Evolution of Horseshoe Crabs

The IDiots are at it again but this time they are aided and abetted by scientists who should know better. The subject is horseshoe crabs, famous as "living fossils" because species that look similar to the four living species were around millions of years ago.

The BBC (United Kingdom) is broadcasting a new television series called "Survivors"¹ staring this month. The first episode is Horseshoe crabs are one of nature’s great survivors. The show is based on a book by Richard Fortey of the Natural History Museum in London, England.

Here's a quotation from the BBC press release where Fortey attempts to explain why horseshoe crabs haven't evolved.

A strange evolution?

Evolution not only brings about ‘improvements’ in body shapes and design that help a species adapt better to its surroundings. It also allows some species to remain basically the same.

‘These creatures tell us that evolution does not move inevitably forwards towards new morphology and new designs,' comments Fortey.

'Evidence for evolution is also found in past designs that endure to the present day. As long as the right habitat endures, then so will some of the creatures that inhabited the distant past.

The Problem With Press Releases

 
Press releases are a problem. Ryan Gregory has found a doozy: Radical Theory Explains the Origin, Evolution, and Nature of Life, Challenges Conventional Wisdom.

You may be tempted to actually read the paper. Don't. First, read what PZ Myers has to say: The comparison to jabberwocky is inevitable.

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Paul Doty (1920 - 2011) and DNA Renaturation

Paul Doty was born in 1920. He died last month (Dec. 5, 2011) at his home in Cambridge, Massachusetts, USA [Paul Mead Doty (1920-2011)]. He was a Professor at Harvard for most of his career.

For many of us, Doty's major contribution to molecular biology was his study of DNA renaturation with his long-time post-doc and collaborator, Julius Marmur (1926 - 1996)¹, a graduate of McGill University in Montréal, Canada. The paper that most of us remember is Marmur and Doty 1962: "Thermal Renaturation of Deoxyribonucleic Acids." This was the first time that the renaturation of complex DNA had been studied in detail and the results have led to many of the common techniques in use today.

Where Is David Attenborough?

 
Jerry Coyne has a little quiz for you as you watch this music video about evolution [An Evolution Music Video]. You should visit his blog website and answer the questions. Sandwalk readers should be able to answer the most difficult question namely, "Figure out where Attenborough is walking at the beginning: it’s a very famous place."

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What's the Difference Between a Human and Chimpanzee?

The number of differences between the human and chimpanzee genomes is consistent with Neutral Theory and fixation by random genetic drift.

How Many Differences?

You can estimate the total number of single nucleotide differences by measuring the rate of hybridization of human and chimpanzee DNA in a technique developed by Dave Kohne and Roy Britten over forty years ago. This technique was applied to human and chimp DNA and the results indicated that the two genomes differed by about 1.5% (reviewed in Britton, 2002). That corresponds to 45 million bp in a genome of 3 billion bp.

This value of 1.5%, rounded up to 2%, gave rise to the widely quoted statement that humans and chimps are 98% identical. Britton (2002) challenged that number by pointing out that humans and chimp genomes differed by a large number of insertions and deletions (indels) that could not have been detected in hybridization studies. He claimed that there was an addition 3.4% of the genome that differed due to indels. That means the the real difference between humans and chimps is closer to 5% and we are only 95% identical!

Much of the difference is due to insertion and deletion of members of gene families. One study shows that the human genome has 689 genes not present in the chimp genome and chimps have 729 genes not present in humans [Mammalian Gene Families: Humans and Chimps Differ by 6%]. That's a total of 1,418 complete genes that are only found in one of the species.

At first glance this looks like 689 completely new genes have evolved in the human lineage since it diverged from our common ancestor with chimpanzees but looks can be deceiving. These genes are members of gene families and all that's happened is that 689 orthologous genes have either arisen by duplication in the human lineage or been lost by deletion in the chimp lineage or 689 new parologous genes have been "born" by gene duplication (or some combination).

Much better date is available today than in 2002 when Britten wrote his paper. We now know by direct comparison that there are at least 30 million single nucleotide differences between human and chimp genomes. There are about 90 million base pair differences as insertion and deletions (Margues-Bonet et al., 2009). The indels (insertions and deletions) may only represent 90,000 mutational events if the average length of an insertion/deletion is 1kb (1000 bp). In fact, more than 75% of indels are less than 5 bp (Britton 2002) so the actual number of mutational events is in the millions. Many of these are undoubtedly due to sequence errors. The latest studies indicate that humans and chimps differ by only 26,500 large indels (>80 bp) (Polavarapu et al., 2011). To a first approximation, the single nucleotide differences are a good measure of the total number of mutational events that have occurred in the two lineages. (underlined portion added on Jan. 25, 2012 - LAM)

Polymorphisms

It's worth noting that many of the differences between the human and chimp genomes are polymorphic within their respective populations. In other words, the variant alleles have not become fixed in the population. This affects the calculations of mutation rate since that calculation assumes that an allele has become fixed in the population by random genetic drift.

The polymorphisms include SNPs, of course, and that's the basis of many studies that look for specific haplotypes associated with disease. At least one of the variants at a given polymorphic locus in humans will be different from the nucleotide in the chimp reference genome. Deletions in the human and chimp genomes can also be polymorphic. Copy number variants (CNVs) in humans have been characterized in a number of studies (Campbell et al. 2011). In terms of total nucleotides, there is more variation in copy number than in single nucleotide polymorphisms (Alkan et al., 2011).

Are the Differences Neutral?

We would like to know if the differences between the human and chimp genomes are neutral alleles or if natural selection has played an important role in fixing these differences. Nobody doubts that many of the changes we see are adaptive in one or other of the lineages but can we recognize those important adaptive changes in a sea of possible neutral changes?

Several lines of evidence suggest that most of the changes are non-adaptive. First, since most (~90%) of the genome is junk, and most of the differences are located in junk DNA, it follows that most of the new alleles had no effect on function.

Second, if we look at the pattern of changes this is what we see for one of the human chromosomes.

The percent identity between humans and chimps fluctuates between 98% and 99% identity and the differences are pretty evenly scattered throughout chromosome 7. Remember, most of that DNA is junk.

Calculating the rate of evolution in terms of nucleotide substitutions seems to give a value so high that many of the mutations must be neutral ones.

Motoo Kimura (1968)The third line of evidence has to do with the mutation rate and fixation in the two lineages. The mutation rate in humans is about 130 mutations per generation based on our knowledge of the biochemistry of DNA replication [Mutation Rates]. A value that's consistent with recent direct measurements [Human Y Chromosome Mutation Rates] [Direct Measurement of Human Mutation Rate]. Michael Lynch (2010) bases his estimate of human mutation rates on a number of other studies. He comes up with a value of about 80 new mutations per generation.

In an evolving population the rate of fixation of neutral alleles is equal to the mutation rate [Random Genetic Drift and Population Size]. How many mutations would we expect in the human lineage since it diverged from a common ancestor with chimpanzees if all of the fixed alleles were neutral? The two species diverged about 5 million years ago. The average generation time in the human lineage is about ten years, so that means 500,000 generations. If the rate of mutation is about 100 new mutations per generation, then we would expect to see about 50 million new mutations in the human lineage. The actual number is about 22.5 million (half of 45 million). We're certainly in the right ballpark.

The actual mutation rate may be lower than we calculate.

We're certainly safe in concluding that the number of differences between humans and chimps is consistent with Neutral Theory and we should accept this as the null hypothesis.

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Alkan C, Coe BP, Eichler EE. (2011) Genome structural variation discovery and genotyping. Nat Rev Genet. 12:363-376. [PubMed]

Britton, R.J. (2002) Divergence between samples of chimpanzee and human DNA sequences if 5%, counting indels. Proc. Natl. Acad. Sci. (USA) 99:13633-13636.

Campbell, C.D., Sampas, N., Tsalenko, A., Sudmant, P.H., Kidd, J.M., Malig, M., Vu, T.H., Vives, L., Tsang, P., Bruhn, L., and Eichler, E.E. (2011) Population-genetic properties of differentiated human copy-number polymorphisms. Am J Hum Genet. 88:317-32. [PubMed]

Marques-Bonet, T., Ryder, O.A., and Eichler, E.E. (2009) Sequencing primate genomes: what have we learned? Annu. Rev. Genomics Hum. Genet. 10:355-386. [PubMed]

Lynch, M. (2010) Rate, molecular spectrum, and consequences of human mutation. Proc. Natl. Acad. Sci. (USA) 107:961-968. [PubMed]

Polavarapu, N., Arora, G., Mittal, V.K., McDonald, J.F. (2011) Characterization and potential functional significance of human-chimpanzee large INDEL variation. Mob. DNA 2:13. [PubMed] [doi:10.1186/1759-8753-2-13]

Monday's Molecule #156

 

This is one of the most important molecules on Earth. Without it we wouldn't be around and neither would most species. The revised structure is shown here. The one shown in the textbooks is wrong and this includes my own recently published edition of Principles of Biochemistry. Oops!

You need to identify the molecule, including the part with the white carbon atoms. You also need to specify how this molecule differs from the one shown in most textbooks.

Post your answer in the comments. I'll hold off releasing any comments for 24 hours. The first one with the correct answer wins. I will only post correct answers to avoid embarrassment.

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 comment.)

Some past winners are from distant lands so their chances of taking up my offer of a free lunch are slim. (That's why I can afford to do this!)

In order to win you must post your correct name. Anonymous and pseudoanonymous commenters can't win the free lunch.

Winners will have to contact me by email to arrange a lunch date.

UPDATE: The molecule is the iron-sulfur-molydenum cluster with bound homocitrate. The central atom was thought to be nitrogen but recent work has shown that it is most likely carbon. The cluster is in the active site of bacterial nitrogenase, an enzyme responsible for fixing atmospheric nitrogen and converting it to ammonia. This is a key part of the nitrogen cycle. The winner is David J. Schuller. I don't know if he will come for lunch.

Winners
Nov. 2009: Jason Oakley, Alex Ling
Oct. 17: Bill Chaney, Roger Fan
Oct. 24: DK
Oct. 31: Joseph C. Somody
Nov. 7: Jason Oakley
Nov. 15: Thomas Ferraro, Vipulan Vigneswaran
Nov. 21: Vipulan Vigneswaran (honorary mention to Raul A. Félix de Sousa)
Nov. 28: Philip Rodger
Dec. 5: 凌嘉誠 (Alex Ling)
Dec. 12: Bill Chaney
Dec. 19: Joseph C. Somody
Jan. 9: Dima Klenchin

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The Modern Molecular Clock

The first molecular phylogenetic trees were constructed from the amino acid sequences of small proteins. One of those proteins was cytochrome c and it turned out to be very useful because homologues could be found in all species, including bacteria.

The original trees were published by Emanual Margoliash but I'm showing a later version here from Fitch and Margoliash (1967). This is a very famous tree that's found in many textbooks. (The version shown here is from Mulligan (2008).)

From the very beginning, the authors of these molecular phylogenetic trees noted that the rate of change in each lineage was approximately constant. You can see that in the tree shown here. The number of changes in the lineage leading to yeast (Saccharomyces) is 17+10+2=31 from the common root. The number of changes in the lineage leading to insects is 31 or 28, depending on the species. The number leading to humans and monkeys is 32.

Margoliash on "Homology" (1969)

Emanuel Margoliash (1920 - 2008) is famous for his studies of the evolution of cytochrome c genes/proteins. His lab sequenced dozens of them and he published some of the first molecular phylogenetic tress back in the early 1960s.

I recently stumbled on a letter he published in Science back in 1969 (Margoliash, 1969). It's about how you define "homology." This is one of my pet peeves. I've been trying to teach people for years that homology refers to the fact that two genes share a common ancestor. It a conclusion based on evidence such as sequence similarity. For example, if two genes/proteins are more than 30% identical over their entire length then you can conclude that they are homologous—they descend from a common ancestor. The conclusion is based on evidence, such as 30% sequence identity. Don't confuse "similarity" and "homology" because they are two different things.¹

Homology is like being pregnant. Either you are or you aren't. You can't be 30% pregnant and you can't be 30% homologous.

I knew that the definition of homology had changed over the years but I didn't know that the dispute over its usage in molecular phylogeny started in the 1960s. Here's the Margoliash letter.

I regret the error in citation (the journal name was given as Nature, rather than Science), which crept in among the 462 references of the review (1) to which Winter, Walsh, and Neurath take exception (Letters, 27 Dec.). In that review, the term homologous was taken to imply, in parallel to universal biological usage, "that the genes coding for the polypeptide chains considered, in all the species carrying these proteins, had at one time a common ancestral gene," and we stated that when this concept is not intended "it would be best to use any of the numerous synonyms of 'similar' and 'similarity' and not appear to be prejudging the issue of evolutionary relations." The "pointed and specific criticism" followed, and was entirely contained in the sentence: "Other definitions may cause confusion and are unlikely to supplant well established biological usages." The "other definitions" referred to the article by Neurath, Walsh, and Winter (2), in which they state, "The term homology as applied to proteins refers to similarity in amino acid sequence," and later, that comparisons of protein structures "must be interpreted on a statistical basis lest we misinterpret random similarities."

On this last score there is no argument. Winter, Walsh, and Neurath will surely agree that in this field erroneous conclusions are likely to arise from the lack of an appropriate statistical distinction between random similarities and similarities of structure greater than can result from random phenomena. An excellent method of performing just such a distinction was published by Fitch (3), and although Neurath, Walsh, and Winter acknowledge it in their article (2), they do not use any acceptable statistical techniques in their comparisons of proteases. Thus, even by their own definition they fail to show "homology."

Homology, in any biological evolutionary context has a generally understood and well-defined meaning, namely the one we have adopted for use in protein primary structure comparisons. One cannot argue that such comparisons represent an area of knowledge separate from evolutionary biology, and that therefore one may use the same words for other meanings, since such protein studies obtain their interest largely in terms of evolutionary concepts and have their major impact in the taxonomic-evolutionary field. Winter, Walsh, and Neurath justify their novel definition of "homology" by maintaining that, without fossil remains, it is not possible to decide whether the structural genes corresponding to a set of present-day proteins are or are not ancestrally related. Apart from the inherent danger of assuming that a problem is insoluble, it may be pointed out that six pages after the definition of "homology," the paper (1) reviewed a statistical method for demonstrating just such ancestral homology. One requires enough primary structures to derive a "statistical phylogenetic tree," as has been possible in the case of cytochrome c (4). From such a tree a simple statistical calculation permits one to approximate the number of residues in a set of proteins that will remain invariant, because of biological necessity, no matter how many species are examined (5). If, in the comparison of any two proteins of this set, the number of identical residues is substantially in excess of the number that remain invariant in the entire set of proteins, then clearly this excess cannot result from functional convergence from different phylogenetic origins, a process yielding analogous structures, and, therefore, it can only be attributed to ancestral homology. In such a procedure, the assumption of the constancy of the genetic code has replaced the fossils of the morphological evolutionist.

Even if one does not accept the validity of such a demonstration, it is difficult to understand why there is an insistence on using the word "homology" for "similarities of protein primary structure greater than random." Any of the over 30 synonyms of "similarity" (6) or a variety of elegant neologisms would do, and prevent an insidious misunderstanding likely to arise in biological literature. Rather than take Alice in her confused trip in Wonderland as a model for logical scientific nomenclature, I prefer to follow the 17th-century poet reacting against a form of debasement of the language then prevalent, and "call a cat a cat" (7).

E. MARGOLIASH
Department of Molecular Biology,
Abbott Laboratories,
North Chicago, Illinois 60064
References

1. C. Nolan and E. Margoliash, Ann. Rev. Biochem. 37, 727 (1968).
2. H. Neurath, K. A. Walsh, W. P. Winter, Science 158, 1638 (1967).
3. W. M. Fitch, J. Mol. Biol. 16, 9 (1966).
4. W. M. Fitch and E. Margoliash, Science 155, 279 (1967).
5. W. M. Fitch and E. Margoliash, Biochem. Genet. 1, 65 (1967).
6. Roget's Thesaurus (St. Martin's Press, New York, 1965).
7. N. Boileau, Satires 1, line 52 (1660). "J'appelle un chat un chat, et Rolet un fripon."

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1. Very few people pay attention to me. I appear to be fighting for a lost cause.

Margoliash, E. (1969) Homology: A Definition. Science 163:127

Understanding Mutation Rates and Evolution

The recent article by physician Joseph A. Kuhn contains a lot of errors and misunderstandings [Physicians Can Be IDiots]. Today I want to focus on one paragraph.

The complexity of creating two sequential or simultaneous mutations that would confer improved survival has been studied in the malaria parasite when exposed to chloroquine. The actual incidence of two base-pair mutations leading to two changed amino acids leading to resistance has been shown to be 1 in 10²⁰ cases (42). To better understand this incidence, the likelihood that Homo sapiens would achieve any single mutation of the kind required for malaria to become resistant to chloroquine (a simple shift of two amino acids) would be 100 million times 10 million years (many times the age of the universe). This example has been used to further explain the difficulty in managing more than one mutation to achieve benefit.

The reference is to The Edge of Evolution by Michael Behe. His book was published in 2007 but I never got around to reviewing it thoroughly—partly because it's so difficult to explain where he goes wrong.¹ Here's my take on one part of the book: The Two Binding Sites Rule. This post covers "chloroquine-complexity clusters" (CCC).

Congratulations Vip!

 

Here's Vipulan Vigneswaran with his fabulous Biochemistry textbook that he won by contributing to Monday's Molecule [And the Winner Is ...]. Vip is studying Chemistry at the University of Toronto.

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Alain de Botton Tells Us the Good Things About Religion

 
Here's a TED talk by Alain de Botton. He claims to be an atheist but he's promoting Atheism 2.0. That's a version of atheism that incorporates all the good parts of religion like how they can brainwash children and con people out of lots of money. And pilgrimage. Let's not forget the value of pilgrimage and the importance of travel. (Think Canterbury Tales!)

There's a certain mysticism about TED talks that I deplore. In order to be a successful TED talker you need to be articulate and clever. You need to be engaging and just a little bit radical—though not too radical. That's just about all it takes to get an enthusiastic standing ovation from the people who comes to listen to these 18 talks. What you're actually saying doesn't really count for anything as this example plainly shows.

The mantra of TED talks is "Ideas Worth Spreading" but if you think about it there aren't very many important new ideas that can be explained in 18 minutes. On the other hand, if you want to spread ideas that your audience already agrees with then TED talks are just the thing for you.

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[Hat Tip: PZ Myers: Alain de Botton is right about one thing.]

James Shapiro Publishes on Evolution News & Views

James A. Shapiro, author of Evolution: a View from the 21st Century has been criticized for being an Intelligent Design Creationist, or at least a sympathizer. He denies it but his denials sound very much like someone who protests too much.

Shapiro has now been allowed to post an article on the main IDiot blog, Evolution News & Views [A Response to Ann Gauger's and Douglas Axe's Comments. I don't agree with his response but that's not the point. Do you know any respectable evolution supporter who would post on a creationist blog?

Can you imagine his University of Chicago Colleague, Jerry Coyne, posting an article on the flagship blog of the Discovery Institute?

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Physicians Can Be IDiots

 

Joseph A. Kuhn is a physician at the Baylor University Medical Center at Dallas. This is a Christian medical center associated with Baylor University in Waco, Texas. Joseph Kuhn published an article in a recent issue of Baylor University Medical Center Proceedings: Dissectring Darwinism.

Kuhn has an M.D. degree. He is not a scientist and he has no obvious expertise in biology and/or evolution. He is a Roman Catholic. He is definitely an Intelligent Design Creationist.

Let's look as what this IDiot has to say ...

The primary conflicts or anomalies with neo-Darwinian evolution lie in the failure of mutation and natural selection to account for the formation of DNA, the information of DNA, or the complexity of the human cell. In all fairness, many physicians, medical students, and college students have not been shown the weakness of Darwinian evolution. They haven’t been shown the failure of the Miller-Urey experiments to explain DNA, RNA, or protein formation; the paucity of fossil data; or the refutations of transitional species based on a growing biochemical understanding of complex systems and the limits of DNA mutation to account for the formation of new DNA, new chromosomes, and therefore new species.

In contrast, how is it possible that the majority of National Academy of Science members (who should know the above weaknesses) fully believe that random mutation and natural selection can explain the origin of DNA and the subsequent generation of a vast array of protein systems within complex cells? It is possible that the biologist, the paleontologist, and the anthropologist are each studying a small portion of the picture and do not have the education and training to see the full picture. More likely, their previous research relies on the established paradigm of Darwinian evolution to provide structure for their work. As the limitations of existing paradigms become apparent, adoption of a new paradigm typically requires at least a full generation, since existing practitioners and scientists often hold on to the old paradigm.

There's so much wrong here that I hardly know where to begin. First, biological evolution, whether it be the outmoded neo-Darwinian model or a more modern version, was never intended to explain the origin of life. We don't know how life originated but that has nothing to do with the truth and power of evolution as an explanatory mechanism.

Second, members of the National Academy of Science—and all other scientists in the USA and many other countries—are not stupid. The idea that they would all fail to see the truth about evolution because they "do not have the education and training to see the full picture" is silly beyond belief. The idea that they might be blind to the truth because they adhere to an incorrect Darwinian paradigm is ridiculous. The idea that a physician at a Christian university might be in a better position to recognize the truth about evolution is something that only a true IDiot could believe.

The standard IDiot talking point these days is that students and the general public are being misled because scientists won't teach all the problems and controversies concerning biological evolution. This is an attitude that completely ignores all the debate and discussion that has been taking place on the internet and in popular books, magazines, and journals over the past four decades. None of the problems and controversies have stood up to close analysis in spite of the fact they have been dogmatically defended by dozens of leading IDiots.

Of course Joseph Kuhn, the physician, knows nothing about this. That's why he writes ...

When the Texas State Board of Education voted to recognize the weaknesses of Darwinian evolution in explaining the origin of the species, it was a result of 3 full days of intense debate and scientific dispute. In 2011, when new textbooks were presented to the State Board of Education, 9 out of 10 failed to provide the mandated supplementary curricula, which would include both positive and negative aspects of evolution (44). Moreover, several of the textbooks continued to incorrectly promote the debunked Miller-Urey origin of life experiment, the long-discredited claims about nonfunctional appendix and tonsils, and the fraudulent embryo drawings from Ernst Haeckel. In essence, current biology students, aspiring medical students, and future scientists are not being taught the whole story. Rather, evidence suggests that they continue to receive incorrect and incomplete material that exaggerates the effect of random mutation and natural selection to account for DNA, the cell, or the transition from species to species.

The Texas State Board of Education guidelines do not propose teaching any other alternatives to Darwinian evolution. Rather, the students of tomorrow and teachers of today should appropriately recognize that there are weaknesses that have been pointed out by reasonable scientists. In this dissection of Darwinism, we have cut into the weaknesses of the fossil evidence for human evolution, the failure of the fossil data to demonstrate substantial transition species, and the awareness of the sudden formation of most species in a short window of time, with no significant subsequent variation. More importantly, this physician-perspective article emphasizes the extreme impossibility of the natural formation or self-formation of billions of nucleotides in a specific sequence, allowing for the coding of RNA and proteins in a complex cell with thousands of interrelated and irreducibly complex functions. The article also enlightens the reader regarding the conflicts and difficulty of using natural selection and mutation to explain the simultaneous or sequential changes in cellular DNA, involving entirely new strands of DNA and thousands of new proteins, which are necessary for the formation of new species.

It's hard to imagine what must be going on inside the head of someone who could write such drivel. Let's say that the Texas Board of Education succeeds in brainwashing students about the "weaknesses" of evolution. Is that going to change the minds of any expert who studies biological evolution for a living? Is that going to lead to a new generation of scientists who accept Intelligent Design Creationism? No, not even in Texas.

Only an IDiot could believe that forcing Intelligent Design Creationism down the throats of students in some parts of southern USA will eventually lead to a "paradigm shift" in thinking about evolution. Only an IDiot physician could believe that he knows more about evolution than the experts. In fairness, you've got to give the creationists some credit for convincing some, otherwise intelligent, people that 99.9% of all scientists are really, really stupid.

UPDATE:Jonathan Wells defends Joseph A. Kuhn, MD ["Shut up," Coyne Explained].

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[Hat Tip: Jerry Coyne in Creationist paper in a medical journal.]

Canadian Blog Awards: Science and Technology

 

Voting for The Canadian Blog Awards ends tomorrow so this is your last chance to pick the best of the best(?).

Most of you will be interested in the science blogs. The category is Best Science and Technology Blog. Here are the finalists ...

Sync.ca

Here at Sync, we strive to bring you the latest in news, reviews and opinions from the tech universe. It′s our way of helping to keep Canadians in sync with tech and gadgets that surround us in our daily lives. Never miss a beat: stay in Sync.

iPhoneinCanada.ca

iPhoneinCanada.ca was started in late 2007 in Vancouver, BC. The site was created to document using the first generation iPhone in Canada. The blog has evolved along with the iPhone and we are now the leading Canadian iPhone authority for news, reviews, tips, tricks and anything else iPhone-related. We are powered by a fantastic iPhone community.

Jon Arnold's Analyst 2.0 Blog

Independent analysis of the IP communications sector - VoIP, Mobile Broadband, IPTV, Unified Communications, Telepresence, Mashups, Web 2.0, Social Media, etc. Plus, my thoughts on all the other things I enjoy during the rest of the day like the Red Sox and great music. And more recently, Smart Grid too!

Hi-Sci-Fi

Creator, producer, writer and host of HiSciFi is Irma Arkus. Over the years, she noticed that the idea of sitting by herself in a studio is unappealing, and potentially dangerously unfunny too. So, Irma had quite a few lovely co-hosts over the years: Andrew Yang, Jevon Ryan, Gregory Milne, and Tarek Suliman. Irma is evidently a man-eater.

BROADCASTING OF HISCIFI

HiSciFi is taped and broadcast live, every Friday at 5:00-6:00 p.m. on CJSF 90.1FM in Burnaby, British Columbia, Canada. Currently, HiSciFi is evaluated for syndication.

www.HiSciFi.com is the place where the show gets a second life as a podcast, and as such can be found at numerous podcast distribution sites, as well as distributed by Mininova.org, PirateBay.com and BTJunkie.org via bit-torrent.

Mark Evens Tech

My company, ME Consulting, creates digital strategies and does tactical execution for startups and entrepreneurs that want to take their marketing efforts to the next level. Having worked for startups, covered them a reporter and consulted with them for the past three years, I understand their goals, and what they need to be successful.

Hmmm ....

There seems to be a slight problem. There are no "science" blogs in the running for best science and technology blog! This is one of my pet peeves. Why can't people understand the difference between science and technology?

When's the last time you saw an actual science project win a Science Fair?

If you really want to cast a vote then go to Best Religion and Philosophy Blog and vote for Canadian Athiest.

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False Dichotomy

 

A false dichotomy is when you are presented with two choices and told that if one is wrong then the other must be correct but there are actually other choices.

Intelligent Design Creationists are very fond of this argument. They tell you that there are only two choices when it comes to explaining biology: either Darwinism or Intelligent Design Creationism. If a given feature of the biological world cannot possibly be explained by Darwinism, then God must exist and he must have designed the feature.

Here's Douglas Axe illustrating the false dichotomy on Evolution News & views [Let Science Be the Arbiter: A Reply to James Shapiro].

As an ID proponent, I've put forward the scientific case for thinking that the thousands of distinct structures that enable protein molecules to perform their specific tasks inside cells cannot have arisen in a Darwinian way. Moreover, the facts of this problem seem to preclude any naturalistic solution, Darwinian or not.

There is no crutch here. The aspects of protein structure that appear to preclude a naturalistic origin have been described in detail. If Shapiro or anyone else were to show in detail how these are overcome by a naturalistic mechanism, then my argument would fall and I would let it fall. But the reverse needs to be true as well. Scientists who personally side with naturalism have to be willing to let naturalism fall, as otherwise they would be guilty of using a crutch to prop it up.

This is actually an attempt to get around the charge of false dichotomy by extrapolating from a rejection of Darwinian explanations to any naturalistic explanation. If Axe is truly able to demonstrate that his "data" cannot possibly be explained by any naturalistic means then it follows logically that the only other type of explanation has to be supernatural. But what Axe is really arguing against is a Darwinian explanation and it's only his lack of imagination and arrogance that allows him to claim that no other naturalistic explanation is possible.

As we have seen time after time, the Intelligent Design Creationists do not have a scientific theory or any kind of scientific explanation for biological phenomena. All they have is criticisms of science—criticisms that are usually based on a lack of knowledge. When will we see an ID explanation of protein folding and function?

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