occur because in many cases differences in amino acids at certain locations (such as those outside the active site) do not require high specificity. Function can be sustained under a variety of different amino acids in certain positions, thus random mutations in the process of common descent with modification will generate polymorphisms in positions which do not affect enzymatic function.
My answer:
The polymorphisms can be due to different functional constraints such as those resulting from necessary DNA binding motifs and microRNA regulatory targets that result in non-synonymous amino acid differences, Also there are possible different functionally significant post-translationtional modifications that are amino acid specific which have not yet been detected due to the difficulty of actually measuring such modifications in all possible contexts.
Another question:
30.Why do eukaryotic genes have introns?
My textbook non-answer:
Prokaryotes have introns, but no spliceosomal introns like Eukaryotes, so I believe Dr. Moran is referring to spliceosomal introns. Honestly, I don’t recall I’ve ever gotten a good answer from evolutionists. I don’t think Lehninger even attempted an answer. Since I don’t have copy of Larry’s textbook, but only Lehninger’s, can I be excused until I can get a hold of Larry’s book? 🙂
My answer:
For multicellular eukaryotes, the introns allow more diversity in gene expression between cell types as they can act as parts of robotic arms in 3D space to position regulatory and transcriptional machinery onto genes. This can happen from introns in other gene in a cis or even trans chromosomal context. Because of histones, chromatin complexes that contain introns are also capable of information processing and storage allowing them to be manipulated according to their histone chemical state to do gene regulation in a 3D manner as shown here:
For unicellular eukaryotes, I don’t have a good answer at this time (and neither do I think anyone else does), except God wanted to make other KINDS of Rube Goldberg machines.
The role of introns that are transcribed or excised is still not well understood. Primate specific Alus are indicated to use introns to make circular dsRNAs that appear important in alternative splicing. Until high throughput methods emerge to sequence proteomes in large scale and detect alternative splices, post translational modifications, glyco conjugation, etc. the role of introns may not be evident to the extent they may effect these (especially alternative splicing).
Papers on the function of introns have been published that list even more roles for introns.
But here is the rest of the exam. I’ll put some answers out in the comment section. Some answers will have to wait until after I finish this semester’s biochemistry evening class at the NIH. 🙂 Anyone else can weigh in with their answers.
1.Where do non-photosynthetic chemoautotrophs get their energy?
2.What is a typical Gibbs free energy change for a metabolic reaction inside a cell?
3.Why can’t you have a lipid monolayer?
4.Why is DNA supercoiled?
5.Which pathway evolved first; glycolysis or glucoenogenesis?
6.Why is methionine an essential amino acid in humans but glutamate is not?
7.Can humans fix carbon dioxide?
8.What are the end products of photosynthesis?
9.How do you create a protonmotive force?
10.How do some species survive without a citric acid cycle?
11.Why is some DNA replication discontinuous?
12.Why does E. coli need so many molecules of RNA polymerase?
13.Why is the ribosome so big and complex?
14.Why are there six codons for arginine but only one for tryptophan?
15.Why is Levinthal’s paradox not a paradox?
16.Why does DNA rich in G/C denature at a higher temperature than A/T-rich DNA?
17.Why are the amino acids sequences of a typical enzyme different in mice and humans?
18.If protein folding is spontaneous then why do cells need chaperones?
19.Why do acids like acetic acid and formic acid have different pKas?
20.Why did you need to learn about the Michaelis-Menten equation?
21.How much of your genome is functional?
22.Why is ATP not an effective allosteric regulator of enzyme activity?
23.What is flux?
24.Why isn’t it correct to say that ATP is an energy-rich compound?
25.What was the point of learning about reduction potentials?
26.Why are transcription and translation separated in eukaryotic cells?
27.Why did it take so long to evolve an oxygen evolving complex in photosynthesis?
28.Why is fat better than sugar for storing energy?
29.Why do we need cholesterol?
30.Why do eukaryotic genes have introns?
31.What’s the point of homologous recombination?
32.How can bacteria survive without mitochondria?
No. They cannot fix carbon dioxide on a net basis because they are not capable of photosynthesis or other chemical pathways that can fix carbon dioxide.
Cholesterols are part of the reactants to create various hormones.
Also cholesterols provide structural support for systems such as lipid rafts and other parts of lipid membranes.
Fats have higher average energy density at 37 kJ/g whereas sugars have an average energy density of 17 kJ/g. Also fats, being hydrophobic can be stored in anhydrous environments whereas sugars bind to water and hence in the hydrated form have their energy density diluted. Thus fatty acids can hold six times the unit energy than sugars per unit mass when hydration is considered.
The reason for the difference is primarily
stcordova,
They can plant trees 🙂
32.How can bacteria survive without mitochondria?
That’s a trick question. Bacteria are mitochondria.
Mung,
Is Larry abusing young adults?
What are the end products of photosynthesis?
Professors giving biochemistry exams.
What was the point of learning about reduction potentials?
So i could impress good-looking women.
I’m just wondering what mark would one of Larry’s student if he quoted the ENCODE?
With the right tools and some duct tape, sure. 😎
😯
????
It may not be effective for some enzyme activity, but it is for others. What am I missing?
Sugar and water.
Specifically the general reaction is, with the end product on the right hand side of the equation:
6C02 + 6H20 -> C6H12O6 + 6O2
One strand (the lagging strand) must be grown in short segments in a direction opposite the moving replication fork. This is because the polymerase grows strands only in the direction of 5′-to-3′, so small Okazaki fragments are duplicated discontinuously so the polymerase can move in it’s natural direction (5′ to 3′)but opposite the direction of the replicaiton fork for short stretches that define the Okazaki fragments.
Delta-G is typically negative.
11. Why is some DNA replication discontinuous?
There are no discontinuities! Are you trying to give ammo to the cretinists?
3. Why can’t you have a lipid monolayer?
With evolution, all things are possible.
http://www.pnas.org/content/105/31/10803.abstract
1. Where do non-photosynthetic chemoautotrophs get their energy?
I love evolution. What the hell is a photosynthetic chemoautotroph?
http://www.biology-online.org/dictionary/Chemoautotroph
I’m guessing Larry had some stupid grad student who hadn’t even completed the course yet come up with at least some of these questions.
The answer I think Larry is expecting:
My answer:
This is fun Sal!
I wonder what a YEC Exit Exam looks like.
Inoraganic sources like Hydrogen or Hydrogen Sulfide, occasionally organic sources like methane.
I didn’t really know the specifics of this till I researched the question. I can see its relevance to the OOL question.
4. Why is DNA supercoiled?
The design reason or the “it just happened, that’s all” reason?
9. How do you create a protonmotive force?
The design reason or the “it just happened, that’s all” reason?
12. Why does E. coli need so many molecules of RNA polymerase?
The design reason or the “it just happened, that’s all” reason?
13. Why is the ribosome so big and complex?
The design reason or the “it just happened, that’s all” reason?
Why questions assume an underlying intelligibility. And the rather obvious implication is an underlying intelligence.
26. Why are transcription and translation separated in eukaryotic cells?
Because transcription and translation are separated in all cells.
What a stupid question.
Mung,
By separated he may mean inside vs outside the nucleus of eukaryotic cells. The nuclear pore complex can flag a mis coded RNA me thinks.
I’m just wondering what happened to all the defenders of science.
We watch a bunch of grown me(the attackers on science) make fools of themselves. Please continue.
Mung,
Right, why.
What does a why question mean in evolution? To most evolutionists the only answer to why questions is, well, it must have given a selection advantage.
To Larry Moran there is another option. Because it wasn’t enough of a selection disadvantage not to.
Mung,
I’m just wondering what the point is.
This is just an amusement park.
Don’t you consider yourself a defender of science Mung?
I love watching IDiots pretend they understand biochemistry.
I prefer watching Morons pretend they understand English.
I love watching evos cower when it comes to supporting the claims of evolutionism
If they understood it they’d advance it, even if inadvertently.
What I love the most is watching arrogant, deceitful, pretentious, ostentatious, ego driven quacks who present their own delusions as facts.
As one once said: “…It’s not a lie, if you believe it…”
I love the irony of reading you write this.
Unfortunately for you phoo, not a miracle worker
Is that the design reason?
Ah, the delicate art of the Gotcha.
Speaking of which, on micelles, if you added new phospholipid units to the ball one by one, at what point would it flip from being a ‘monolayer’ to being a bilayer? Conversely, how complete is the cross-sectional diagram of the bilayer?
Since you love watching us pretend, you can at least tell us if our pretend answers are right, like:
or
I want to see how well a creationist can pretend he understands evolution and biochemistry according to the gospel of Larry.
What’s your answer to this question?
I made up the following answer. I just pulled it out of the air from imitating the usual storyline of Darwinists. What’s wrong with my pretend answer?
Moved a comment to Guano. Calling other people names, no matter how cleverly you think you’re doing it, is against the rules.
stcordova,
More to the point, I think, what do you think is wrong with it? Your preferred answer contained an awful lot of appeal to undiscovered constraint – ‘can be due […] possible [ …] not yet been detected***’. Enzymatic differences can be observed at every taxonomic level – including within the same organism, due to misreads and contributions from both alleles in heterozygotes, so there is reason to suppose that some component of the mouse-human difference is due to that. You can’t rule out differential constraint as well, so a complete answer would allow for both.
*** … I think the OoL can be due to possible things that have not yet been detected too, if you find that kind of reasoning convincing!
Regarding micelles, apparently I wasn’t the only one who found this question troubling:
Over at Larry’s Blog, Bryan challenged Larry:
That’s actually what I thought at first when I saw the question, and when I saw Bryan’s response, I thought to myself, “friggin right!”
How does Larry respond:
How’s that for critical thinking on my part, bwahaha! 🙂
stcordova,
You missed my point in your rush to brag. Why are micelles monolayers? Would a micelle with too many subunits to be spherical still be a monolayer? It’s a simple question of topology.
You are playing by his rules no matter how much you complain.The more you break the rules ,the easier it is to dismiss your complaints.
The layer of lipids on the micelle mono-layered isn’t, we don’t have bilayered micelles do we? 🙄
In any case, the issue is moot now, Larry is effectively withdrawing the original question and replacing it with:
Regarding monolayers, someone at Larry’s blog also pointed out something related to this:
Yikes, Larry. Talk about confusing your poor students.
You are probably correct sir. But another case of asking for a design reason.
Can you imagine giving the stock evolutionist answer to all these questions and still getting a passing grade?
Regarding this question,
As in what reaction? Larry has something in mind, obviously, and I don’t know what answer he is fishing for.
Here is an example of ATP being an allosteric regulator of enzyme activity:
Help me Allan, help me. I’m stuck on this question.
You can google for yourself this phrase:
I get three hits, and guess where they pretty much all land?
stcordova,
You missed it again. Take a ‘monolayered’ micelle. Stick your thumb in it on one side, then mould it round until it forms a spherical cavity, with just a single pore (itself edged in phospholipid ‘heads’). What have you got? A bilayer. Where did the ‘second layer’ come from?
Point being, a bilayered membrane is just a deformed micelle.