The eyes of Anomalocaris

Look with your puny camera eyes! Some new specimens of Anomalocaris, the spectacular Cambrian predator, have been discovered in South Australia. These fossils exhibit well-preserved eyes, allowing us to see that the bulbous stalked balls on their heads were actually fairly typical compound eyes, like those of modern insects.

Anomalocaris eyes from the Emu Bay Shale. a–d, Eye pair, SAM P45920a, level 10.4 m. a, b, Overview and camera lucida drawing. Scale bars, 5 mm. Grey fill in b represents visual surface, the proximal part in the upper eye extrapolated from the lower eye. c, Detail of ommatidial lenses located by horizontal white box in a. Scale bar, 1 mm. d, More complete eye, showing transition between visual surface and eye stalk (white arrows). Scale bar, 2 mm. e, Detail of ommatidial lenses in counterpart SAM P45920b. Scale bar, 0.3 mm. es, eye stalk; I.c., Isoxys communis; us, undetermined structure; vs, visual surface. Tilted white box in a represents area analysed using SEM-EDS.

The cool part of this discovery: the investigators were able to count the density of lenses and estimate how many were present in the intact eye. The number is 16,000 ommatidia in each eye, which is more than a little impressive: to put it in context, Drosophila has about 800. The emphasis on high-resolution vision suggests that Anomalocaris was diurnal predator in shallow water.

Oh, and just in case you’re one of those strange beings who isn’t instantly familiar with what the anomalocarids looked like, here’s a video to remind you.

Paterson JR, García-Bellido DC, Lee MS, Brock GA, Jago JB, Edgecombe GD (2011) Acute vision in the giant Cambrian predator Anomalocaris and the origin of compound eyes. Nature 480(7376):237-40.

(Also on Sb)

Why I am an atheist – Fester60613

I am an atheist because the gods presented to me in my youth are:

  • All loving – while providing the perfect vehicle of hatred and bigotry for their followers.

  • Omniscient – except when the intervention of a God is desperately needed.

  • Benevolent – while children suffer and die, while women are humiliated and tortured and slain in barbarous fashions simply because they are women.

  • Conflicted – “Heal the sick, clothe the naked, feed the hungry” but also “kill them all – men, women, children, animals and trees.”

  • Afflicted by Munchausen by proxy syndrome – “I’ll kill my son so you will love me more.”

  • Misogynistic

  • Used by the international criminal Pope Benedict XVI to assist in the cover up of an international conspiracy to sexually abuse children.

  • Unworthy of my praise, my devotion, and my worship.

And other reasons too numerous to mention.

United States

The ghouls’ new game

Hitch is barely cold and already the ghouls are coming for the corpse. It’s the strangest approach, too — they’re all sounding like Mormons, trying to retroactively baptize him in their faith.

Case #1: Ross Douthat. But then you knew that Christian hack would do his best to turn an atheist’s death into a moral fable for his faith. He compares his literary gifts to G.K. Chesterton and C.S. Lewis and thereby, by some strange rambling logic, claims him as a kindred spirit, actually cites Hitchens denying that he was going to abandon his lifelong and strongly held principles and convert on his deathbed, only to then concludes that Hitchens wouldn’t have given in to atheistic despair. It’s appalling, sleazy, and contemptible, and exposes Douche-hat as someone completely incapable of comprehending any other perspective than his god-bothering own.

Do go read Charles Pierces’s takedown. If the NY Times had any sense, they’d fire Douthat on the spot (because he’s a fucking dimwitted ghoul), and put Pierce in his place (because he actually has talent and perspicacity).

Case #2: Scott Stephens. Stephens is the religion editor at ABC Online, and he actually makes Douthat look good. Douthat at least is constrained by the Times in his length; Stephens has a kind of spirit-infused theological diarrhea that he pours onto the page. I swear, I blacked out several times trying to read the whole thing — I think he was trying a novel argument for the soul by doing his best to make mine sick to the point of pining for mortality.

His obit is a weird one that simultaneously tries to be generous in its praise while sinking to new depths. One of the running themes seems to be ‘Hitchens got fat’, with comments like “his increasingly corpulent body”, “overindulged jowls”, “bloated, hirsute complexion” (that last one is strange) — aha, I thought, so that’s what Conservapædia looks like dressed up with a clerical collar and a thesaurus.

But then, he tries to “distill the essence” of Hitchens, and concludes that he was, at heart, a Christian. He quotes Hitchens saying that the Pope was one of his three most deeply hated people in the world (the others being bin Laden and Kissinger), and then declares that Hitchens’ anti-totalitarianism was exactly like the Pope’s.

Yet, on the other hand, it was precisely the form of rigorously Christocentric humanism advocated by Pope Benedict and his predecessor, Pope John Paul II, that constituted the most powerful and persuasive critique of the totalitarian regimes of Eastern Europe. Moreover, it was from Christianity itself that Hitchens derived his keen sense of the illegitimacy, the idolatry of totalitarian power.

And then he quotes Hitchens acknowledging the contribution of Christianity.

The greatest contribution of Christianity in my life is the reminder of the complete ephemerality of human power, and indeed human existence – the transience of all states, empires, heroes, grandiose claims, and so forth. That’s always with me, and I daresay I could have got that from Einstein … and from Darwin. But the way I got it and the way it is implanted in me is certainly by Christianity.

That’s from a public conversation he had with his brother. But Stephens doesn’t bother to mention what Hitchens said further down:

If anything could prove what I so much believe, which is that we are not made by God and never were and could not have been, but that many, many gods have been made by men and women and it is precisely the other way around, the basic claim of materialism — if nothing else could persuade me of that obvious truth, the behavior of religion itself would be enough.

Hitchens was always blunt and plain-spoken about his opinion of religion. He would not ever deny that he was a product of a Western and English culture that had religion wrapped around its roots (like a parasitic fungus, I would say), he was also explicit in his denial of the validity of god-belief, and was frank in his accusations of the folly of faith. For a Christian to now try and put the mantle of Christianity on him is repulsive and disrespectful — it’s like witnessing the desecration of a corpse. The corpse may not mind anymore, but it’s still a distasteful spectacle and gives the lie to any pretense of appreciation of the person who once resided in that body.

But then, that’s what ghouls do.

It’s also such peculiar behavior. When popes die, you don’t find atheists lining up to write encomiums in which they claim that he was really an atheist, deep down, and that he lived as a humanist rather than a Catholic. When William Lane Craig dies, no one will speculate that he denied the gods on his deathbed; when Scott Stephens croaks, no one will winnow through his columns, straining occasional words and phrases out of context to suggest that maybe he really was sympathetic to atheism after all. They are who they are, deluded dunces who invoke no sense of envy in us at all.

And maybe that’s the explanation. Hitchens was a man of palpable talent and immense rhetorical skill, and maybe we should recognize it as flattery that these Christians desperately wish to appropriate him.

But there is one thing anyone who read his works could know: Hitchens was an atheist, without qualification.

Yet another apologist simpers feebly

Paul Wallace (who?) is declaring victory in the conflict between science and religion, with the most specious reasoning. His big general argument is that the New Atheists are old.

This year has marked, I believe, the beginning of the end of the war between science and religion. Creationism cannot last. The New Atheists are now old (or departed).

That little dig about “departed” atheists is, clearly enough, a rather nasty reference to Christopher Hitchens, and the link goes to a religious argument about whether he’s in hell or not. It is revealing that these Christians can’t even try to make a rational argument without playing ghoul. But it’s also wrong; as an activist in the atheist movement for about 15+ years, what has been most notable to me is how much younger the movement gets every year. As has been pointed out many times, the fastest growing segment of the religious question is the Nones, who reject the whole mess.

After that little falsehood, Wallace’s arguments disintegrate rapidly. His sole tactic is to list 10 people, marginal or tangential to the whole movement on either side, and point and say, “Look! They don’t hate religion! Therefore, we’re winning.” It’s a pathetic and irrational effort. Here is his list of the Big 10 reconciling science and religion.

10. Karl Giberson, science & religion writer and former physicist, for reminding evangelicals that science is not the enemy

Right. The Karl Giberson who was squeezed out of the website he cofounded, as Biologos cozies up to fundagelical literalists? It seems to me that the real lesson here is that the evangelicals are reminding Giberson that science is the enemy.

9. Jon Huntsman, U.S. Ambassador to China, former Governor of Utah, candidate for the 2012 Republican nomination for president, for decoupling conservative politics and creationism

Huntsman was the only Republican candidate for president to speak out for the scientific views on evolution and global warming. He also doesn’t stand a prayer of getting the nomination. His position is a confirmation that the Christian majority hates science. And mormons.

8. Jon Stewart, political satirist, for shining light on American Atheists’ frivolous lawsuit against the inclusion of the Ground Zero cross in the 9/11 memorial museum

I wasn’t that enthusiastic myself, but I don’t think it was frivolous. I think the “ground zero cross” highlights the stupidity of Christianity — to think, they found two metal bars that had been welded at right angles to one another in some wreckage!

7. Nidhal Guessoum, astrophysicist, for reminding us that, in the minds of nearly 1.6 billion people, “science and religion” does not mean “science and Christianity”

Somehow, the fact that they found a guy who favors good science, and is also a member of a religion that has discouraged science to the point that only 10-20% of its members accept evolution (which Wallace comes right out and admits), is regarded as a victory for religion? So to some people, “science and religion” means “science and Islam”, and the overwhelming majority of them detest science.

6. Jack Templeton, surgeon, president and chairman of the John Templeton Foundation, for bringing science into the church

Hmmm. Reactionary fundamentalist Christian who donates substantial sums of money to defeat gay marriage initiatives and also strains to coopt science to support his religious beliefs is supposed to be an example of religion and science finding a middle ground? It looks more like moral and scientific bankruptcy to me. He’s a guy trying to bring the church into science, not vice versa.

5. Chris Stedman, interfaith activist and super-swell atheist guy, for decoupling atheism from science, and for being the face of a kinder, gentler atheism

Fuck “kinder, gentler atheism”. Finding one smiley apologist for faith who is too craven to confront the real lies of religion does not convince me that the New Atheism is in decline at all. These pandering compromisers will always be popular with the subset of the population that dreads rocking the boat…and they’ll always be the ones fighting against change and for the status quo.

4. Rachel Held Evans, author, speaker, blogger, for making science & religion her thing, but not her main thing

Who? Wallace seems impressed that Evans is not a biblical literalist. So? That’s been common for quite some time.

3. All Those People Who Are Not Backing the Ark Park, for keeping the sure-to-be-divisive Ark Encounter from its scheduled August groundbreaking

What? The majority of Christians in Kentucky are in favor of the nonsensical giant ark, and somehow this tells Wallace that religion and science are reconciled?

2. Tenzin Gyatso, the 14th Dalai Lama, for reminding us that being ethical does not depend on belief in a personal God—nor, particularly, on science

I have never been sympathetic to the Dalai Lama. Sure, he smiles a lot — that seems to be the sole criterion for thinking he’s a hero of religion — but he represents a misogynistic, theocratic tyranny that wants to get back in power in the homeland of Tibet. Charismatic tyrants may be one kind of religious ideal, but not mine.

1. Terrence Malick, filmmaker, for reminding us that art may be the most compelling way to reconcile science & religion

Haven’t seen his movie. Not really interested in seeing it, either. I don’t think an art-house movie represents the state of religion in this country, and especially since Wallace mainly seems to like it for its biblical roots, it’s not exactly a slice of scientific thought, either.

That’s it. That’s Wallace’s great groundswell of pro-religious, pro-science belief that is sweeping the country — 10 marginal characters who meet Wallace’s criterion of being nice and non-confrontational. I’m sorry, but cherry-picking the population for the wimpiest set of useless apologists (or twisting their positions to hide their actual agendas) is not very impressive.

Although I did think it entirely appropriate to see Stedman and Templeton on the same list. Both are playing exactly the same game from different sides of the playing field.

(I am not alone in finding Wallace risible. Greg Laden has commented, and Ian Cromwell tears him a new one. Expect more of the freethought to rise to point and laugh at Wallace in the near future.)

And now…Ophelia makes the interesting point that the apologists are actually divisive and increase the combativeness.

Steve Pinker’s hair and the muscles of worms

I’ve been guilty of teaching bean-bag genetics this semester. Bean-bag genetics treats individuals as a bag of irrelevant shape containing a collection of alleles (the “beans”) that are sorted and disseminated by the rules of Mendel, and at its worst, assigns one trait to one allele; it’s highly unrealistic. In my defense, it was necessary — first-year students struggle enough with the basic logic of elementary transmission genetics without adding great complications — and of course, in some contexts, such as population genetics, it is a useful simplification. It’s just anathema to anyone more interested in the physiological and developmental side of genetics.

The heart of the problem is that it ignores the issue of translating genotype into phenotype. If you’ve ever had a basic genetics course, it’s quite common to have been taught only one concept about the phenotype problem: that an allele is either dominant, in which case it is expressed as the phenotype, or it’s recessive, in which case it is completely ignored unless it’s the only allele present. This idea is so 19th century — it’s an approximation made in the complete absence of any knowledge of the nature of genes.

And the “one gene, one trait” model violates everything we do know about the phenotype and genotype. Every gene is pleiotropic — it influences multiple traits to varying degrees. Every trait is multigenic — multiple genes contribute to the expression of every phenotypic detail. The bean-bag model is totally inadequate for describing the relationship of genes to physiology and morphology. Instead of a bean-bag, I prefer to think of the genome as comparable to a power spectrum, an expression of the organism in a completely different domain. But I wrote about that previously, and I’ll make this explanation a little simpler.

Here’s the problem: you can’t always reliably predict the phenotype from the genotype. We have a skewed perspective on the problem, because historically, genetics has first searched for strong phenotypes, and then gone looking for the genetic cause. We’ve been effectively blind to many subtle phenotypic effects, simply because we don’t know how to find them. When we go the other way, and start by mutating known genes and then looking for changes in the phenotype, we’re often surprised to discover no detectable change. One of the classic examples is the work of Elkins (1990), who found that mutating a neural cell adhesion gene, Fasciclin I, did not generate any gross defects. Mutating another gene, a signal transduction gene called Abelson tyrosine kinase, similarly had no visible effects. Mutating the two together, though — and this is a major clue to how these strange absences of effect could work — did produce gross and obvious effects on nervous system development.

Providing another great example, Steve Pinker examined his own genome, and discovered that his genes said he was predisposed to be red-haired and at high risk for baldness. If you’ve seen Steve Pinker, you know he’s neither.

How can this be? As any geneticist will tell you, the background — the other alleles present in the organism — are important in defining the pattern of expression of a specific gene of interest. One simple possibility is that the genome contains redundancy: that a trait such as adhesion of axons in the nervous system or the amount of hair on the head can be the product of multiple genes, each doing pretty much the same thing, so knocking out one doesn’t have a strong effect, because there is a backup present.

Genetic interactions provide a general model for incomplete penetrance. Representation of a negative (synergistic) genetic interaction between two genes A and B.

So Steve Pinker could have seen that he has a defective Gene A, which is important in regulating hair, but maybe there’s another Gene B lurking in the system that we haven’t characterized yet, and which can compensate for a missing Gene A, and he has a particularly strong form of it. One explanation for a variable association between an allele and the phenotype, then, is that we simply don’t have all the information about the multigenic cause of the phenotype, and there are other genes that can contribute.

This doesn’t explain all of the observed phenomena, however. Identical twins who share the same complement of alleles also exhibit variability in the phenotype; we also have isogenic animal lines, where every individual has the same genetic complement, and they also show variability in phenotype. This is the problem of penetrance; penetrance is a genetics term that refers to the likelihood that an individual carrying an allele will actually express the phenotype associated with that allele…and it’s not always 100%.

Again, the explanation lies in the other genes present in the organism. No gene functions all by itself; its expression is dependent on a cloud of other proteins — transcription factors, enhancers, chaperones — all of which modulate the gene of interest. We also have to deal with statistical variation in the degree of expression of all those modulatory factors, which vary by chance from cell to cell, and so the actual degree of activation of a gene may follow a kind of bell curve distribution. In the cartoon below, the little diamonds represent these partners; sometimes, just by chance, they’ll be present in sufficiently high numbers to boost Gene B’s output enough to fully compensate for a defective Gene A; in other cases, just by chance, they’re too low in concentration to adequately compensate for the absence.

Genetic interactions provide a general model for incomplete penetrance. A model for incomplete penetrance based on variation in the activity of genetic interaction partners.

What the above cartoon illustrates is the concept of developmental noise, the idea that the cumulative total of statistical variation in gene expression during development can produce significant phenotypic variation in the absence of any differences in the genotype. Developmental noise is a phrase bruited about quite a bit, and there’s good reason to think it’s valid: we can see quantitative variation in gene expression with molecular techniques, for instance. But at the same time we have other concepts, like redundancy and canalization, that work to buffer variation and produce reliable outputs from developmental processes, so we don’t have many good examples where we can directly correlate subtle variation at the molecular level with clear morphological differences.

To test that, we have to go to simple animal models (it turns out that Steve Pinker is a rather intractable experimental animal). And here we have a very nice example in the nematode worm, C. elegans. In these experiments, the investigators were dealing with an isogenic strain — the genetic background was identical in all of the animals — raised in a uniform environment. They were looking at a mutant in the gene tbf9, which causes defects in muscle formation, but only 50% penetrance; that is, half the time, the mutants appeared completely normal, and the other half of the time they had grossly abnormal muscle development.

Genetic interactions provide a general model for incomplete penetrance. Inactivation of the gene tbx-9 in C. elegans results in an incompletely penetrant defect, with approximately half of embryos hatching with abnormal morphology (small arrow).

See the big red question mark? That’s the big question: can we trace the abnormal phenotype all the way back to random fluctuations in the expression of other genes in the animal? Yes, they can, otherwise it would never have been published in Nature and I wouldn’t be writing about it now.

In this case, they have a situation analogous to the Gene A/Gene B cartoons above. Gene B is tbx-9; Gene B is a related gene, a duplicate called tbx-8 which acts as a redundant copy. In the experiments below, they knock out tbx-9 with a mutation, and then measure the quantity of other genes in the system using a very precise technique of quantitative fluorescence. Below, I’ve reproduced the entirety of their summary figure, because it is awesome — I just love the idea of being able to count the number of molecules expressed in a developing system. In order to avoid overwhelming everyone, though, I’ll just describe a couple of the panels to give you the gist of the work.

First, just look at the top left panel, a. It’s a plot of the level of expression of the tbx-8 gene over time, where each line in the plot is a different animal. The lines in black are in the wild type animal, with fully functional copies of bothe tbx-8 and tbx-9, and you should be able to see that there’s a fair amount of variation in expression, about two-fold, in different individuals. The lines in green are from animals mutant for tbx-9; it’s messy, but statistically what happens when tbx-9 is knocked out, more tbx-8 gene product is produced.

Panel e, just below it, shows the complementary experiment: the expression of tbx-9 is shown for both wild type (black) and animals with tbx-8 knocked out. Here, the difference is very clear: tbx-9 levels are greatly elevated in the absence of tbx-8. This shows that tbx-8 and tbx-9 are actually tied together in a regulatory relationship where levels of one rise in response to reduced levels of the other, and vice versa.

(Click for larger image)

Early inter-individual variation in the induction of ancestral gene duplicates predicts the outcome of inherited mutations. a, Quantification of total green fluorescent protein (GFP) expression from a tbx-8 reporter during embryonic development in WT (black) and tbx-9(ok2473) (green) individuals. Each individual is a separate line. a.u., Arbitrary units. b, Boxplot of tbx-8 reporter expression (a) showing 1.2-fold upregulation in a tbx-9 mutant at comma stage (~290 min, P=1.6×3 10-3, Wilcoxon rank test). c, Expression of tbx-8 reporter in a tbx-9(ok2473) background for embryos that hatch with (red) or without (blue, WT) a morphological defect. d, Boxplot of c showing tbx-8 expression is higher in tbx-9 embryos that develop a WT phenotype (blue) compared with those that develop an abnormal (red) phenotype at comma stage (P= 6.1×10-3). e, Expression of a ptbx-9::GFP reporter in WT (black) and tbx-8(ok656) mutant (green). f, Boxplot of tbx-9 reporter showing 4.3-fold upregulation at comma stage (~375 min, P=3.6×10-16). g, Expression of tbx-9 reporter in a tbx-8(ok656) mutant background, colour code as in
c. h, Boxplot of g showing tbx-9 expression is higher in tbx-8 embryos that develop a WT phenotype (P=0.033). i, Expression of a pflh-2::GFP reporter in WT (black) and flh-1(bc374) mutant (green). j, Boxplot of flh-2 reporter expression (i) showing 1.8-fold upregulation in a flh-1 mutant at comma stage (~180 min, P=2.2×10-16). k, Bright-field and fluorescence image of an approximate 100-cell flh-1; pflh-2::GFP embryo. Red arrow indicates the local expression of flh-2 reporter quantified for flh-1 phenotypic prediction.
l, Boxplot showing higher flh-2 reporter expression at approximate 100 cells for WT (blue) compared with abnormal (red) phenotypes (P=0.014). Boxplots show the median, quartiles, maximum and minimum expression in each data set.

Now skip over to the right, to panel c. All of the lines in this plot are of tbx-8 expression in tbx-9 mutants, and again you see a wide variation in levels of gene expression. In addition, the lines are color-coded by whether the worm developed normally (blue), or had the mutant phenotype (red). The answer: worms with low tbx-8 levels were more likely to have the abnormal phenotype than those with high levels.

Panel g, just below it, is the complementary analysis of tbx-9 levels in tbx-8 mutants, and it gives the same answer.

Obviously, though, there is still a lot of variability unaccounted for; having relatively high levels of one or the other of the tbx genes didn’t automatically mean the worm developed a wild-type phenotype. There’s got to be something more that is varying. Look way back to the second cartoon I showed, with the little diamonds representing the cloud of transcription factors and chaperone proteins that modulate gene expression. Could there also be correlated variation there? And yes, there is. The authors looked at a chaperone protein called daf-21 that is associated with the tbx system, and found, in mutants for tbx-9, that elevated levels of daf-21 were associated with wildtype morphology (in blue), while lowered levels of daf-21 were associated with the mutant phenotype.

(Click for larger image)

Expression of daf-21 reporter in a tbx-9(ok2473) mutant background. Embryos that hatch into phenotypically WT worms (blue) have higher expression than those hatching with a morphological defect (red) at the comma stage (P=1.9×10-3).

I know what you’re thinking: there isn’t a perfect correlation between high daf-21 levels and wildtype morphology either. But when they do double-label experiments, and take into account both daf-21 and tbx-8 levels in tbx-9 mutants, they found that 92% of the animals with greater than median levels of expression of both daf-21 and tbx-8 had wildtype morphology. It’s still not perfect, but it’s pretty darned good, and besides, it’s no surprise that there are probably other modulatory factors with statistical variation lurking in the system.

What should you learn from this? Developmental noise is real, and is a product of statistical variation in the degree of expression of multiple genetic components that contribute to a phenotype. We can measure that molecular variation in living, developing systems and correlate it phenotypic outcomes. None of this is surprising; we expect that the process of gene expression is going to be a bit noisy, especially in these transcriptional regulators that are present in low concentration in the cell, anyway. But the other cool thing we can observe here is that having multiple noisy systems that interact with each other can produce a more reliable, robust signal and contribute to the fidelity of developmental outcomes.

Burga A, Casanueva MO, Lehner B (2011)
Predicting mutation outcome from early stochastic variation in genetic interaction partners. Nature 480(7376):250-3.

Elkins T, Zinn K, McAllister L, Hoffmann FM, Goodman CS (1990)
Genetic analysis of a Drosophila neural cell adhesion molecule: interaction of fasciclin I and Abelson tyrosine kinase mutations. Cell 60(4):565-75.

(Also on FtB)

Steve Pinker’s hair and the muscles of worms

I’ve been guilty of teaching bean-bag genetics this semester. Bean-bag genetics treats individuals as a bag of irrelevant shape containing a collection of alleles (the “beans”) that are sorted and disseminated by the rules of Mendel, and at its worst, assigns one trait to one allele; it’s highly unrealistic. In my defense, it was necessary — first-year students struggle enough with the basic logic of elementary transmission genetics without adding great complications — and of course, in some contexts, such as population genetics, it is a useful simplification. It’s just anathema to anyone more interested in the physiological and developmental side of genetics.

The heart of the problem is that it ignores the issue of translating genotype into phenotype. If you’ve ever had a basic genetics course, it’s quite common to have been taught only one concept about the phenotype problem: that an allele is either dominant, in which case it is expressed as the phenotype, or it’s recessive, in which case it is completely ignored unless it’s the only allele present. This idea is so 19th century — it’s an approximation made in the complete absence of any knowledge of the nature of genes.

[Read more…]

von Däniken poisons everything

Gah, the stupid, it burns. Ridley Scott is making a kind of prequel to Alien called Prometheus, which sounds fun; I liked the first two movies in the Alien franchise. But his rationale dismays me, and makes me regard Scott as a bit dim.

"The (space) journey, metaphorically, is about a challenge to the gods," Scott said. But Scott’s ambitions with Prometheus go far beyond simply restarting a hit franchise. The British director said the film’s storyline, and script by David Lindelof, was partially inspired by the writings of legendary Swiss sci-fi writer Eric van Daniken.

Van Daniken, author of 1968 bestseller Chariot of the Gods, is best known as the first proponent of the so-called ancient astronaut theory, which holds that aliens kick-started civilization on earth. "NASA and the Vatican agree that is almost mathematically impossible that we can be where we are today without there being a little help along the way," Scott said. "That’s what we’re looking at (in the film), at some of Eric van Daniken’s ideas of how did we humans come about."

I had to laugh at the claim that von Däniken was a “sci-fi writer”. He wasn’t. He was a pseudo-science writer who believed that his nonsense about aliens helping the Egyptians construct the pyramids (and other belittlings of human abilities) was actual history. I’ve read a couple of his books, many years ago, and they were so hopelessly inane and incompetently supported that I rejected them as a high school student. It doesn’t say much about Scott’s scientific discrimination that he can be inspired by that drivel, and it is just about as damning to his competence at recognizing a good story that he mistook it for a sci-fi novel.

I also don’t consider the opinion of a bunch of engineers or a gang of theological thugs to be of much value in assessing the likelihood of evolutionary events — the authorities he cites are not authorities in the subject he’s discussing. I have a strong suspicion that Scott is making crap up, doesn’t know much about what either NASA or the Vatican has said, and probably hasn’t even read any of von Däniken’s books, but is only vaguely echoing the ‘common knowledge’ of blithering Hollywood celebrities.

My expectations for this movie have plummeted, though. Those Hollywood celebrities should never ever speak, because they always seem to confirm that they’re vacuous and credulous.