Last week's molecules (right) [Monday's Molecule #237] were α-D-glucopyranosyl-(1➝4)-β-D-glucopyranose, the β anomer of maltose and α-D-glucopyranosyl-(1➝6)-α-D-glucopyranose, the β anomer of isomaltose. The winner is Dean Bruce. A surprising number of people got it right.
This week's molecules (below) are related. They are cytoplasmic (PDB 2P8U left) and mitochondrial (PDB 2WYA right) versions of very important enzymes. The human versions are shown. Name the enzymes and the products bound in the active sites (complete common name of the product). Mutations in one of the genes coding for one of these enzymes cause a rare genetic disease. Which one? Why are there no known diseases associated with genetic defects in the gene for the other version of the enzyme?
Email your answer to me at: Monday's Molecule #238. The first one with the correct answer wins. I will only post the names of winners 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.)
I'm in San Diego (California, USA) attending Experimental Biology 2014 (EB2014). This is a large meeting of several differnent societies. The one I belong to is ASMBM (American Society for Biochemisty & Molecular Biology).
I'm mostly interested in the sessions on teaching. The two I went to yesterday were on "Measuring Success in Undergraduate Education" and "Mentoring and Networking: Preparing for the Future."
There are far too many science talks. It's a bit overwhelming. I tend to focus on the plenary sessions where you can get an overview of a subject. This is where I'm most likely to find new material for my textbook. (No luck so far.)
All the cool people are here. 
Here's Voet & Voet (Don Voet and Judy Voet). I also met John Tansey and several of the other authors on the paper covering ASMBM Core Concepts [see ASBMB Core Concepts in Biochemistry and Molecular Biology: Molecular Structure and Function ].
We've had some interesting discussions. I don't think I've convinced them, yet.
Sometimes you just want to throw up your hands and say something very rude. This is one of those times.
Salvador Cordova is trying to explain non-Darwinian evolution to his friends over on Uncommon Descent [Cost of maintenance and construction of design, neutral theory supports ID and/or creation].
Here's the punchline ....
But if most evolution is non-Darwinian, maintenance much less construction of design cannot be explained by Darwinism, then the case for ID is strengthened.
Now if most evolution had been non-Darwinian, one would rightly argue it would have been a random walk, and thus not much better than a tornado going trough a junkyard. Creationist have seized on this and said, "well we’re not a junkyards, therefore some non-random process must have created designs in nature, hence we are designed". In contrast, Larry Moran and friends have said "evolution is a random walk and we are obviously junkyards and you’re an IDiot if you think biological organisms are mostly functional."
It's very, very, difficult for me to believe that Cordova isn't lying through his teeth. He can't be that stupid, can he?
The faculty at most Canadian universities are unionized. Faculty unions are important for negotiating fair salaries and benefits but they play a much more important role in defending academic freedom and protecting faculty from administrators who don't understand what a university should be about. I served for many years on the Grievance Committee and I can assure you that conflict between faculty members and administrators is common. In 99% of cases, the issues are resolved by negotiations between the union and the administration.
We don't have a union at the University of Toronto. Instead, we have an "Association" that functions a lot like a union without the right to strike. Right now the University of Toronto Faculty Association (UTFA)is negotiating with the university to set up ways for faculty to play a more direct role in governance issues. Those negotiations have nothing to do with certification (unionization).
I suppose there's another option. University faculty members could abandon collective bargaining and rely entirely on the goodwill of administrators, much like the situation in the business world where you can be fired if the boss doesn't like you. I suppose it's possible that academic freedom could be protected entirely by the administration and individual faculty members could fend for themselves if administrators ever abused their authority.
That's apparently what some professors in the Rotman School of Management want. They wrote letters to the President of the University protesting an imaginary move toward certification. I assume they misunderstood what the University of Toronto Faculty Association was doing because they don't read the newsletters that all us received.
Here's one of the letters from Roger Martin, Premier’s Chair in Competitiveness and Productivity in the Rotman School of Management. It illustrates quite nicely why schools of management and business don't belong on university campuses.
Dear President Gertler:
I am writing to express in the strongest possible terms how outraged I am by UTFA’s decision to attempt certification. UTFA does not represent anything related to me, nor, I suspect, does it represent the faculty of the Rotman School.
The notion of unionization of employees who make six figure salaries and have job security and protection of the sort enjoyed by professors is ridiculous on its face. It is really an insult to all real laborers who fought for the right to unionize and collectively bargain. Those workers coped with subsistence wages, unsafe and inhumane work environments, and absolutely zero job security. They didn’t have intellectually rewarding jobs in completely safe environments with lifetime job security. Collective bargaining was put in place to protect basic human rights, not to enable highly paid employees to argue for richer dental plans.
It is simply outrageous that that the ideologues who purport to represent us even raise the notion. They should be embarrassed. Sure they can say that it happens at other Universities in Canada. But when ever was that robust logic for doing something incredibly stupid and destructive?
We simply can’t let University of Toronto be ruled and ruined by ideologues. This is a fight for the future of a great institution. UTFA, when not run by ideologues, works perfectly well and creates a positive dialogue with university administration and a pleasant work environment for the faculty.
My fond hope is that this gambit is defeated by the weight of faculty members across the University. Failing that, I believe that my colleagues at the Rotman School will disassociate themselves from the bargaining unit and refuse to be represented by a completely foreign force. But in the end, if that can’t happen, it will be a sad day for me. I can’t insult every brave union activist in history who fought for human rights for workers by accepting becoming a member of one of the cushiest unions on the planet. That is not the way to live a principled life.
Sincerely,
Roger Martin
Premier’s Chair in Competitiveness and Productivity
Rotman School of Management
University of Toronto
In case some of you aren't familiar with unions, let me explain what would have to happen if UTFA ever wanted to certify. There would have to be a vote and a majority of faculty members would have to vote in favor of forming a union. That vote would be called by a group of faculty members and there's absolutely nothing that the President of the University of Toronto could do to stop it. It falls under labor laws of the province.
The current President knows this and I'm certain that he would have no objection to a certification drive if there ever was one. Apparently there are several professors in the Rotman School of Management who think that the President of the University could put a stop to certification. They must think the President functions like the CEO of a big corporation. (But even a corporate boss couldn't stop certification, so I don't know what they were thinking. Maybe they don't think.)
The one good thing about the letter from Roger Martin is the suggestion that the faculty at the Rotman School of Management might want to dissociate themselves from the university if the faculty ever forms a union. That might be a good reason for certification. If we play our cards right, the entire school of management might leave the university.
Last week's molecules (above) [Monday's Molecule #236] were the stereoisomers of L-threonine (D-threonine, L-allotheronine, and D-allothreonine). Nobody got the right answer so there was no winner last week. I guess that one was too hard.
It's not going to get any easier. This week's molecules (right) are related. You need to give the common names of each one and the complete IUPAC names. You'll have to be very careful in identifying and naming each one of the stereoisomers.
Email your answer to me at: Monday's Molecule #237. The first one with the correct answer wins. I will only post the names of winners 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.)
A few Intelligent Design Creationists are beginning to learn about evolution. A few days ago, I speculated about what would happen if they really did start to understand modern evolutionary theory and the massive amount of data that supports the basic facts of evolution [What would happen if Intelligent Design Creationists understood evolution?].
Vincent Torley has responded. He illustrates the problems they will face and reveals some of the rationalizations that they might use to avoid the most severe symptoms of cognitive dissonance [see Professor Larry Moran poses five questions for the ID movement].
Let's take a look at what has to say. Remember that Vincent Torley doesn't speak for all Intelligent Design Creationists but he does have posting privileges on Uncommon Descent and he is frequently praised by some of the ID leaders who post there. I think we can assume that his views are typical.
Here's his response to each of the five questions.
I stumbled across an article in Science & Education that caught my eye. The authors discuss the way genetics is taught in introductory university courses (McElhinny et al. 2014). They quote several sources that define the core concepts of genetics that students must learn.
Here's the list ...
- DNA is the universal information molecule in living organisms, encoding genes and allowing for genetic variation within and genetic continuity between generations (DNA);
- Mendelian patterns of inheritance are directly related to the mechanisms of meiosis (MENDELIAN);
- Traits result from the expression of one or more genes working alone or together, with the environment, often in unpredictable ways (GENE EXPRESSION);
- The activities of genes and the environment regulate all developmental processes (GENES + ENVIRONMENT);
- Genetic variation underlies variation in traits, which is the basis for the differential survival and reproduction that allow populations to evolve (VARIATION); and
- The ability to analyze and manipulate genetic information raises a variety of complex issues for individuals and society (GENES + SOCIETY).
These six concepts for genetic literacy will hereafter be referred to as the core genetics concepts.
This is a strange list. Let me explain why.
- The structure of DNA and how it is expressed should be covered in other mandatory courses, including introductory biology and biochemistry. You should not have to spend any time at all on these topics in a genetics course. (P.S. DNA does not "encode genes.") You may want to spend some time on the biochemistry of recombination if it's not covered elsewhere. Students should understand Holliday junctions and how they are resolved.
- Mendelian genetics is important. Students should learn and understand the three laws he discovered. They should also learn about meiosis and sex. However, it's important for students to understand that simple transmission genetics is not limited to diploid eukaryotes. Bacteria also do genetics.
- Traits (phenotype) are due to information in DNA (not just genes) but most of those traits have very little to do with the external environment.
- Of course the activities of genes regulate development. They also regulate the citric acid cycle, photosynthesis, and protein synthesis. Surely you don't want undergraduates to think that development is the only thing that's important in genetics?
- It's important for students to understand that populations contain genetic variation. That means they have to learn about MUTATION and how it happens. They also have to learn why there's so much variation in populations—one of the most important discoveries in genetics in the last century. The answer is Neutral Theory and random genetic drift. No genetics course should leave out this important concept, especially because so few students will have never heard of it before enrolling in the course.
- Discussions about cloning, GM foods, and personal genomes are interesting but, unfortunately, there are very few scientists who can handle those issues in a genetics course. The important core concept is to get the science right and make sure students understand that getting the science right is absolutely essential whenever you discuss controversial issues.
- POPULATION GENETICS is an essential core concept in an introductory genetics course. You can't teach students about the genetics of EVOLUTION without it.
The authors discovered that only the first three "core concepts" were taught in every genetics course. Variation and mutation were taught in only 88% of the courses they surveyed. Only 63% covered GENES + ENVIRONMENT and only 9% covered GENES + SOCIETY.
McElhinn et al. (2014) discuss one possible change in the curriculum. It's a suggestion originally made by Dougherty (2009) and echoed by Redfield (2012). The idea is to "invert" genetics courses by beginning with coverage of poplations, variation, and complex traits. I strongly disagree with Rosie Redfield's proposal [see Questions for Genetics Students] but what surprises me in the McElhinny et al (2014) paper is that they can seriously list those core concepts without mentioning mutation and population genetics.
McElhinny, T.L., Dougherty, M.J., Bowling, B.V., and Libarkin, J.C. (2014) The Status of Genetics Curriculum in Higher Education in the United States: Goals and Assessment. Science and Education 23:445-464.
[doi: 10.1007/s11191-012-9566-1]
Redfield, R. J. (2012) "Why do we have to learn this stuff?’’—A new genetics for 21st century students. PLoS Biology, 10, e1001356 [doi: 10.1371/journal.pbio.1001356]
Branko Kozulic has asked me to post some additional comments. I'm happy to do so since it reflects a sincere attempt to learn about evolution and come to grips with the concepts of neutral alleles and random genetic drift. We should encourage the creationists to continue this effort whenever possible.
As usual, my policy is not to comment on posts from guests, especially those that disagree with my views. So here's Branko Kozulic's latest take on the "evidence" as he see it.
I thank Professor Moran for posting my text.
This reply to the comments has grown in size much more than initially anticipated. At the outset, to prevent misunderstandings, I declare my complete ignorance of paleontology and, in general, that my ignorance is by far larger than my knowledge. And I am prepared to repeat this as many times as the readers are willing to read it.
From this discussion up to date, it seems that we do not have a simple model that could show the fixation of 22,000,000 mutations. And that no simple model will work becomes evident, for example, with just a glance at the Beerli & Felsenstein paper.
The referring of our colleague McBride to the Li & Durbin paper provides an opportunity to touch upon two other topics. In addition to the Li & Durbin article, I have carefully read also the paper by Gronau et al., dealing with the same topic. Both research groups started with the data derived from the sequenced genomes of several humans (7 and 6, respectively) from various sub-populations, with the goal of illuminating past fluctuations of the effective population size. Both groups arrived at similar results: thus the first paper reports for the Yoruba population the Ne of 15,313 ± 559, while the second paper gives the range of 7,500 to 10,500. Given this congruence of the results and the quality of the journals in which the results are published, I have no doubts about correctness of the results: I trust in internal consistency of these results. But they depend on certain starting assumptions, like all other results that are an outcome of scientific models. Now it´s time to look closer at the starting assumptions of these models because there is an external inconsistency – with another set of experimental data – as will become apparent in view of other three papers.
Figure 1 of Nielsen et al., paper shows multiple (up to 21) synonymous and non-synonymous substitutions in thousands of chimp proteins compared to the related human proteins. In the second paper Behe & Snoke conclude that in order to generate a new function that requires mutations of two amino acids, like forming a disulfide bridge, 108 generations are needed with a population size of at least 109. In the third paper, Lynch countered that much smaller populations could reach this goal in less time. Now, if we take the human population size from the above two studies (Ne about 104) for the population size in Figure 3 of the Lynch article, we can see that it would take 108 generations for the arrival of a new function, even if the two changed amino acid were any 2 of 50 (with a high s = 0.01). For humans, 108 generations mean 2 Billion years: an impossibly long period. Needless to say, a new function requiring 3, 4 … up to 21 amino acid changes would take much longer than 108 generations. And yet there about 3,000 proteins with 3 amino acid substitutions, over 1,000 proteins with 5 substitutions, etc. A contradiction is thus evident between the experimental data on the one side and the Lynch model plus Li & Durbin and Gronau et al., modeled results on the other, by a wide margin. Therefore, either the starting assumptions of the Lynch model, or of the human population size models, or of both, are false.
Furthermore, we should not lose sight of singletons/orphans found in all sequenced genomes. Population genetics – which deals with changes of allele frequencies in populations – necessarily will remain “agnostic” in relation to the singletons: they are, simply put, beyond its horizon.
Some of the comments referred to religious implications. I deny the existence of direct contact between scientific conclusions and religion. In my view, each particular scientific conclusions must pass through the filter of philosophy and exit at the other side as part of a general statement (universal); then universals are incorporated into a philosophical system, and that philosophical system may or may not be in accordance with philosophy (or theology) of a religion. The only level at which the implications of scientific conclusions can be meaningfully discussed is the philosophical level, in my opinion.
Allow me to conclude with additional philosophical thoughts. Science is no democracy, but a dictatorship. A dictatorship of experimental data: and only of experimental data. Can a scientist ignore the experimental data that contradict his favorite theory without betraying his vocation of scientist? I do not think so.
Moreover, I do not expect other scientists to provide answers to all my questions; nor can I answer all their questions: this is the normal state of affairs.
I wish to extend my thanks to all participants, especially Professor Felsenstein, for their courtesy shown during this discussion.
Beerli, P. and Felsenstein, J. (2001) Maximum likelihood estimation of a migration matrix and effective population sizes in n subpopulations by using a coalescent approach. Proc. Natl, Acad. Sci. (USA) 98:4563–4568. [doi:10.1073/pnas.081068098]
Behe, M.J. and Snoke, D.W. (2009) Simulating evolution by gene duplication of protein features that require multiple amino acid residues. Protein Science 13:2651–2664. [doi: 10.1110/ps.04802904]
Gronau, I., Hubisz, M.J., Gulko, B., Danko, C.G., and Siepel, A. (2011) Bayesian inference of ancient human demography from individual genome sequences. Nature Genetics 43:1031–1034. [doi: 10.1038/ng.937]
Li, H. and Durbin, R. (2011) Inference of human population history from individual whole-genome sequences. Nature 475:493–496. [doi: 10.1038/nature10231]
Lynch, M. (2009) Simple evolutionary pathways to complex proteins. Protein Science 14:2217–2225. [doi: 10.1110/ps.041171805]
Nielsen, R., Bustamante, C., Clark, A.G., Glanowski, S., Sackton, T.B., Hubisz, M.J., Fledel-Alon, A., Tanenbaum, D.M., Civello, D., White, T.J., Sninsky, J.J., Adams, M.D., and Cargill, M. (2005) A Scan for Positively Selected Genes in the Genomes of Humans and Chimpanzees. PLoS Biology doi: 10.1371/journal.pbio.0030170
Branko Kozulic has asked me to post his reply to Branko Kozulic has questions about fixation. My policy is to post letters like this without comment. We can discuss it in the comments.
I think it's an excellent example of the difficulties that many creationists will face when they try to come to grips with modern evolutionary biology.
Here's what he wants to say ...
Since Professor Moran has kindly addressed the questions I have raised, I feel obliged to respond here. But I must add that my response will be restricted to one topic only, and therefore this reply should not be construed to have the same purpose as the earlier discussion.
I find only a few minor contentious issues in Professor Moran´s post, so I prefer not to bother the readers with details about them. In my opinion, it is important that we have started to look at the core issue – the average fixation of about 100 mutations per generation, or 22,000,000 in 5,000,000 years, according to the genetic drift model - in terms of close to real-life conditions. Now we see that the simple genetic drift model needs extension, to include population splitting and recombining that leads to the postponement of fixation (I thank Professor Felsenstein for improving the clarity of this point). Furthermore, we see that in expanding populations the fixation rate is lower than the average. Thus, in today´s human population, the fixation rate per generation is close to zero. In order to compensate for the lower than the average fixation rates in some generations, it is necessary to postulate higher than the average fixation rates in other generations, if one wishes to account for the 22,000,000 fixed mutations in 5,000,000 years.
Let us consider the most dramatic case, mentioned in the comments, leading to the maximal fixation rate: the shrinking of a whole population to just a single couple, 2Ne = 2. Today we know that two unrelated human individuals differ in 1 nucleotide per about 1,000 nucleotides, so that each one of us carries about 3,000,000 SNPs. This is the maximal number (actually the maximal number is smaller because a fraction of SNPs is always in the heterozygous state) that can be fixed in this dramatic case. An interesting thing comes out to light now: the average of 100 fixed mutations per generation may result from the values that span a range of over six orders of magnitude, from less than 1, to over 1,000,000.
This raises the question of the meaning of the term “genetic drift model”. Can we maintain to be talking about the genetic drift model if the essential postulate of that model – mutation rate equals fixation rate – does not hold, because while the mutation rate changes little, the fixation rate can vary over six orders of magnitude? I think not. Drastic scenarios, known as “bottlenecks”, do not belong to the genetic drift model, in my opinion.
Now the important question is this: During the 5,000,000 years, what is the number of mutations that would have been “delayed to fix” because of the expansion of the human population, and/or due to the splitting-recombining, so that we must postulate dramatic events (“bottlenecks”) to account for their fixation? In other words, how many mutations were fixed in “bottlenecks” and how many by the ordinary course of genetic drift, in percentage? I doubt anyone can provide a verifiable answer (I kindly ask Professor Felsenstein to correct me if I am wrong). If for a “bottleneck” we take 2Ne significantly larger than 2, then many more “bottlenecks” need to be postulated in order to account for the same number of “delayed to fix” mutations. Is it possible to account for all the fixed synonymous mutations found in the human and chimp genomes by invoking fewer than two “bottlenecks” with 2Ne = 2? So that only 6 Million mutations are fixed in the “bottlenecks”, while 16 Million are fixed by genetic drift? I do not know.
And here is an additional complication. According to Wikipedia (since Professor Moran has relied on that source in his post, I follow suit):
Early humans (before Homo sapiens)
Early members of the Homo genus, i.e. Homo ergaster, Homo erectus and Homo heidelbergensis, migrated from Africa during the Early Pleistocene, possibly as a result of the operation of the Saharan pump, around 1.9 million years ago, and dispersed throughout most of the Old World, reaching as far as Southeast Asia. The date of original dispersal beyond Africa virtually coincides with the appearance of Homo ergaster in the fossil record, and the associated first emergence of full bipedalism, and about half a million years after the appearance of the Homo genus itself and the first stone tools of the Oldowan industry. Key sites for this early migration out of Africa are Riwat in Pakistan (1.9 Mya), Ubeidiya in the Levant (1.5 Mya) and Dmanisi in the Caucasus (1.7 Mya).
If correct, this information means that the time available for fixation of 22,000,000 mutations is reduced by about 2 Million years - to just about 3 Million years - because after migrating out of Africa different human sub-populations fixed different neutral mutations, due to the stochastic nature of the process. All specific human-chimp genetic differences (= all humans have them, no chimp has them, or vice versa) must have been fixed before the out of Africa migration. Is it possible to construct a genetic drift model (without “bottlenecks, with reasonable numbers) able to account for all the fixations, now within 3 Million years? I doubt it, but am willing to review a model that could dispel my doubts.
Let´s suppose that there are indeed 22 Million fixed synonymous mutations between the two genomes. I have no principal problem with that, or any other, experimentally established number. Whatever the exact number may turn out to be, scientists will continue looking for a model that fits the data best. In my opinion, no model should be rejected a priori. In order to contribute more constructively to this discussion, I ask: Why not test a model that uses 2Ne = 2 for the starting human population? With this model, for example, in the first generation 15 Million synonymous mutations might be fixed. Therefore, this model does not require multiple “bottlenecks” (perhaps just one) to account for a large fraction of the fixed mutations; while a smaller fraction - the 7 Million remaining mutations – could then be fixed in many subsequent generations in an expanding and splitting-recombining human population according to the population genetics theory.
One could argue that the starting Ne = 2 model is preferable in view of the principle known as Occham´s razor. But I would be the first one to disagree with such argumentation. Only in view of other experimental data found in the sequenced genomes one should decide which model is the preferred one; if the genome sequence data contradict one of any two models, the bad model should be rejected; and if the data contradict both, both models should be rejected.
I hope the above makes clear my thinking on this topic.
This one is from five years ago, reposted today at eggs2.
There's an interesting phenomenon taking place over on one of the main Intelligent Design Creationist websites. It started when a philosphopher, Vincent Torley, tried to understand how the sequences differences between chimpanzees and humans could be explained by evolution. In the beginning, he was skeptical of the explanation I offered and he was supported by a biochemist creationist named Branko Kozulic. Kozilic assured him that his skpeticism was justified and the population geneticists were wrong.
Then an amazing thing happened. Salvador Cordova, another well-known creationist, posted a comment on one of Torley's blog posts. You can see it as comment #39 on Branko Kozulic responds to Professor Moran. Cordova was responding to comments posted by Nick Matzke and "WD400" on that same post. Here's what Sal Cordova said,
Branko Kozulic is trying to understand how so many neutral alleles could be fixed in the human and chimpanzee populations (species) over the past five million years. He's not happy that Vincent Torley conceded the point that it was possible.
There are two relevant posts on Uncommon Descent: Branko Kozulic Responds and Branko Kozulic responds to Professor Moran, Part II.
I'll respond to the second one since it is more specific. He begins with ...
The idea of 100 mutations being fixed in the human population in each generation over a period of 185,000 generations, or 5,000,000 years, has always appeared intuitively unrealistic to me, possibly because I am primarily a practical scientist.
Many things in science seem counter-intuitive. That's why you have to make an effort to understand the science. In this case, you've been arguing against evolution for many years so you've had plenty of opportunity to get beyond intuition.
Vincent Torley was initially very skeptical when I described the differences between human and chimpanzee genomes and explained that those differences could be accounted for by evolution. He didn't want to believe that was true because it didn't fit into his views of how humans came to be.
After resisting for a week or so, he finally came to the realization that what the scientists are saying is correct [When I’m wrong].
Professor Moran and I disagree on many things, and I’m sure we’ll have many lively exchanges in the future, but it would be downright churlish of me not to acknowledge that my attempts to show that the neutral theory could not account for 22.4 million mutations arising in the human lineage over the last five million years have failed. I also wish to state that I had no intention of giving any offense to Professor Moran in our exchange of views, and that I have always striven to remain as polite as possible, while publicly disagreeing with him. The next time I’m dining out, I shall order a glass of red wine and silently toast him.
Thank-you Vincent Torley. I greatly respect you for taking the time to understand evolution and to listen to the explanations of evolutionary biologists.
I think you can see how your initial biases affected your ability to understand evolution. That's why you tried so hard to prove that population genetics was wrong when you didn't understand it and had only heard of the explanation for the first time a few days earlier.
Now Torley wants to address a different point. He wants to show us that creationists are more open-minded and less biased than evolutionary biologists [A question of bias].
In today’s post, I’d like to explain why I believe that evolutionary biologists who regard evolution as an unguided process are more ideologically biased than people who believe that God made us – whether through a process of (a) direct creation or (b) guided evolution. The distinction between the latter two positions is totally irrelevant, from Professor Moran’s perspective ...
It's a long post. Torley describes seven different arguments in support of his position.
