01 August 2009

Carnival of Evolution 14

Welcome to Quintessence of Dust and to the 14th Edition of the monthly Carnival of Evolution. Thanks for stopping by, and for supporting scientific carnivalia, members of a taxon that seems to be flirting with extinction.

One good reason to visit a carnival: brain stimulation. Brain Stimulant offers some thoughts and speculations on Free Will and the Brain, touching briefly on themes of selection and adaptation, and he doesn't charge as much as the clinic would.

Another good reason: you can bump into real scientists, the kind who actually work on evolution. Ryan Gregory has a day job as an expert on genome evolution, but somehow finds the time to blog at Genomicron. Recent entries there include fascinating pictures of ongoing field work. For this month's carnival, be sure to read two reviews of the ideas of Stephen Jay Gould, focusing on controversial papers by Gould published in 1980 and 1982. You may find that you have been misinformed about Gould's positions, and you'll surely learn more about evolution.

Michael White at Adaptive Complexity is another blogging scientist, and he writes very clearly about parasitic DNA in Selfish Gene Confusion.

David Basanta is a biologist who runs a cool blog called Cancerevo: Evolution and cancer, which is subtitled "Studying cancer as an evolutionary disease." Check it out, and don't miss his recent piece on Stem cells and ecosystems.

Zen Faulkes is a biologist who blogs at Neurodojo. That's cool enough, but the subtitle of that blog is "Train your brain." Hey, this could be a theme for the whole carnival! He recently wrote about a walking bat in New Zealand. Bat evolution...we can't get enough of that. I've written about it myself.

Brains and their origins come up in an extensive discussion of early animal evolution at AK's Rambling Thoughts. The post is The Earliest Eumetazoan Progression.

At The Loom, the peerless Carl Zimmer discusses AIDS in chimps and the relevance of the story to conceptions of scientific progress. AIDS and The Virtues of Slow-Cooked Science is engrossing and important. And John Wilkins discusses some new fossil apes in an excellent recent post at Evolving Thoughts.

John Lynch reviews a new book on Alfred Russell Wallace. Caveat lector. Brian at Laelaps takes us on a historical tour of the work of Florentino Ameghino. Are those elephants or not? Brian's discussion is typically excellent.

At The Spittoon, AnneH discusses new findings concerning both the past and the future of the mammalian Y chromosome.

Hoxful Monsters is a future host of this carnival; Nagraj recently reviewed some recent work on pattern formation in the development of spiders. Wonderful evo-devo stuff.

Someone at Wired wrote some swill about the "10 Worst Evolutionary Designs" which annoyed a few smart bloggers. At Deep-Sea News, Dr. M sets the record straight. The title is self-explanatory: Worst Evolutionary Designs? No! Brilliant Solutions to the Complexity of Nature and Constraints.

Larry Moran at Sandwalk is attending a conference entitled Perspectives on the Tree of Life. He's posted reviews of days one and two so far.

And that's our carnival. Thanks for reading, and on the way out I hope you'll look at my nearly-complete series on Notch and deep homology.

Next month's edition will appear at Southern Fried Science. To submit posts, use the submission form found at the Carnival of Evolution site. And if you like the carnival, help us promote it with a link, and/or consider hosting. More info at the carnival site.

29 July 2009

Carnival of Evolution 14: Call for Submissions

The 14th edition of the excellent Carnival of Evolution will go up here at Quintessence of Dust this Saturday, 1 August 2009. Send submissions and links, to your own work or to good stuff you've seen elsewhere. Images welcome too!

03 July 2009

Deep homology and design: why Notch?

The Notch signaling pathway is a golden oldie of genetics in two ways. First, it's a system that was first described at the dawn of modern genetics – named by its founder, Thomas Hunt Morgan – and used to establish some of the most basic principles of "the physical basis of heredity," as Morgan put it. (His book by that title is a founding document of modern genetics, describing in 1919 what we now call chromosomes without any knowledge of their chemical makeup.) Second, it's a system now known to be as ancient as animals themselves.

Why Notch? The name refers to the appearance of some of the first mutant fruit flies described by Morgan and his colleagues in their famous work in the early 20th century. They found flies with notched wings, and found that the trait was dominant.

Figure 1 from T.H. Morgan, "The Theory of the Gene." American Naturalist 51:513-544, 1917.

So aside from its importance in evolution and development, Notch is of historical interest to genetics. Now, Morgan was interested in Notch (the gene name is capitalized because the original trait is dominant, in case you're wondering) because of its mode of inheritance, not specifically because of its biological effects. (I mean, who cares about flies with notched wings?)

But twenty years later, things got more interesting when a different mutation in Notch was found to cause a weird (and lethal) overgrowth of the nervous system. Interesting... then, as geneticists began to probe the genetics of animal development 50 years after Morgan's initial discoveries, using the fruit fly as a model, Notch started turning up again and again. Problems in Notch signaling led to developmental problems all over the place: brain, eyes, gut, wings, bristles.

By the beginning of the 1990's, geneticists had figured out why its activity is so central to proper development: Notch controls a crucial type of cell-to-cell interaction that leads to a change in cell fate. And they had found Notch signaling in animals of every kind, including in humans, mediating the same kinds of inductive developmental interactions. It's not as complicated as it might sound – in such an interaction, two cells interact physically (they have to touch) and after the interaction one or both of the cells changes its developmental fate, choosing to become, say, a nerve cell or a skin cell. That weird brain overgrowth in the flies with no Notch activity results from a failure of cells to communicate in this way, such that all the cells on the outside of the fly's head become brain cells. (Flies, like most animals, prefer to have some skin over their brains, but in these mutants there's very little skin and lots of extra brain. Ick. See Figure 1 of this recent paper in BMC Biology for pictures; the green stain indicates nerve cells and the second animal down has the nasty trait.)

The point is that Notch signaling involves direct cell contact, and typically leads to cells making decisions about what to do when they grow up. So how does it work? Well, we know an awful lot about this particular system, and there are myriad details of mechanism and control that I'm going to skip. The very basic outline is as follows. Some cells make the Notch protein, which is a receptor. Other cells make the Delta protein, which is the signal that activates the receptor. (One useful analogy is that of locks and keys: Notch is the lock, Delta is the key.) Both proteins are displayed on the cell surface. When the two cells come into contact, the Delta protein on one cell activates the Notch protein on the other. When Notch becomes activated, it gets chopped into at least two pieces. One piece leaves the surface of the cell and travels inward to the nucleus of the cell. There, in collaboration with other proteins, it causes changes in gene expression, meaning that some genes are turned on or up and others are turned off or down.

This mode of signaling is unique and extraordinary. What we have is a signaling system that takes cell-to-cell contact and converts it directly into changes in gene expression.

Now, let's think carefully about this. We have a system of receptors and activators, in the form of Notch proteins (there are at least four in humans) and Delta proteins (there are several in humans, in a few different protein families), which serve a critical and unique purpose in cell-to-cell signaling. The function is conserved in all known animals, and that's not surprising – having cells send messages to their immediate neighbors, directing them to adopt particular fates, is key to constructing tissues and organs. I hope you'll agree that we should expect to see these inductive mechanisms in the development of complex organisms. More to the point, one should expect this regardless of one's stance on questions of "intelligent design."

Here's what is surprising. The same Notch proteins are used for this purpose in every known animal. And here's why that's surprising: as far as we know, there's no reason to insist on those particular proteins playing those particular roles. It's easy to envision – and then design and create – a set of locks and keys that bear no resemblance to Notch or Delta but that can accomplish these somewhat basic purposes just as well. There's no need for such a specific solution to a basic challenge. Why does every animal use Notch? Recall the previous post in this series and how we approached this question of common design. Here, again, are our options.
  1. These inductive signaling events could only be accomplished by Notch. There is a design constraint, currently unknown, which forces that choice. It may seem that the system could have been effectively constructed using a different lock-and-key combination, but in fact it could not function (or function well) any other way.
  2. These inductive signaling events could be mediated in various ways, but the choice of Notch has been forced by common ancestry. The earliest animals settled on this choice, and their descendants have used it ever since.
  3. These inductive signaling events could be mediated in various ways, but an intelligent designer has repeatedly chosen Notch for reasons known only to her/him/it.
Option #1 is, in my view, unreasonable. The system is not complicated in its basic design. There are no clear constraints on the choice of lock and key. A designer who is crafting an organism from the ground up need not select that particular lock/key combination, and someone who intends to argue otherwise needs to demonstrate how that particular combination is superior.

Option #3 is, I think, perfectly reasonable. The only problem is that one must know quite a lot about the designer to begin to surmise her/his/its goals and proclivities. Without that knowledge, it is no more reasonable to assume a preference than it is to assume a constraint.

The point is not that we can ever rule out preferences or other characteristics of a creator or designer. The point is that we can rarely make explanatory use of them. Consider that while we may assert that the Creator/Intelligent Designer prefers that pine trees have needles, we would not advance that as a useful explanation for why pine trees have needles. Specifically, we would never advance that as an alternative explanation in place of one that notes that today's pine trees have the same needles that last century's pine trees had, by virtue of biological ancestry.

Notch signaling represents one of the classic examples of deep homology. It seems to me that design theorists need to deal with deep homology before they can ever be taken seriously as scientific thinkers. Deep homology is crying out for explanation, and those who believe that the biosphere cries "design" are remiss in not offering a serious design-based explanation for the fact that every animal on the planet uses the same lock-and-key mechanism to achieve basic cell-to-cell inductive communication.

Next, we'll look at a recent and very interesting example of new findings that illustrate the striking conservation of Notch-mediated developmental events – an example of deep homology that could arise from the very root of animal ancestry.

19 June 2009

Weekly sampler 24

1. Get your genome sequenced for $48,000. I would so do this. In the meantime, we bought the Matheson family DNA test for my dad for Father's Day.

2. I'm following this series at Siris: Philosophical Sentences explained. You know the old chestnuts: Cogito ergo sum, God is dead, virtue is its own reward, cleanliness is next to godliness... heh. Brandon tells us where they came from and a little about them. Latest installment is Santayana's famous quote etched at Dachau.

3. A very cool illusion that, like all good ones, tells us something interesting about how the brain processes visual information. Don't click till you're ready to follow these instructions: display the image on your computer screen so that you can slowly back away from the screen and still see the image. The idea is to view it up close then back up at least a few meters.

4. Two of my favorite bloggers, John Lynch (of Satan's University) and John Wilkins (from Down Under) have left ScienceBlogs and set up shop independently. Lynch formerly blogged at Stranger Fruit and his new place is called a simple prop. Wilkins is an important antidote to brainless anti-religious bellowings from Coyne and like-minded simps. Both are skeptics who know a lot about evolution. Recent important posts: Lynch on The Roots of ID and Wilkins on The Demon Spencer.

5. Strangest species discovered in the last year. The ghost slug wins for weirdness, but the big news is that someday we might be able to drink decaf that's still coffee.

6. Becoming Creation is an important blog by a homeschooler, evolutionary creationist, accomplished biologist and good guy: Doug Hayworth. Up right now is an interview with Denis Lamoureux, author of Evolutionary Creation.

7. A recent piece in the Chronicle of Higher Education presents a very interesting take on teaching science in the context of religion (and other social influences). The concluding paragraph:
Science professors should explicitly engage the rich social and ethical context of the subjects that they teach, engaging new generations of students in the science that so many now fear and reject. A careful, thoughtful approach to teaching the sensitive issue of evolution represents merely the beginning of a challenging, less-traveled-by path, but one that could, nevertheless, make all the difference.
8. My research concerns some very interesting proteins called formins. Michael Behe's scholarship includes a focus on the malaria parasite, P. falciparum. A recent paper reports that a formin protein in P. falciparum is critically involved in the process by which the parasite invades red blood cells. I always knew that Professor Behe and I were destined to be collaborators.

10 June 2009

Theistic embryology: the talk

I previously posted the abstract of a talk I gave at Calvin last month in which I test-drove my "theistic embryology" metaphor that I'll present at the North American Paleontological Convention in Cincinnati in two weeks. Now the audio and my simple slides are posted on Calvin's e-zine, Minds in the Making. Lots of jokes. And now my name's spelled right.

About halfway through, I refer to "10 dangers of theistic evolution" at Answers in Genesis. Later I read from Jerry Coyne's steaming pile. And speaking of steaming piles, I then read from one of my favorite posts in The Cesspool. In case you wanted to follow along.

09 June 2009

Deep homology and design: common design and its implications

Consider these not-so-random samples from the animal world: a cockroach, a zebrafish, a mouse. What do these creatures have in common?

Left to right: American cockroach (Periplaneta americana), zebrafish (Danio rerio), house mouse (Mus musculus). Cockroach image from Wikimedia Commons, zebrafish and mouse from Wellcome Images.

Well, they're all animals and that means they're all eukaryotes, for example. They all have DNA-based genomes. They all like water to some extent. They all have muscles that cause them to move. And so on.

But let's think of them in a different way. Let's think of them as things that exhibit design. (Not Design. Just design.) We see similarities like the ones we just listed, and we see some dramatic differences. Insect, exoskeleton, open circulatory system. Fish, gills, egg-laying. Mammal, milk, hair, live birth, temperature control. We can see elements of common design (limbs and joints, eyes, nerves) and elements of specialized design (lungs, fins, antennae).

Now let's forget everything we know about common descent and adopt an Intelligent Design perspective. This isn't hard to do: just think of each animal as a machine that was designed to be the way it is. The machines have some common design elements and some specialized design elements. Now this is important: let's assume that each machine was designed separately, such that design decisions were made on a case-by-case basis (for each type of machine, not for each individual machine). In other words, let's think of the cockroach as designed from the ground up to be a cockroach, and the fish and the mouse likewise. Simple, right? I think so.

Now, let's look under the hood of each machine and ask detailed questions about how it's built, again with the assumption that it was designed. Not just its overall structure, but also the procedures used for its assembly. Let's look, in other words, at its molecular machinery – machinery for signaling between cells and tissues, machinery for signaling within individual cells, machinery for directing gene function during development and normal function. And let's focus specifically on the signaling systems in these creatures and in their developmental stages. What would we expect to see? Well, let's consider some basic scenarios.

1. Maybe the signaling systems will be roughly the same – or even largely the same – in all three animals. This would imply that such systems are hard to assemble and perhaps even harder to tune and maintain, and therefore we would conclude that there are very few ways to make a working system. The only other explanation would refer to preferences on the part of the designer, who was unconstrained by design limitations but nevertheless insisted on doing things a certain way.

2. Maybe the signaling systems will differ between the three animals, to such an extent that it is clear that the choice of a system is somewhat arbitrary, arbitrary in the sense that the choice of a particular system is largely independent of the context or the function that is specified. The implication is that there are plenty of ways in which cells and molecules can communicate, and no strong constraints on the designer's choices.

Now of course we may find examples of both scenarios in our analysis. Perhaps some signaling systems will appear to be highly constrained while others will be largely different among the three species. The point, though, is this: when examining machines that were separately designed, common design implies either design constraint or designer preference. Divergent design implies a lack of design constraint. There are no further options: either the designer was constrained, or she wasn't; if unconstrained, she could nevertheless choose a favorite scheme and leave the impression that she was somehow constrained.

Designer constraint could arise in various ways. It could be that a particular signaling system is uniquely suited to a particular purpose. It could be that a particular signaling system is highly robust to damage or other challenges. It could be that there are only a handful of different possibilities due to limitations in the raw materials. One variation of that last possibility would look a lot like how evolution is known to work: the designer tweaks the system a little at a time, working with the materials supplied by each generation and therefore constrained by common descent.

Design proponents can be stunningly cavalier about all this. "Common elements in animal biology? Well of course! Common design!" But wait: common design implies either design constraint (that was the best way to do it – or the only way to do it) or designer preference (she just happens to like it that way), and those are dramatically different from an explanatory standpoint.

It turns out that signaling systems in animal development are so universally conserved that they require an extraordinary explanation. The commonality of the elements is so striking that it took most biologists by surprise when it first became evident, and remains one of the most remarkable facts of developmental biology today. We'll look at some recent advances in this area of evo-devo in posts to come.

But one last thing: I'd like to try a thought experiment to illustrate how we might approach questions of signaling in animal cells and embryos. Consider a group of 50 people who have agreed to help with your experiment. You divide them into pairs and tell each pair to send one person out of the room. Then you tell the remaining people to greet their partners upon their return, using a single word of their choosing that is certain to convey the greeting. You observe that all of the people employ either "hello" or "hi" for this purpose.

Question: would you conclude that "hello" and "hi" are uniquely suited for the task, and that no other word could possibly have worked? I hope you would seek another explanation and perhaps consider trying the experiment in, say, Shanghai or Guadalajara. You would conclude, I wager, that the word itself is of little explanatory value. In other words, the choice of a word was constrained, but not by anything specific to the word itself. In Shanghai, it's "ni hao." Maybe somewhere it's "duuuuuuude." And in a matter of minutes, you could change it to "ahoy" or "blorp" or anything you want.

And if you really wanted to probe the notion of constraint in human conversation, you would ask your 25 pairs of subjects to come up with an identifying word or phrase that they could call out to find each other in the dark. You would find, of course, that the choice of that word or phrase would be almost completely unconstrained.

What does all this have to do with signaling systems and design? That's for next time. Till then, blorp.

08 June 2009

Deep homology and design: a new series

Recently I was reading a superb review article [doi] on the subject of a famous and important cellular signaling pathway called the Notch pathway. The author, Mark Fortini of Thomas Jefferson University, quoted James Puckle (an 18th-century English inventor and writer) on the "wonderful frame of the human body" in which "so many strings and springs" which all must "be in their right frame and order" for life and concluding that "it is next to a miracle we survived the day we were born." (If you must know, it's maxim #914 in The Club, in a section called "Death.")

This reminded me of some personal tragedy in our own family, after which Puckle's conclusion was repeated almost verbatim. It also reminded me of my need to write about the amazing homology of developmental signaling mechanisms in animals. For many months, I've listed an article on "deep homology" as the subject of my next Journal Club. But this topic won't fit into one article review, so I've decided to turn it into a little series.

Here's what Fortini writes in his introduction, after quoting Mr. Puckle:
Surprisingly, research over the past few decades has revealed that the orderly differentiation and arrangement of these many physiological ‘‘strings and springs’’ are controlled by a relatively small number of developmental signaling pathways. These pathways, including the Notch, Ras/MAPK, Hedgehog, Wnt, TGFβ, and JAK/STAT pathways, among others, are widely conserved throughout the animal kingdom and they cooperate throughout development to pattern a diverse array of tissues in different animal species.
The lingo might seem strange, but I hope the point is clear. The vast diversity of animal life, with "endless forms most beautiful," is assembled through the action of a small set of signaling systems. And, remarkably, the systems are used in the same ways in animals that couldn't be more different in behavior or structure.

This fact raises interesting questions about design and evolution. Why so few systems? Why are they used again and again, for the very same purpose? Are these choices forced by design constraints of some kind, or is there another explanation? Could it have been otherwise? Can it be otherwise? I'll tackle those questions while discussing some recent experiments in evolutionary developmental biology, or evo-devo.

And what of this phrase "deep homology"? It was coined by some of the founding minds of evo-devo – Neil Shubin, Cliff Tabin and Sean Carroll – as they considered the fact that animal limbs of every kind are "organized by a similar genetic regulatory system that may have been established in a common ancestor." And we mean limbs of every kind: whale flippers, fish fins, bat wings, human arms, and, amazingly, insect limbs. Such disparate structures may not be evolutionarily homologous (meaning that they were modified from a common ancestor) but the signaling systems that create them are homologous.

This, then, is deep homology: the sharing of signaling mechanisms that are used to create diverse (though often functionally similar) animal structures. So please join me, and maybe we'll lure interesting commenters into the discussion.

12 May 2009

Theistic embryology controversy: a developing story

Get it? Heh. Anyway, go to Clashing Culture to see further discussion of the TE test.

09 May 2009

Weekly sampler 23

Okay, so not really weekly.

1. John Farrell has an interesting discussion of protein folding as a problem or challenge for evolutionary theory. His post includes quotes from experts with whom he has corresponded, and he cites the primary literature. (You know, peer-reviewed research articles written by people who are actually trying to understand the biochemistry of an early earth.) Here he's quoting Nick Matzke:
Even the very first polypeptides were pretty certainly not assembled all-at-once-from-scratch from a pool of 20+ kinds of amino acids in even proportions, in D- and L-form, as creationists and various beknighted physicists blithely assume. Probably the first time a proto-tRNA grabbed an amino acid and made a short chain, the chain was composed of glycine and few common hydrophobic amino acids and was quite short. Cavalier-Smith (2001) suggests that the original function may have just been a hydrophobic tail for association with a membrane. All of the improbability statistics are irrelevant in this sort of scenario, chirality isn't an issue, etc.
Let's go with 'benighted' lest anyone confuse an ignoramus in Glendora, California with, say, Sir John Polkinghorne.

2. I never really finished my junk DNA series, but there's still work to be done: falsehoods about non-coding DNA are beyond rampant. Recently at Adaptive Complexity, Michael White scored a direct hit on one of the major issues in this bogus controversy, and as usual it's a basic scientific principle (in this case, the concept of a null hypothesis). His post is required reading for those interested in any aspect of evolutionary genetics and especially those who have seen the standard genomic arguments of intelligent design creationists. Hat tip: Sandwalk.

3. Christians (and others) will find ThinkChristian.net interesting and provocative. I'll be writing there regularly starting this month. About science. And stuff.

4. Alister McGrath on Augustine on Darwin. His (very) basic point is a good one and he equivocates at the right times. But he seems to be allergic to randomness. After mentioning Augustine's emphasis on "divinely embedded causalities," he claims that "Augustine has no time for any notion of random or arbitrary changes within creation." More specifically, McGrath explores notions in Augustine's The Literal Meaning of Genesis that sound like ideas from a thoughtful design advocate. (Ideas, I'll add, that were articulated just as well by Howard Van Till in a slightly different context.) But, like most design proponents, he inveighs against randomness and then identifies it with Darwin:
Augustine would have rejected any idea of the development of the universe as a random or lawless process. For this reason, Augustine would have opposed the Darwinian notion of random variations, insisting that God's providence is deeply involved throughout. The process may be unpredictable. But it is not random.
I wonder if McGrath has thought hard about this. He may be right about Augustine, but I think it's a mistake to take such a hard line against "random variations." Why do so many people think that "embedded causality" is inconsistent with "random variation"? I don't get it.

5. And speaking of randomness, our reading group ("Random Readers") recently tackled some articles on determinism and evolutionary theory. We focused on a paper by Roberta Millstein titled "How Not to Argue for the Indeterminism of Evolution: A Look at Two Recent Attempts to Settle the Issue.” The "attempts to settle the issue" were responses to a paper that Millstein describes as a "full fledged defense of evolutionary indeterminism" that put the debate over evolutionary determinism "into high gear." That paper is "The Indeterministic Character of Evolutionary Theory: No 'No Hidden Variables' Proof But No Room for Determinism Either" by Robert N. Brandon and Scott Carson. Wait, Scott Carson? Yes, the same Scott Carson who writes one of the blogs I regularly follow: An Examined Life.

6. An answer to the famous question, "What is it like to be a bat?" Hat tip: Very Short List.

02 May 2009

Theistic embryology: the gathering storm

On Friday in the Christian Perspectives in Science seminar at Calvin College I gave a little talk on theistic evolution. The idea was to get some feedback on the simple ideas that I'll present at a symposium at the North American Paleontological Convention (NAPC) in Cincinnati in June. The symposium is titled "The Nature of Science and Public Science Literacy" and it's part of Education and Public Outreach Day at the NAPC. Here's the title and abstract of both the symposium talk and the seminar I gave at Calvin.
Why is there no controversy surrounding theistic embryology? Dissecting critical responses to theistic evolution.

Those who simultaneously express Christian belief and affirm evolutionary theory are said to espouse a position called "theistic evolution." The view holds the peculiar distinction of being reviled by both hard-line creationists (who call it "appeasement") and prominent atheist commentators (who deride it as fallacious). I argue that these critics typically fail to articulate objections that are specific to the view. Most creationist critics of theistic evolution object to one or both of these characteristics of the view: 1) its reliance on naturalistic explanation, a feature common to all scientific theorizing; or 2) its embrace of "random" causal events, a feature common to myriad scientific explanations. Most atheist critics of theistic evolution object to its openness to supernatural explanation, a feature of religious belief in general. Such criticisms, valid or not, fail to address anything specific to theistic evolution. In other words, attacks on theistic evolution are usually attacks on theism or attacks on evolution, but rarely represent specific criticisms of the theistic evolution position. To better understand the controversy surrounding theistic evolution, I propose that critiques of the position be considered in light of a lesser-known position we may (with tongue in cheek) call "theistic embryology." Theistic embryology describes the thinking of those who simultaneously express Christian belief and affirm basic theories in human developmental biology. Although the logic is indistinguishable from that of theistic evolution, the view is uncontroversial and the term "theistic embryology" is practically non-existent. I suggest that critiques of theistic evolution be subjected to the "theistic embryology test." Most critiques that claim to identify weaknesses in theistic evolution make arguments that are equally damaging to "theistic embryology" and so fail the test. Critiques that fail this whimsical test are likely to be arguments against belief, or against naturalistic explanation, and should be considered as such.